The Evaluation of Renal Transplant Candidates:

Clinical Practice Guidelines

 MUNKSGAARD
International Publishers Ltd.
35 Nørre Søgade, DK-1016 Copenhagen K, Denmark
ISBN: 87-16-16453-9
ISSN: 1601-2577

Financial support for the development of these guidelines was provided by the Ame-
rican Society of Transplantation. All authors and reviewers volunteered their time
and effort. Some of the publication costs were supported by an unrestricted grant
from Fujisawa Healthcare, Inc.

Printed in Denmark by P. J. Schmidt A/S, Vojens

 Copyright C Munksgaard 2001
ISSN 1601-2577

The Evaluation of Renal Transplant Candidates:

Clinical Practice Guidelines
Bertram L. Kasiske1, Charles B. Cangro2, Sundaram Hariharan3, Donald E. Hricik4,
Ronald H. Kerman5, David Roth6, David N. Rush7,
Miguel A. Vazquez8 and Matthew R. Weir2
for The American Society of Transplantation
1
Department of Medicine, Hennepin County Medical Center, University of Minnesota, Minneapolis, MN,
2
Department of Medicine, University of Maryland, Baltimore, MD,
3
Department of Medicine, Medical College of Wisconsin, Milwaukee, WI, 4Department of Medicine,
Case Western Reserve University, University Hospitals of Cleveland, Cleveland, OH,
5
Department of Surgery, University of Texas, Houston, TX,
6
Department of Medicine, University of Miami, Miami, FL, USA,
7
Department of Medicine, University of Manitoba, Winnipeg, Canada,
8
Department of Medicine, Southwestern Medical Center, University of Texas, Dallas, TX, USA
 Copyright C Munksgaard 2001
American Journal of Transplantation 2001; Suppl. 1: Vol. 2: 5–95
Munksgaard International Publishers ISSN 1601-2577

Contents

Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7 Pulmonary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 43
Purpose . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7 Cardiovascular Disease . . . . . . . . . . . . . . . . . . . . . . . . 44
Scope . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7 Psychosocial . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 52
Intended Users . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7 Genitourinary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 55
Endocrine . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 58
Methods and Results . . . . . . . . . . . . . . . . . . . . . . . . . 7 Coagulopathies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 61
Organization Scheme . . . . . . . . . . . . . . . . . . . . . . . 9 Age . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 62
Medications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 63
The Process . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9 Histocompatibility . . . . . . . . . . . . . . . . . . . . . . . . . . . . 64
Cancer . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12
Infections . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 22 Acknowledgments . . . . . . . . . . . . . . . . . . . . . . . . . . . 66
Recurrent Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . 28
Gastrointestinal . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 38 References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 67
 The Evaluation of Renal Transplant Candidates: Clinical Practice Guidelines
Introduction
Purpose
These guidelines are designed to facilitate the evaluation of
candidates for renal transplantation. Although they are meant
to be comprehensive, they cannot cover every possible as-
pect of the evaluation. Each renal transplant candidate is dif-
ferent and each faces unique clinical and psychosocial chal-
lenges resulting from end-stage renal disease (ESRD). It is
not possible to precisely define an evaluation process that
will adequately meet the needs of each individual. On the
other hand, the large amount of often conflicting information
pertaining to the evaluation of renal transplant candidates
make guidelines particularly helpful. It is in that spirit that
these guidelines were developed. They are intended to be an
aid, not a rigid set of rules, and as such their limitations
should be clearly recognized.
Scope
These guidelines cover issues pertinent to the assessment of
potential adult or pediatric renal transplant recipients. This tar-
get population is different from the general population, in that
they all have ESRD, or marked, progressive declines in renal
function that will soon result in ESRD. The patients targeted
in these guidelines also differ from most ESRD patients in
several important respects:
O The patients covered by these guidelines are facing elec-
tive surgery. The assessment and preparation of patients
with ESRD for any elective surgery may be similar to that
outlined in these guidelines, although the ethical and
moral issues pertaining to the use of living donors and/or
the limited supply of cadaveric kidneys may be unique to
the present population.
O The patients covered by these guidelines are patients who
will likely live longer than most patients with ESRD. As a
result, screening tests that may not be cost-effective for
some ESRD patients, e.g. screening for certain cancers,
may be cost-effective for the patients who are being re-
ferred for possible transplantation.
O The patients covered by these guidelines are being evalu-
ated and treated to better tolerate the risks and compli-
cations of the immunosuppressive medications.
Intended Users
These guidelines were designed to be used by physicians
and health care workers who evaluate potential renal trans-
plant recipients. They were not specifically developed for pri-
mary care physicians, but referring physicians may neverthe-
less find them useful. In addition, these guidelines may be
helpful to trainees at all levels who wish to learn about renal
transplantation. To the extent that these guidelines are evi-
dence-based, they may also be useful for those seeking to
identify future research needs. Finally, some health care plan-
ners and policy makers may find the guidelines helpful in
2001; Suppl. 1: Vol. 2: 5–95
understanding what is involved in the evaluation of renal
transplant candidates.
Methods and Results
The guidelines were developed by a subcommittee (the
authors) of the Clinical Practice Guidelines Committee of the
American Society of Transplantation, pursuant to a mandate
of the Society’s Board of Directors. They are an updated ver-
sion of guidelines previously developed on behalf of the
American Society of Transplantation (1). Work began in June
1999, and was completed in June 2000. The areas covered
were arbitrarily divided into sections (Table 1). Each section
was divided into specific topics. The recommendations are,
as much as possible, evidence-based.
For each recommendation we reviewed the pertinent medical
literature found by searching MEDLINE and bibliographies
from recent publications. However, in the absence of scien-
tific evidence we also relied on our personal experiences and
the opinions of colleagues. We did not limit our review to
topics for which there were adequate scientific data, but
rather covered all topics that we and others felt were perti-
nent, and made recommendations based on the best evi-
dence available. We graded the strength of the evidence sup-
porting each recommendation using the system developed
by the Canadian Task Force on the Periodic Health Examina-
tion (2) and adopted by the U.S. Preventative Services Task
Force (3). Accordingly, recommendations are graded A, B, C,
D, or E when:
A. There is good evidence to support the recommendation
that the condition be considered in the evaluation pro-
cess.
B. There is fair evidence to support the recommendation that
the condition be considered in the evaluation process.
C. There is poor evidence regarding the inclusion of the con-
dition in the evaluation process, but recommendations
may be made on other grounds.
D. There is fair evidence to support the recommendation that
the condition be excluded from consideration in the evalu-
ation process.
E. There is good evidence to support the recommendation
that the condition be excluded from consideration in the
evaluation process.
Draft versions of the guidelines were circulated among sub-
committee members, and each version was discussed and
revised. A consensus draft was then sent to other individuals
with expertise in specific areas covered by the guidelines.
These individuals were asked to review specific areas, and
invited to comment on any aspects of the guidelines. In virtu-
ally all instances, revisions were made as suggested by these
7
Kasiske et al.

Table 1: Table of contents

Section Table number
The process 2. The evaluation process
3. The timing of transplantation
4. Donor source
Cancer 5. Cancer
6. Renal cell carcinoma
7. Wilm’s tumor
8. Bladder cancer
9. Anogenital malignancies
10. Carcinoma of the uterine cervix
11. Carcinoma of the uterine body
12. Testicular cancer
13. Thyroid and other endocrinologic tumors
14. Kaposi’s and other sarcomas
15. Breast cancer
16. Colorectal cancer
17. Prostate carcinoma
18. Liver cancer
19. Multiple myeloma
20. Lymphoma and posttransplant lymphoproliferative disorders
21. Leukemia
22. Malignant melanoma
23. Non-melanoma skin cancer
24. Lung cancer
Infections 25. Human immunodeficiency virus
26. Tuberculosis
27. Cytomegalovirus
28. Infections in peritoneal dialysis patients
29. Dental infections and gingival hyperplasia
30. Influenza A and B
31. Pneumococcal infections
32. Childhood infections and immunizations
Recurrent disease 33. Consensus estimates of the rate of disease recurrence
34. Focal segmental glomerulosclerosis
35. Immunoglobulin A nephropathy
36. Henoch-Schoenlein purpura
37. Membranoproliferative glomerulonephritis
38. Idiopathic membranous glomerulonephritis
39. Hemolytic uremic syndrome/thrombotic thrombocytopenic purpura
40. Antiglomerular basement membrane/Goodpasture’s disease
41. Vasculitis including Wegener’s granulomatosus
42. Systemic lupus erythematosus
43. Primary oxalosis
44. Cystinosis
45. Fabry’s disease
46. Alport syndrome and antiglomerular basement membrane disease
47. Sickle cell disease
48. Amyloidosis
49. Mixed essential cryoglobulinemia
50. Waldenström’s macroglobulinemia
51. Immunoglobulin light chain deposition disease
52. Progressive systemic sclerosis (scleroderma)
Gastrointestinal 53. Colonic diverticulae
54. Peptic ulcer disease
55. Cholelithiasis
56. Liver disease
57. Hepatitis B Virus
58. Hepatitis C Virus
Pulmonary 59. Postoperative atelectasis, pneumonia, and respiratory failure

8 2001; Suppl. 1: Vol. 2: 5–95

 The Evaluation of Renal Transplant Candidates: Clinical Practice Guidelines

Table 1: (Contd.)
Section Table number
Cardiovascular 60. Ischemic heart disease
61. Left ventricular hypertrophy
62. Congestive heart failure
63. Cerebral vascular disease
64. Peripheral vascular disease
Psychosocial 65. Cognitive dysfunction and the ability to give informed consent
66. Chemical dependency
67. Mental illness
68. Noncompliance
Genitourinary 69. Ensuring adequate urinary drainage posttransplant
70. Approach to patients with a dysfunctional urinary excretory system
71. Native kidney nephrectomy
Endocrine 72. Obesity
73. Diabetes
74. Hyperparathyroidism
Coagulopathies 75. Preventing posttransplant graft thrombosis
Age 76. Advanced age
Medications 77. Anticipating posttransplant drug interactions
Histocompatibility 78. Blood group
79. Tissue typing
80. Crossmatch
81. Pretransplant sensitization

individuals, who are listed in the Acknowledgments. Since
transplantation is a rapidly changing field, portions of these
guidelines may soon become outdated. We cannot predict
what new developments may affect the way in which pa-
tients are evaluated for transplantation, nor can we know
when such information is likely to become available. How-
ever, we feel that these guidelines should be reviewed and
updated in 3 years.
Organization Scheme
Each topic is accompanied by a table that gives a structured
overview, including some or all of the following five items:
1) a list of potentially helpful screening tests,
2) a list of possible prophylactic measures that could be
undertaken,
3) the incidence or prevalence of the problem being con-
sidered,
4) the potential rationale for actions that could be taken,
5) our recommendations for specific actions.
The list of screening tests includes procedures that are poten-
tially useful, not procedures that are necessarily indicated.
The list of possible prophylactic measures similarly includes
potential steps that could be taken prior to transplantation,
but are not necessarily indicated. The incidence or prevalence
of the problem includes information pertinent to ESRD pa-
tients before and/or after transplantation. The rationale gives
the reasoning behind any of the major actions that could be
taken.
The Process
The evaluation (Table 2) is designed to meet the needs of
both the renal transplant candidates and the transplant cent-
er. For renal transplant candidates the process should provide
adequate information and education to allow informed,
shared decision-making. Ultimately, renal transplant candi-
dates need to decide not only whether they want to undergo
transplantation, but also whether they will accept a kidney
from a living donor (if a living donor is an option). Some po-
tential recipients on the cadaveric kidney waiting list may also
need to decide whether they are willing to accept a kidney
from a ‘‘marginal’’ cadaveric donor (Table 4).
In assessing the potential risks and benefits of transplan-
tation, the transplant team must first and foremost consider
what is in the best interests of the potential recipient. The
transplant evaluation may be most efficient and cost-effec-
tive if consideration is given to the order, or sequence, of
information gathering (Fig. 1). The evaluation starts when a
patient is referred to the transplant center. At this time it may
be expedient to gather some basic information on the candi-
date. This might include information on insurance coverage
to determine if transplantation is a viable option financially.

2001; Suppl. 1: Vol. 2: 5–95 9

Kasiske et al.

Table 2: The evaluation process

Rationale The evaluation of renal transplant candidates is costly and consumes valuable resources. It is important to identify
patients who are not suitable for transplantation in the most cost-effective manner possible.
Recommendations (C) The evaluation process should be as efficient as possible, and should minimize the number of tests and pro-
cedures that may ultimately prove to be unnecessary. However, potential benefits of testing include not only increas-
ing quality-adjusted life years for the recipient, but also maximizing the use of donated kidneys (a benefit to donors
and/or their families, and to society).

Information on the patient’s medical history, family history
(including potential living donors) and laboratory results may
also be collected at this time. An initial interview, or infor-
mation session, can then be scheduled.
The initial information session is a critical step in the evalu-
ation process. The patient should be encouraged to attend
with family members and/or friends, if possible. During the
session the patient should learn about the risks and benefits
of transplantation. Some patients may decide that they do
not want to proceed with the evaluation, thus obviating the
need for additional tests and procedures. The initial infor-
mation session is also extremely useful for the transplant
center. During this session it may be possible to identify one
or more obvious barriers to successful transplantation. Com-
mon examples of important barriers include ischemic heart
disease (IHD), substance abuse and/or medical noncompli-
ance. Patients with a major, potential barrier to transplantation
can be referred to appropriate specialists to be sure that the
barrier can be removed before additional tests are obtained.
For example, a patient with active substance abuse can be
referred for appropriate chemical dependency counseling
and additional evaluation can be deferred until a documented
period of abstinence has elapsed. Urologists and caregivers
with expertise in nutrition are particularly helpful for evalu-
ating children. Most transplant centers develop a network of
specialists, e.g. a psychologist, a psychiatrist, a gastro-
enterologist and a cardiologist, who become familiar with the
transplant evaluation process. These affiliated members of
the transplant team can be extremely helpful in ensuring a
comprehensive and cost-effective evaluation process. An ini-
tial interview and evaluation that efficiently identifies patients
who are not suitable for transplantation helps to avoid situ-
ations whereby patients believe that they are candidates for
transplantation when they are not.
Additional study of the best approach to the transplant evalu-
ation process is clearly warranted.
The timing of transplantation should maximize the use of the
patient’s own kidneys, but avoid the morbidity and expense
of access placement and dialysis treatments (Table 3). Pre-
emptive transplantation with a living related, living unrelated
(emotionally related) or cadaveric renal transplant requires
advanced planning and careful estimation of when a patient
will reach ESRD. Outcomes after preemptive transplantation
have been as good or better than outcomes after transplan-
tation preceded by dialysis in adults (5–10) and children (11–
14). Perfectly timed cadaveric transplantation is often not
possible, due to the long waiting time required to received a
cadaveric kidney. For patients listed in 1996, the median (and
95% confidence intervals) waiting times in months for a ca-
daveric transplant in the US were: 33.0 (31.6–34.5, nΩ7782)
for blood group O, 17.6 (16.7–18.5, nΩ5524) for group A,
40.2 (38.0–42.8, nΩ1225) for group B, and 8.1 (7.2–9.2, nΩ
638) for group AB (15). Patients need to be advised that sim-
ultaneous preparation for both dialysis and transplantation
should be made. Early placement on the cadaveric transplant
waiting list may help minimize the typical 1–4-year waiting
time. However, patients must have an estimated or measured
glomerular filtration rate that is not more than 20 ml/min to
accrue waiting time on the United Network for Organ Sharing
(UNOS) waiting list.

Once it is clear that a potential candidate still desires trans-

plantation, and that there are no major, obvious barriers, the
remainder of the evaluation can be completed. The need for
specific tests is in part determined by the medical and
psychological profile of the patient. These tests and pro-
cedures are detailed in the guidelines that follow. There are
few formal studies examining the process of transplant evalu-
ation. However, it is intuitively obvious that identifying candi-
dates who will ultimately not receive a transplant as early as
possible is a cost-effective, efficient use of scarce resources.
At least one retrospective review has substantiated this (4). Figure 1: The renal transplant candidate evaluation process.

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 The Evaluation of Renal Transplant Candidates: Clinical Practice Guidelines

Table 3: The timing of renal transplantation

Rationale Ideally, renal transplantation should be delayed long enough to maximize the use of the patient’s own kidneys. On
the other hand, preemptive transplantation can sometimes allow patients, especially children, to avoid the morbidity
and expense of acquiring a dialysis access and initiating dialysis treatments. Preemptive transplantation requires
advanced planning and careful attention to the rate of renal disease progression. Early referral to a transplant center
is mandatory.
Recommendations (C) Candidates should be referred to a transplant center as soon as it appears probable that renal replacement
therapy will be needed within the next 6–12 months.
(C) Some candidates who are not yet on dialysis should be considered for preemptive transplantation.
(C) The medical status of patients on the cadaveric transplantation waiting list should be reviewed at least every 2
years. Patients who are diabetic, older than 65, or have a medical condition that could change relatively quickly
should be reviewed at least annually.
(C) Candidates should be informed that placement on the cadaveric waiting list does not guarantee transplantation,
since changes in their medical status may delay or preclude transplantation.

Table 4: Donor source

Rationale Outcomes after renal transplantation are strongly influenced by the choice of the donor. Excellent data are available
to advise renal transplant candidates concerning the relative likelihood of successful transplantation from living re-
lated, living unrelated (emotionally related) and cadaveric donors.
Recommendations (C) Renal transplant candidates should be informed of the risks and benefits (to the donor and/or recipient) and of
the risks of using a particular donor, and should be allowed to refuse that donor based on medical grounds.

The waiting time for cadaveric transplantation is often several
years, and during this time the patient’s risk and suitability for
transplantation may change (Table 3). There are few data on
the frequency and/or timing of events that may change the
suitability for transplantation of a patient on the waiting list.
However, we recommend that the medical status of patients
on the cadaveric transplantation waiting list be reviewed at
least every 2 years, and more often if the patient is diabetic,
older than 65, or has a medical condition that could change
relatively quickly.
The evaluation of potential living kidney donors is beyond the
scope of these guidelines (Table 4). However, renal transplant
candidates may play an important role in deciding the ulti-
mate donor source. For example, renal transplant candidates
may decide not to accept a kidney from a particular living
donor because he/she does not want that potential donor to
suffer the discomfort of donor nephrectomy, or to be ex-
posed to even the small risk of donation. Similarly, renal trans-
plant candidates may decide not to accept a kidney from a
particular donor if the kidney from that donor has an in-
creased risk of a poor outcome. Therefore, it is important for
renal transplant candidates to fully understand the risks and
benefits associated with the use of a particular donor.
Specifically, renal transplant candidates should know that the
best results are obtained from living donors who are siblings
with 2 haplotype matches (16). The survival of transplants
from 1- and 0-haplotype matched living relatives is similar,
and while it is not as good as human leukocyte antigen
(HLA)-identical transplants, it is better than that of cadaveric
kidney transplants (16). Good results have also been reported
with donors who are not blood relatives, e.g. a spouse, a
life-long companion with strong emotional attachment or an
altruistic donor with no direct relationship to the recipient (16–
19). In general, kidneys from living donors are less likely to
have delayed graft function and more likely to have long-term
function compared to cadaveric donor kidneys (20, 21). Living
unrelated renal transplantation has also been encouraged by
the relatively low risk of the procedure.
In many centers, laparoscopic donor nephrectomy has re-
duced the morbidity of kidney donation and thereby encour-
aged living donors to donate (22–26). Laparoscopic donor
nephrectomy reduces the postoperative convalescence time
and enables donors to return to work quickly (22,24,25).
Laparoscopic donor nephrectomy is technically more difficult
than standard donor nephrectomy, and there may be a higher
incidence of delayed graft function, especially in the hands
of inexperienced surgeons. Although there do not appear to
be other adverse consequences for the donor or recipient
compared to standard donor nephrectomy, few long-term
follow-up data are available and the potential exists for a
greater incidence of late complications from peritoneal ad-
hesions in the donor who undergoes laparoscopic donation.
In general, strategies to expand the donor pool and thereby
alleviate the growing shortage of cadaveric organs and the
dramatic increase in waiting times have created new oppor-
tunities for renal transplant candidates on cadaveric waiting
lists (27,28). Some of the newer strategies include the use
of: non-heart beating donors (29), donors with long-standing
hypertension and mild renal dysfunction, or kidneys with ana-
tomic abnormalities (30,31). Several transplant centers have
used dual renal transplants from the same donor in order to
optimize the amount of renal mass transplanted from older

2001; Suppl. 1: Vol. 2: 5–95 11

Kasiske et al.

Table 5: Cancer
Incidence Although the incidence varies by tumor type, the overall incidence of cancer in hemodialysis patients is higher than
in the general population.
Rationale It is generally accepted that immunosuppression increases the morbidity and mortality of cancer. Effective screening
and treatment of cancer prior to transplantation could reduce the risk of posttransplant malignancy. It is prudent to
allow sufficient time between the treatment of malignancy and transplantation to exclude patients who will otherwise
develop recurrence.
Recommendations (A) Patients should be screened for cancer at the time of evaluation and while on the waiting list, following recom-
mendations for the general population.
(B) An appropriate disease-free interval before transplantation should be used to reduce the risk of recurrence (see
tables that follow for specific types of cancer).

donors with reduced glomerular filtration rate (32–39). Al-
though there are no controlled trials in this area, centers
transplanting dual ‘‘marginal’’ kidneys into one recipient have
generally reported that patient and graft survival rates are
comparable to those of single kidney transplants that are not
from marginal donors (35,36). They have also reported that
graft survival and/or renal function from dual kidney trans-
plants is better than that from single marginal donor kidneys
(34,37,38). Transplantation of two pediatric kidneys into adult
recipients has also been associated with patient and graft
survivals comparable to those of single cadaveric transplants
from adult donors (40).
If the use of a marginal cadaveric kidney is contemplated,
renal transplant candidates should be fully informed of the
risk and benefits. A marginal kidney can be defined as one
that confers a higher than expected risk of graft failure or
medical complications for the recipient (41). Characteristics
of a marginal donor might include: age ⬎60 years, whether
other organs were removed from the donor, positive hepatitis
C antibody, serum creatinine ⬎2.0 mg/dl, hypertension and
non-heart beating donor status (41,42). Renal transplant can-
didates should be allowed to refuse a marginal kidney and
instead remain on the waiting list.
Cancer
Cancer is responsible for 1–4% of deaths in the dialysis
population (Table 5)(43). Patients with ESRD receiving dialy-
sis have an increased risk of cancer compared to the general
population (44). This relative risk of cancer is especially high
for younger patients and for specific organs (44). Data on the
standardized incidence ratio (ratio of observed-to-expected
cancers) has been recently published from the dialysis regis-
tries in three continents, and include data from the United
States Renal Data System, the European Dialysis and Trans-
plant Association, and the Australia and New Zealand Dialysis
and Transplant Registry (44). This report includes information
on cancer risks for dialysis patients based on follow-up of
over 800 000 patients for an average of 2.5 years and is the
most complete information available on malignancies in the
ESRD population (44). Previous analyses have suggested
that cancer screening applied to the entire dialysis population
may not be cost-effective (45). Nevertheless, subgroups of
dialysis patients who have longer life expectancies (such as
renal transplant candidates) may have much to gain from
screening (46). The ethical imperative to maximize the bene-
fit from donor kidneys, a scarce resource, should also be
taken into consideration.
Although cancer is responsible for 9–12% of deaths in renal
transplant recipients (43), it is not clear what effect pretrans-
plant screening may have on reducing the incidence of post-
transplant malignancies. Posttransplant immunosuppression
likely inhibits surveillance mechanisms that otherwise
counteract the development of malignant cell growth (47,48).
Thus, it is reasonable to assume that eliminating malig-
nancies or premalignant lesions prior to transplantation may
help to reduce the incidence of posttransplant malignancy.
However patients with ESRD who have been successfully
treated for their cancer are generally considered to be suit-
able candidates for renal transplantation. Review of previous
reports and especially data on recurrent cancers (posttrans-
plant) from the Cincinnatti Transplant Tumor Registry (CTTR)
allows us to suggest some general guidelines on waiting
times between treatment of the specific cancers and renal
transplantation. In the CTTR, 54% of cancer recurrences oc-
curred in patients who had their pretransplant malignancies
treated within 2 years of transplantation, 33% of recurrences
occurred in patients treated 2–5 years before transplantation
and 13% of recurrences occurred in patients treated more
than 5 years before transplantation (47). While these stat-
istics may provide general guidelines, the risk of tumor recur-
rence has to be balanced against the benefits of renal trans-
plantation for each individual patient.
Most patients treated for cancer benefit from a waiting
period prior to renal transplantation. For most patients pre-
viously treated for cancer, it appears prudent to recommend
a minimum waiting period of 2 years. In the case of some
cancers at increased risk for recurrence, a longer waiting in-
terval, e.g. 5 years, should be considered. Some patients with
cancers incidentally discovered at the time of evaluation may
not require a waiting period prior to renal transplantation.
Dialysis patients have a high risk of renal cancer, especially
in younger patients and in those with ESRD from toxic, infec-

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 The Evaluation of Renal Transplant Candidates: Clinical Practice Guidelines

Table 6: Renal cell carcinoma

Possible screening Urinalysis and urine cytology
Radiographic imaging of the native kidneys, e.g. ultrasound, computerized tomography, and/or magnetic resonance
imaging
Incidence Renal cell cancer is 3.3–9.9 times more common in dialysis patients than in the general population. The recurrence
rate for clinically apparent renal cancers after renal transplantation is 27%. Incidentally discovered renal cancers recur
in only about 1%.
Rationale Mortality for recurrent renal cancer after kidney transplantation has been reported to be as high as 80%. Most
recurrences (59%) of renal cancers occur when patients who have suffered from symptomatic renal cancer while
on dialysis are transplanted less than 2 years after treatment of their cancers.
Recommendations (C) Patients at high risk for renal cell carcinoma should be screened with both radiographic imaging (ultrasound,
computerized tomography and/or magnetic resonance imaging) and urine cytology.
(B) For patients with symptomatic renal cell carcinoma, a waiting time of at least 2 years after surgical removal is
recommended before transplantation. Some large (Ø5 cm) and/or invasive renal cancers may warrant a 5-year
waiting period.
(B) No specific waiting time is recommended for small (⬍5 cm) renal cell cancers discovered incidentally, i.e. at the
time of native kidney nephrectomy that is performed for other reasons.

Table 7: Wilm’s tumor

Possible screening Urinalysis
Radiographic imaging of the native kidneys, e.g. ultrasound, computerized tomography, and/or magnetic resonance
imaging
Mutations in the WT1 gene (high risk patients).
Incidence The recurrence rate after renal transplantation for patients who have been treated for Wilm’s tumor is 13%.
Rationale Mortality for recurrent Wilm’s tumor after renal transplantation is 80%. Most patients who develop recurrences after
renal transplantation have been transplanted less than 2 years after treatment of their tumors.
Recommendations (C) There is no evidence for or against screening renal transplant candidates for Wilm’s tumor.
(B) Wait a minimum of 2 years after treatment of Wilm’s tumor before proceeding with renal transplantation.
(B) Due to the high risk of developing Wilm’s tumor, patients with Denys-Drash syndrome should undergo bilateral
nephrectomy prior to transplantation.

tious or obstructive uropathies (Table 6)(44). The standard-
ized incidence ratio of renal carcinoma in the dialysis popula-
tion was 9.9 (95% confidence interval 7.7–12.3) in Australia
and New Zealand, 3.3 (3.1–3.6) in Europe and 3.7 (3.5–3.9)
in the US (44). Patients with ESRD from analgesic nephro-
pathy, Balkan nephropathy or Chinese-herb nephropathy are
at especially high risk for urothelial malignancies (49–51). The
duration of time on dialysis increases the relative risk of renal
cancer for dialysis patients (44). Acquired cystic disease in-
creases in prevalence with the duration of dialysis and may
be associated with increased risk of renal cancer in ESRD
patients (52,53). However, some evidence suggests that ac-
quired cysts may regress after transplantation (54). Renal
carcinomas are relatively common in renal transplant recipi-
ents and have a high mortality rate (47,55). Recurrent renal
cancer after renal transplantation is associated with a mor-
tality rate of 80% (47). There is no evidence that screening
all renal transplant candidates is effective in reducing mor-
tality from renal cell carcinoma, although studies using radio-
logical screening have led to a diagnosis of renal cell cancer
in 3.4–3.9% of asymptomatic renal transplant candidates
(53,56). However, patients at especially high risk for renal
cancer (such as those outlined above) may benefit from
screening prior to renal transplantation.
Incidentally discovered renal neoplasms in ESRD patients
have a very low recurrence rate after renal transplantation
(1%), and only those tumors which are large or extend be-
yond the renal capsule warrant a waiting time before trans-
plantation (47,57). Symptomatic renal carcinomas are much
more serious, with overall recurrence rates of 27% (with 59%
recurrence in patients who are treated less than 2 years be-
fore transplantation, 33% recurrence in patients treated be-
tween 2 and 5 years before transplantation, and 8% recur-
rence in patients treated for cancer more than 5 years before
transplantation) (47). A waiting time of 5 years between treat-
ment of renal cancer and transplantation would eliminate
most recurrences and is recommended for large (⬎5 cm),
symptomatic renal cancers. A waiting time of 2 years would
eliminate more than half of all recurrent renal cancers and is
appropriate for most other patients with smaller renal can-
cers. At the end of the waiting period, appropriate radio-
graphic imaging, usually with computerized tomography and/
or magnetic resonance imaging, is needed to ensure that the
patient remains disease-free.
Most recurrences of Wilm’s tumor occur in patients treated
for their cancers 2 years or less before renal transplantation
(Table 7)(47). Factors associated with recurrences include

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Kasiske et al.

Table 8: Bladder cancer

Potential screening Urinalysis
Urine cytology
Voiding cystourethrogram
Cystoscopy
Incidence Bladder cancer is 1.4–4.8 times more common in dialysis patients than in the general population. The rate of
recurrence after renal transplantation is 29%.
Rationale The mortality for recurrent bladder cancer after renal transplantation is 38%. Most patients with carcinomas of the
bladder who develop recurrences after renal transplantation have been treated for their cancers less than 2 years
before transplantation. Patients with in situ or non-invasive papilloma tumors have a very low risk of recurrence.
Recommendations (C) It is unnecessary to screen all renal transplant candidates for bladder cancer; however, high-risk patients may
benefit from screening.
(B) Renal transplant candidates with bladder cancer should wait at least 2 years between treatment of their bladder
cancer and transplantation.
(B) Patients with in situ cancer or non-invasive papillomas need not delay transplantation.

Table 9: Anogenital malignancies

Possible screening History and physical examination (with pelvic examination in women)
Anoscopy, sigmoidoscopy and/or colonoscopy
Incidence There are no data on the recurrence rate of anogenital cancers after renal transplantation
Rationale Metastases and death from anogenital cancer can occur in renal transplant recipients. Lesions are treatable. Immuno-
suppression favors the progression of anogenital cancers.
Recommendations (B) History and physical examination (with pelvic examination in women) should be part of the pretransplant evalu-
ation.
(C) There are insufficient data to recommend or not recommend waiting times between the treatment of anogenital
carcinomas and renal transplantation.

incomplete tumor removal and metastases (55). The presence
of pulmonary metastases, unlike abdominal metastases, do
not appear to increase mortality or risk of recurrence (58,59).
Patients who have been treated more than 5 years before
transplantation have a favorable prognosis (60). It is therefore
recommended to wait at least 2 years after treatment of Wilm’s
tumor before proceeding with renal transplantation. There are
no studies investigating the effectiveness of screening for
Wilm’s tumor prior to transplantation.
Denys-Drash syndrome (DDS) is a rare autosomal recessive
disorder arising from heterozygous mutations in the Wilm’s
tumor suppresser gene, WT1 (61,62). The syndrome ac-
counted for 13/6230 (0.3%) of ESRD among individuals
aged 20 and younger in 1994–98 (63). The features of DDS
include Wilm’s tumor, XY gonadal dysgenesis and ESRD sec-
ondary to diffuse mesangial sclerosis, but expression of these
features is variable. Because of the risk of Wilm’s tumor, pa-
tients with DDS should undergo bilateral nephrectomy either
upon initiation of dialysis or at transplant. Some clinicians ad-
vocate preemptive bilateral nephrectomy and early transplan-
tation as soon as the diagnosis of DDS is established, al-
though there is no consensus on the optimal timing of neph-
rectomies in this condition. The same considerations may
also be applicable in other rare congenital conditions that
have been linked to mutations in WT1 (64,65).
The risk of bladder cancer is increased in dialysis patients,
especially for those with renal failure secondary to toxic, in-
fectious or obstructive nephropathies (Table 8) (44). The
standardized incidence ratio of bladder cancer in the dialysis
population was 4.8 (95% confidence interval 3.6–6.2) in
Australia and New Zealand, 1.5 (1.4–1.7) in Europe and 1.4
(1.3–1.5) in the US (44). Patients with bladder carcinoma in
situ or non-invasive papillomas tend to have a low risk of
recurrence of their bladder cancers and do not require a wait-
ing period (60). Invasive bladder carcinoma has a high recur-
rence rate after renal transplantation (29%) (47). The mor-
tality from recurrent bladder carcinoma after transplantation
is 38% (47). Most patients with recurrent bladder carcinoma
in the CTTR received therapy for their cancer less than 2
years before transplantation (60). It is recommended to allow
a minimum of 2 years’ waiting time between treatment of
bladder cancer and renal transplantation to eliminate most
recurrent bladder cancers (60). There are no studies that pro-
vide data on whether routinely screening renal transplant
candidates for bladder cancer is effective. It is reasonable to
screen renal transplant candidates with ESRD secondary to
toxic, infectious or obstructive uropathies, or those who be-
long to other high risk groups such as patients exposed to
industrial carcinogens, patients previously treated with cyclo-
phosphamide or those with a history of infection with Schis-
tosoma hematobium.

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 The Evaluation of Renal Transplant Candidates: Clinical Practice Guidelines

Table 10: Carcinoma of the uterine cervix

Possible screening Cervical cytology and pelvic examination
Incidence Cervical cancer is 1.6–4.0 times more common in dialysis patients than in the general population. The recurrence
rate after renal transplantation is approximately 6%.
Rationale Renal transplant recipients with recurrent disease have high mortality. Favorable prognostic factors for patients
treated with cancer of the uterine cervix prior to renal transplantation include in situ lesions and a delay in transplan-
tation of more than 2 years after treatment.
Recommendations (B) Cervical cytologic and pelvic examination should be performed every 1–3 years in women aged 20–65 years.
(B) Patients with localized, successfully treated carcinoma of the uterine cervix may benefit from a waiting period of
2, and in some cases 5 years prior to transplantation.
(C) It is not clear what waiting time is best for renal transplant candidates with invasive carcinoma of the uterine
cervix.

Table 11: Carcinoma of the uterine body

Possible screening Cervical cytology and pelvic examination
Incidence Uterine carcinoma is 0.8–1.0 as common (i.e. not significantly different) in dialysis patients than in the general
population. The recurrence rate after renal transplantation is 4%.
Rationale The mortality rate for renal transplant recipients with recurrent cancer of the body of the uterus is high. Recurrence
rates of cancers of the uterine body are lower for patients receiving a transplant more than 2 years after treatment
of their cancers.
Recommendations (B) Cervical cytologic and pelvic examination should be performed every 1–3 years in women aged 20–65 years
(who have a cervix).
(B) Patients with cancer of the body of the uterus should wait at least 2 years after treatment of their cancer before
renal transplantation.

The incidence of vulvovaginal and penile cancers is increased
in dialysis patients compared to the general population (Table
9) (44). There are no data regarding recurrence rates of ano-
genital malignancies when treated prior to renal transplan-
tation. There is growing evidence that many if not most
anogenital malignancies are caused by cutaneous viral infec-
tions. Genital warts (condylomata acuminata), squamous
intraepithelial neoplasias and anogenital squamous cell carci-
nomas have been linked to human papilloma virus (HPV)
infection, particularly HPV 16 (66–69). Not surprisingly,
immunosuppression appears to play a very important role in
the progression of anogenital carcinomas, and some lesions
may regress after discontinuation of immunosuppression
(70). There have been variable responses to reinstitution of
immunosuppression in a limited number of reported patients
(70). There are insufficient data to make recommendations
regarding waiting times between treatment of anogenital car-
cinomas and renal transplantation, or regarding the efficacy
of screening. However, physical examination with visualiza-
tion of the penis, vulvovaginal and anal mucosa would be
expected to detect most lesions. Patients with lesions should
be referred for evaluation and treatment prior to transplan-
tation.
The risk of cancer of the uterine cervix is increased several-
fold in dialysis patients when compared to the general popu-
lation (Table 10) (44). The standardized incidence ratio of cer-
vical cancer in the dialysis population was 4.0 (95% confi-
dence interval 2.4–6.6) in Australia and New Zealand, 1.6
(1.3–1.8) in Europe and 2.5 (2.2–2.8) in the US (44). Carci-
nomas of the uterine cervix are also more common in renal
transplant recipients (71). The recurrence rate among treated
patients is 6% (47). Cervical carcinoma has been linked to
viral infection, especially with the HPV virus (68,72–74). Im-
munosuppression associated with renal transplantation in-
creases the incidence and mortality of cervical carcinoma.
The mortality for renal transplant recipients with recurrent cer-
vical carcinoma is high (60). Favorable prognostic factors in
renal transplant recipients with cancer of the uterine cervix
prior to transplantation included in situ lesions (58% of
lesions) and treatment more than 5 years before transplan-
tation (54%) (47,60). Patients with localized, successfully
treated cancer of the uterine cervix may reduce their risk of
recurrence by waiting 2–5 years before transplantation. It is
not clear what waiting time is best for renal transplant candi-
dates with more invasive carcinomas of the uterine cervix.
Although there are no prospective studies for dialysis or
transplant patients, it is prudent to recommend cervical cy-
tology screening (Papanicolaou testing) and pelvic examina-
tion for all women who are or have been sexually active and
who have a cervix (75). The optimal frequency of cervical
cytology screening has not been established, but should be
at least every 3 years (76), and in some patients at higher
risk (such as immunosuppressed renal transplant recipients)

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Kasiske et al.

Table 12: Testicular cancers

Possible screening Medical history and physical examination
Incidence The recurrence rate of testicular cancer after renal transplantation is 5%.
Rationale Testicular cancer in the general population causes widespread metastases and high mortality. Close surveillance in
renal transplant recipients has been effective in preventing mortality from recurrent disease. Most patients with
testicular cancers (and no recurrences) have received a renal transplant more than 2 years after treatment of their
cancers.
Recommendations (C) It is prudent to perform testicular examination as part of the evaluation of transplant candidates.
(B) Patients with testicular cancers should wait a minimum of 2 years between treatment of their cancers and renal
transplantation.

Table 13: Thyroid and other endocrine tumors

Possible screening Medical history and physical examination with palpation of the thyroid gland
Incidence Thyroid carcinoma is 1.9–5.9 times more common in dialysis patients than in the general population. The recurrence
rate after renal transplantation is 7%.
Rationale Many thyroid cancers in dialysis patients have favorable features (low-grade papillary tumors, accidentally discovered
tumors during parathyroidectomy). The mortality rate from recurrent thyroid cancer is low. A favorable prognostic
indicator for thyroid cancer is waiting more than 2 years before transplantation.
Recommendations (C) Medical history and physical examination with palpation of the thyroid gland should be part of the routine
pretransplant evaluation.
(B) Wait at least 2 years after treatment of thyroid cancers before renal transplantation.

more frequent testing may be prudent (77). The role of
screening for HPV remains to be determined.
Patients on dialysis have a similar incidence of cancer of the
body of the uterus as the observed incidence in the general
population (Table 11) (44). The standardized incidence ratio
of uterine cancer in the dialysis population was 1.0 (95%
confidence interval 0.4–2.4) in Australia and New Zealand,
0.0 (0.7–1.0) in Europe and 0.0 (0.8–1.0) in the US (44).
The recurrence rate after transplantation is 4%. Patients with
recurrent cancer of the body of the uterus have high mortality
(60). Most patients with cancer of the body of the uterus
were transplanted more than 2 years after treatment of their
cancer and 50% of patients were transplanted more than 5
years after treatment of their cancer (47, 60). It is recom-
mended to wait at least 2 years after treatment of cancer of
the body of the uterus before renal transplantation.
Testicular cancers, although relatively uncommon, constitute
one of the most important cancers in young men (78). The
recurrence rate of testicular cancer after renal transplantation
is 5% (Table 12) (47). Testicular cancers include seminomas,
teratomas, embryomas, choriocarcinomas, mixed cell and
unclassified tumors (60). No deaths have been reported in
the CTTR from recurrent testicular cancers (60). Most pa-
tients had an interval exceeding 2 years between treatment
of their neoplasms and transplantation, including waiting
periods exceeding 5 years before transplantation for 58%
(60). It is recommended to wait a minimum of 2 years prior
to renal transplantation for patients treated for testicular can-
cer. No firm guidelines have been established in the general
population regarding screening for testicular cancer (78).
Although no prospective data are available, it is prudent to
discuss testicular self-examination with patients and for
physicians to perform testicular examination as part of the
evaluation of renal transplant candidates as in the general
population (76). Patients at increased risk for testicular can-
cer, such as those with a history of cryptorchidism or testicu-
lar atrophy, should undergo screening for testicular cancer as
part of their pretransplant evaluation.
The frequency of cancers of the thyroid and endocrine
glands in dialysis patients is more than 2-fold higher than in
the general population (Table 13) (44, 79). The standardized
incidence ratio of thyroid and other endocrine malignancies
in the dialysis population was 5.9 (95% confidence interval
3.3–10.7) in Australia and New Zealand, 1.9 (1.5–2.3) in
Europe and 2.4 (2.1–2.8) in the US (44). The incidence ap-
pears to be even higher in young women on dialysis (80).
In some reports, renal transplant recipients also have a
higher incidence of thyroid cancers (71,80). The recurrence
rate for thyroid cancer is 7% (47). Several cancers were in-
cidental findings during parathyroidectomy for hyperpara-
thyroidism (60). Favorable features of patients with thyroid
cancers include treatment more than 5 years before trans-
plantation in 35% of patients, and the presence of low

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 The Evaluation of Renal Transplant Candidates: Clinical Practice Guidelines

Table 14: Kaposi’s and other sarcomas

Possible screening Medical history and physical examination
Incidence The recurrence rate of sarcomas after renal transplantation is 29%.
Rationale Patients with extensive disease, visceral involvement and/or metastases have high mortality. Most patients with
recurrent sarcomas after renal transplantation have received their transplants less than 2 years after treatment of
their cancers.
Recommendations (C) Patients should be screened by history and physical examination.
(B) Consideration should be given to measuring antibodies to human herpes virus-8 in patients who are at high risk
for Kaposi’s sarcoma, e.g. patients from endemic areas such as Africa and the Middle East. Patients who are antibody
positive may wish to forego transplantation due to the high risk of posttransplant Kaposi’s sarcoma.
(B) Patients who have had Kaposi’s sarcoma following a prior transplant may wish to forego another transplant due
to the high likelihood of recurrence.
(B) Wait at least 2 years prior to transplantation for patients treated for Kaposi’s or other sarcomas.

Table 15: Breast cancer

Possible screening Medical history and physical examination
Mammography
Possible prophylaxis Tamoxifen and/or raloxifene
Incidence Breast cancer is 0.8–1.5 times as common (i.e. not significantly increased) in dialysis patients compared to the
general population. The rate of recurrence for breast cancer after renal transplantation is 23%.
Rationale The mortality rate for recurrent breast cancer after renal transplantation is 76%. Breast cancer has a high rate of
recurrence and high mortality after renal transplantation, even when most patients wait more than 2 years after
treatment before undergoing transplantation.
Recommendations (C) Breast examination should be performed as part of the pretransplant evaluation and annually thereafter.
(A) Women age 50–69 should undergo mammography annually.
(B) Women age 40–49 should undergo mammography annually.
(B) Women younger than 40 or older than 69 who are at increased risk for breast cancer should also be considered
for mammography.
(B) Most patients with invasive breast cancer should wait at least 5 years before transplantation, although a wait of
only 2 years can be considered for patients with some early-stage breast cancers.
(C) Women at increased risk for breast cancer may be offered tamoxifen to reduce this risk, if the potential for risk
reduction appears to outweigh the risk of therapy.

grade papillary carcinomas in 59% of patients (47). The
mortality rate from recurrent thyroid cancer is 10% (60). It
is recommended to wait at least 2 years prior to renal trans-
plantation in patients treated for thyroid carcinomas.
Sarcomas are rarely seen in the dialysis population, but are
relatively common in renal transplant recipients (81–83).
Sarcomas treated prior to transplantation recur in 29% after
transplantation (Table 14) (47). Waiting 2–5 years reduces
the chances of recurrence (60). Patients who have been
successfully treated for posttransplant Kaposi’s sarcoma
have a very high rate of recurrence if they are re-trans-
planted and immunosuppression is re-instituted (84,85).
It has recently become evident that human herpes virus-8
(HHV-8) may be the cause of many, if not most, cases of
Kaposi’s sarcoma (86–91). In a recent study, 17/25 (68%) of
renal transplant recipients who had HHV-8 antibodies de-
veloped Kaposi’s sarcoma, compared to only 1/33 (3%) sero-
negative patients (92). In another study, 9/32 (28%) with
antibodies to HHV-8 developed Kaposi’s sarcoma after renal
transplantation (93). In this retrospective study, 32/400 (8%)
of patients were antibody positive, suggesting that routine
screening was warranted in this population (93). Altogether,
these studies suggest that screening for HHV-8 may be indi-
cated in populations at increased risk for Kaposi’s sarcoma.
Risk factors include African or Middle East origin, past infec-
tion with hepatitis B, a family history of Kaposi’s sarcoma,
homosexual orientation and a prior history of Kaposi’s sar-
coma (87,88,90–92). Patients who are HHV-8 antibody posi-
tive may wish to forego transplantation.
Breast is the most common site for cancer (excluding non-
melanoma skin cancer and in situ cancer of the uterine cer-
vix) in female ESRD patients (Table 15) (80). The standard-
ized incidence ratio of breast cancer in the dialysis popula-
tion was 1.5 (95% confidence interval 1.1–2.0) in Australia
and New Zealand, 1.0 (0.9–1.0) in Europe and 0.8 (0.8–
0.9) in the US (44). Female renal transplant recipients ap-
pear to have a lower relative risk of breast cancer than the
general population, possibly due to an effect of enhanced
surveillance on mortality and/or lead-time bias (48,83,94).

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Kasiske et al.

Table 16: Colorectal cancer

Possible screening Fecal occult blood
Sigmoidoscopy
Colonoscopy
Double contrast barium enema X-ray
Incidence Colon cancer is 0.9–1.2 times as common (i.e. not significantly increased) in dialysis patients compared to the
general population. The recurrence rate of colon cancer after renal transplantation is 21%.
Rationale The mortality rate for recurrent colorectal cancer after renal transplantation is 63%. There is a high rate of recurrence
of colon cancer for patients transplanted 2–5 years after treatment of cancer.
Recommendations (A) Patients at average risk for colorectal cancer should initiate screening by age 50 with annual fecal occult blood
testing and sigmoidoscopy every 5 years, or total colon examination either by colonoscopy (every 10 years) or by
double contrast barium enema (every 5–10 years). Patients at higher risk for colorectal cancer will need earlier and
more frequent screening, including total colon examination.
(B) Patients previously treated for colon cancer should wait at least 5 years before renal transplantation. Patients
with Dukes A or B1 colon cancer have lower recurrence rates and could have shorter waiting periods prior to renal
transplantation.

The rate of recurrence for previously treated breast cancer
after renal transplantation is 23% (47). This high rate of re-
currence occurred even with a waiting time exceeding 2
years after treatment of the cancer for most patients, and
a waiting time longer than 5 years for 51% of patients (47).
Factors associated with an increased risk of recurrence of
breast cancer included nodal involvement, bilateral disease,
inflammatory carcinoma and previous bone metastasis. Re-
current breast cancer after renal transplantation has a mor-
tality of 76% (47).
Dialysis patients who are treated for breast cancer should
wait at least 5 years prior to renal transplantation. A shorter
waiting period of 2 years may be safe for some patients with
early-stage breast cancers (47). Screening for breast cancer
should include clinical breast examinations and mammo-
graphy performed annually for women between the ages of
50 and 69 years, with screening at an earlier age and in older
women who are at high-risk (76,95). The American Cancer
Society recommends annual mammography for women of
average risk beginning at age 40 and cessation of annual
screening determined not by age but by comorbidity (96).
Breast self-examination starting at age 20 and performed
every month is also recommended by the American Cancer
Society. In addition, the American Cancer Society recom-
mends clinical breast examination every 3 years between the
ages of 20 and 40 and every year for women over 40 (96).
Women with a history of breast cancer are at increased risk
for a second primary breast cancer. Additional risk factors
include a family history of breast cancer in a mother and/or
sister, proliferative benign breast disease (particularly atypical
hyperplasia), radiolographically dense breasts or calcifi-
cations, early age at menarche and late age at first birth.
It has recently been recommended that women in the gen-
eral population at increased risk for breast cancer (at least
1.7% over 5 years) ‘‘may be offered tamoxifen to reduce their
risk’’ (97). Defining appropriate candidates for tamoxifen re-
quires assessment of potential risk reduction from tamoxifen,
taking into account the risk of breast cancer risk based on
age, race, family history, etc. This risk reduction must then be
weighed against the risk of adverse effects of tamoxifen, tak-
ing into account an individual’s risk for endometrial cancer,
stroke, vascular events and fractures. Risk-benefit indexes
have been developed for women in the general population
(98). How these calculations apply to patients with ESRD is
unclear. In contrast to tamoxifen, raloxifene is not generally
recommended for breast cancer risk reduction per se (97).
The incidence of colorectal cancer in the dialysis population
does not appear to be increased (Table 16). The standardized
incidence ratio of intestinal cancer (excluding stomach and
liver) in the dialysis population was 1.1 (95% confidence in-
terval 0.9–1.5) in Australia and New Zealand, 0.9 (0.9–1.0)
in Europe and 1.2 (1.1–1.2) in the US (44). The incidence of
colon cancer in renal transplant recipients is not elevated dur-
ing the first 10 years after renal transplantation, but in some
reports appears to markedly increase 10–20 years after trans-
plantation (80). The recurrence rate of colon cancer after re-
nal transplantation is 21% (47). Mortality from recurrent colon
cancer after renal transplantation may be as high as 63%
(47). Most patients with previously treated colon cancer and
recurrence after transplantation (73%) had received their
transplants 2–5 years after treatment of their cancers. It is
recommended to wait at least 5 years before transplantation
for patients treated for colon cancer. Patients with Dukes A
or B1 colon cancer have lower recurrence rates, and a shorter
waiting period of 2 years may be appropriate (47).
There is general consensus that individuals in the general
population should begin colorectal cancer screening by age
50 using annual fecal occult blood testing with sigmoidosco-
py performed every 5 years, or a total colon examination
either by colonoscopy (every 10 years) or by double contrast
barium enema (every 5–10 years) (99–105). Digital rectal
examination should be performed at the time of the sig-
moidoscopy or the total colon examination (every 5–10
years) (100). There continues to be debate over the relative

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 The Evaluation of Renal Transplant Candidates: Clinical Practice Guidelines

Table 17: Prostate cancer

Possible screening Digital rectal examination
Prostate specific antigen (PSA)
Incidence Prostate cancer is 0.7–1.2 times as common (i.e. not significantly increased) in dialysis patients compared to the
general population. The recurrence rate of prostate cancer after renal transplantation is 18%.
Rationale Renal transplant recipients with metastatic prostate cancer at presentation have a mortality rate of 33%. Nearly one
half of all recurrences of prostate cancer have occurred in patients who have received a transplant less than 2 years
after treatment of their cancers.
Recommendations (C) Digital rectal examination and PSA determination should be offered annually beginning at age 50 to men who
have a life expectancy of at least 10 years and to younger men who are at high risk for prostate cancer. Information
should be provided to patients about the risks and benefits of screening.
(B) Patients with prostate cancer should wait at least 2 years after treatment of their disease before renal transplan-
tation. Patients treated for localized lesions may not require a waiting interval.

merits of different screening strategies (106), and patient
preferences should probably be taken into account (107). In-
dividuals at higher risk for colorectal cancer, including those
with previous adenomatous polyps or colon cancer, family
history of colorectal cancer or adenomatous polyps in first
degree relatives, family history of familial adenomatous
polyposis or hereditary non-polyposis colon cancer, or indi-
viduals with inflammatory bowel disease should undergo
earlier and more frequent screening, including total colon ex-
amination (76,100).
Prostate cancer is the most common noncutaneous cancer
and the second leading cause of death in American men
(Table 17) (108). The standardized incidence ratio of prostate
cancer in the dialysis population was 1.2 (95% confidence
interval 0.9–1.7) in Australia and New Zealand, 0.9 (0.8–1.0)
in Europe and 0.7 (0.6–0.7) in the US (44). As the age of
renal transplant recipients increases, more patients are in the
age group at risk for prostate cancer (109). For patients
treated for prostate cancer, the rate of recurrence after renal
transplantation is 18% (47). Forty percent of recurrences of
prostate cancer in the CTTR were reported in patients who
received a transplant less than 2 years after treatment of their
prostate cancer (60). Diagnosis and treatment of localized
prostate cancer after renal transplantation is associated with
good results compared with the high mortality (33%) for pa-
tients diagnosed when they have metastatic disease at the
time of their diagnosis of prostate cancer (109). It is
recommended to wait a minimum of 2 years after treatment
of prostate cancer and consideration of renal transplantation
(47). Although the data are limited, patients with focal malig-
nancies in the prostate may not require a waiting interval be-
tween treatment of their malignancy and renal transplantation
(47).
There is no general consensus on whether to recommend
routine screening for prostate cancer in men in the general
population (76,108,110,111). In the case of renal transplant
candidates, it appears prudent to follow the recommenda-
tions of the American Cancer Society that both digital rectal
examination and prostate specific antigen (PSA) be offered
annually, beginning at age 50, to men who have a life expect-
ancy of at least 10 years (112). Men younger than 50 years
of age but at high-risk for prostate cancer, e.g. African Ameri-
cans and those with 2 or more first degree relatives with
prostate cancer, may benefit from screening starting at an
earlier age. Information should be provided to patients about
the risks and benefits of screening. Screening for prostate
cancer in asymptomatic men may detect tumors at a more
favorable stage. Mortality from prostate cancer has de-
creased, but it has not been established that this is a direct
result of screening. A positive screening test for prostate can-
cer forces patients to decide on additional diagnostic and, in
many cases, therapeutic interventions (112). Total PSA can
be used to screen patients on dialysis independent from the
dialysis procedure and membrane. Nevertheless, free PSA
can be removed with high flux dialysis membranes (113).
Dialysis patients have an increased risk of liver cancer (Table
18) (44,79). The standardized incidence of liver cancer in the
dialysis population was 1.5 (95% confidence interval 0.5–
4.6) in Australia and New Zealand, 1.2 (1.0–1.4) in Europe
and 1.5 (1.3–1.7) in the US (44). Renal transplant recipients
also have an increased risk of hepatobiliary tumors (83).
Chronic infection with hepatitis viruses is common in both
dialysis patients and renal transplant recipients, and is prob-
ably responsible for the increased risk of liver cancer in these
populations (44,83,114). There are few data to suggest that
routine screening effectively decreases the risk of posttrans-
plant liver cancer. In a case report, fulminate hepatocellular
carcinoma occurred only 50 days after renal transplantation
in a patient who was hepatitis B surface antigen and e-anti-
gen positive (115). Thus, it may be reasonable to screen high-
risk individuals with radiographic imaging and alpha-feto-
protein.
There are no reports of renal transplantation in patients pre-
viously treated for liver cancer. Although the outcomes of liver
transplantation for hepatic cancer have improved in recent
years, there is still a high rate of recurrence and high mortality
from recurrent cancer (116,117). At this time, renal transplan-
tation is not recommended for ESRD patients previously
treated for liver cancer. Long-term survivors from liver cancer
who are unable to receive adequate dialysis need individual

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Kasiske et al.

Table 18: Liver cancer

Possible screening Alpha-fetoprotein
Radiographic imaging of the liver with ultrasound, computerized tomography, and/or magnetic resonance imaging
Incidence Hepatic carcinoma is 1.2–1.5 times more common in dialysis patients than in the general population. There are no
data on renal transplantation after treatment of liver cancer.
Rationale There is a high rate of recurrence and mortality in patients undergoing liver transplantation for liver cancer. Although
there are no data on renal transplantation after treatment of liver cancer, the recurrence rate and mortality for liver
cancer is very high in all patient populations.
Recommendations (C) Renal transplantation is not generally recommended for ESRD patients treated for liver cancer, unless it is part
of a strategy that also includes liver transplantation.

Table 19: Multiple myeloma

Possible screening Serum and urine immunoelectropheresis
Incidence Multiple myeloma is 3.2–5.2 times more common in dialysis patients than in the general population. About 67%
recur after transplantation.
Rationale The incidence of multiple myeloma is high among hemodialysis patients and roughly 2/3 of patients will have a
recurrence after renal transplantation.
Recommendations (B) Patients should be counseled that multiple myeloma frequently recurs after renal transplantation, although the
relative rate of recurrence for comparable patients on hemodialysis vs. transplantation is unknown.
(C) Patients with active myeloma should probably not undergo renal transplantation.
(C) Monoclonal gammopathy of unknown significance is not an absolute contraindication to transplantation.
(C) There are insufficient data to suggest an appropriate disease-free waiting time between myeloma remission and
renal transplantation.

consideration of their circumstances by the transplant cen-
ters.
The risk of multiple myeloma is increased in the dialysis
population compared to the general population (Table 19)
(44,79). The standardized incidence ratio of multiple myel-
oma in the dialysis population was 3.2 (95% confidence in-
terval 1.8–5.8) in Australia and New Zealand, 3.7 (3.3–4.2)
in Europe and 5.2 (5.0–5.3) in the US (44). The recurrence
rate of multiple myeloma after renal transplantation is 67%
(47). Similarly, a high proportion of patients with monoclonal
gammopathy of unknown significance develop multiple my-
eloma posttransplant (47,60,118). However, monoclonal gam-
mopathy of unknown significance may not be an absolute
contraindication to transplantation (118). Active multiple myel-
oma with marrow infiltration and associated pancytopenia
predisposes the patient to infections and sepsis. Indeed, in-
fection is the most important cause of death for patients with
multiple myeloma as cause of their ESRD and who undergo
renal transplantation (119–121). Recurrence of paraproteine-
mias after transplantation does not necessarily lead to allo-
graft failure, and there have been reports of prolonged patient
and renal allograft survival in some instances (120,121). It is
not clear whether outcomes for comparable patients with
multiple myeloma are better on dialysis or following trans-
plantation. Likewise, there are insufficient data to make rec-
ommendations on appropriate waiting times between re-
mission and transplantation. There is a case report describing
the successful treatment of myeloma using cyclophos-
phamide, antithymocyte globulin and thymic irradiation fol-
lowed by simultaneous bone marrow and HLA-matched kid-
ney transplantation (122).
Lymphomas appear to be more frequent in ESRD than in the
general population in some, but not all, studies (Table 20)
(44,79). The standardized incidence ratio of non-Hodgkin’s
lymphoma in dialysis patients was 1.4 (95% confidence in-
terval 0.8–2.6) in Australia and New Zealand, 0.6 (0.5–0.9)
in Europe and 1.7 (1.5–1.8) in the US (44). The standardized
incidence ratio for Hodgkin’s disease in dialysis patients was
4.7 (95% confidence interval 1.8–12.5) in Australia and New
Zealand, 1.0 (0.7–1.5) in Europe and 1.6 (1.3–2.1) in the US
(44). Others have also reported that the risk of non-Hodgkin’s
lymphoma is significantly increased in renal transplant recipi-
ents (83,123).
The posttransplant recurrence rate is 11% for patients with
Hodgkin’s or non-Hodgkin’s lymphoma prior to transplan-
tation (47). More than 75% of patients with lymphomas had
been treated for their cancers at least 5 years before renal
transplantation and were presumably cured of their malig-
nancies (47,60). A minimum waiting period of at least 2 years
is recommended after treatment of lymphomas prior to con-
sideration for renal transplantation.
Growing evidence implicates infection with the Epstein-Barr
Virus (EBV) in posttransplant lymphoproliferative disorders
(PTLD) and some lymphomas. (However, not all PTLD are as-

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 The Evaluation of Renal Transplant Candidates: Clinical Practice Guidelines

Table 20: Lymphoma and posttransplant lymphoproliferative disorders (PTLD)

Possible screening Medical history and physical examination
Antibodies to the Epstein-Barr Virus (EBV)
Possible prophylaxis Antiviral agents, e.g. acyclovir and ganciclovir (posttransplant)
Vaccination
Incidence Lymphomas are 0.6–4.7 times as common (i.e. not significantly increased) in dialysis patients compared to the
general population. The recurrence rate for lymphoma is 11%. The incidence of EBV-associated PTLD varies with
the patient population, but may be as high as 15% in children.
Rationale Most patients with lymphoma prior to transplantation who remained free of disease received their transplants ⬎5
years after successfully completing cancer treatment. Thus, a disease-free interval prior to transplantation may effec-
tively prevent cases of lymphoma recurrence. Although most adults are EBV antibody-positive by the time of trans-
plantation, many children have not yet acquired antibodies. Thus, screening children and their donors for antibody
evidence of immunity to EBV could help predict individuals at increased risk for posttransplant EBV-associated PTLD
(including lymphomas). Children who are high-risk could theoretically benefit from antiviral prophylaxis during periods
of intensive immunosuppression and possibly monitoring for active EBV infection with polymerase chain reaction
(PCR) detection of EBVS.
Recommendations (C) Routine medical history and physical examination should be part of the pretransplant evaluation.
(B) Patients with Hodgkin’s or non-Hodgkin’s lymphoma should wait at least 2 years after successful treatment
before transplantation.
(C) Measuring antibodies to EBV in pediatric transplant candidates could help identify a high-risk population that
would benefit from posttransplant antiviral prophylaxis and monitoring.

Table 21: Leukemias

Possible screening Medical history and physical examination
Complete blood count
Incidence Leukemias are 0.6–1.9 times as common (i.e. not significantly increased) in dialysis patients compared to the general
population. The incidence of leukemias in hemodialysis patients is similar to that found in the general population.
Rationale Although there are few data available, immunosuppression associated with renal transplantation could increase the
risk of recurrence and diminish the chances of survival in patients with leukemia. Therefore, it is reasonable to wait
for at least 2 years after successful treatment of leukemia before renal transplantation.
Recommendations (C) Medical history, physical examination and a complete blood count should be part of the routine pretransplant
evaluation.
(C) Patients with leukemia that has been successfully treated should wait for at least 2 years before renal transplan-
tation.

sociated with EBV (124).) Since EBV is sensitive to antiviral
agents such as acyclovir and ganciclovir, it may be possible to
prevent complications related to EBV infection such as PTLD
(125,126). Unfortunately, there are no large, randomized, con-
trolled trials establishing the benefits of antiviral prophylaxis for
EBV in transplant recipients. A recent meta-analysis of acyclo-
vir treatment of infectious mononucleosis in the general popu-
lation was negative, casting some doubt on the in vivo efficacy
of antiviral treatment of EBV (127). Most adults have had infec-
tion with EBV by the time of transplantation, and have anti-
bodies to EBV (128). Thus, it is unlikely that the measurement
of pretransplant antibodies in adult recipients and donors will
identify a population at high-risk for EBV infection transmitted
with the donor kidney. On the other hand, many children have
not yet acquired antibodies to EBV (129), and the incidence of
EBV-associated PTLD is high among pediatric renal transplant
recipients (129,130). Thus, the measurement of EBV anti-
bodies in pediatric renal transplant candidates and donors
could help to identify a high-risk group that may benefit from
prophylactic antiviral agents posttransplant. This strategy has
not been rigorously tested in controlled trials. Studies are
underway to determine the safety and efficacy of vaccination
with purified EBV pp350, or vaccinia virus expressing gp350
(131–133). Finally, successful retransplantation has been re-
ported in two individuals (disease-free follow-up 18 and 26
months posttransplant) who lost their previous allograft in the
management of PTLD (134).
Leukemia has a standardized incidence ratio of 0.6 to 1.9
in the dialysis population (Table 21) (44). The standardized
incidence ratio of leukemia in the dialysis population was 0.6
(95% confidence interval 0.2–1.7) in Australia and New Zea-
land, 0.8 (0.7–1.0) in Europe and 1.9 (1.7–2.0) in the US (44).
There have been reports of renal transplantation after suc-
cessful treatment of leukemia, but the data available at this
time are too limited to make any specific recommendations
on waiting periods prior to transplantation (135,136). Simi-

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Kasiske et al.

Table 22: Malignant melanoma

Possible screening Medical history and physical examination
Incidence The recurrence rate for malignant melanoma after renal transplantation is 21%.
Rationale Most patients with recurrent disease will die from their melanoma. Most patients with recurrent malignant melanoma
after renal transplantation have undergone their transplants less than 5 years after treatment of their cancers.
Recommendations (C) A thorough skin examination should be part of the pretransplant evaluation.
(B) Patients with malignant melanoma should generally wait 5 years before renal transplantation. A shorter waiting
period of 2 years may be adequate for patients with in situ and very thin melanomas.

Table 23: Non-melanoma skin cancer

Possible screening Medical history and physical examination
Incidence The incidence of new or recurrent cancers in patients with a previous diagnosis of non-melanoma skin tumors is
48% after renal transplantation.
Rationale Aggressive skin cancers can cause severe local tissue destruction, widespread metastases and death. Close to half
of patients with nonmelanoma skin cancers (excepting basal cell carcinomas) will have recurrent and/or new cancers
of the skin after renal transplantation. A waiting period of 2 years may eliminate some recurrences; however, many
patients with skin cancers will have recurrences irrespective of the time between treatment of the skin cancer and
renal transplantation.
Recommendations (C) A thorough skin examination with treatment of suspicious lesions should be part of the pretransplant evaluation.
(C) It is not known whether waiting for a period of time before transplanting patients who have nonmelanoma skin
cancers has any effect on the chances of recurrence.
(C) Basal cell carcinomas are generally benign and do not require a waiting period.

larly, too few data are available to make recommendations approaches due to their more aggressive behaviors (47). The
regarding specific types of leukemias. role of cutaneous viral infections in the pathogenesis of skin
cancer, e.g. with HPV, remains speculative (138,139).

The recurrence rate for malignant melanoma after renal trans-
plantation is 21% in the CTTR data (Table 22) (47). Patients
with recurrent disease usually die from their melanoma (60).
More than half of the recurrences occurred in patients re-
ceiving their allograft less than 5 years after treatment of their
malignant melanoma. A waiting period of at least 5 years is
therefore recommended for most patients with melanomas
prior to renal transplantation (47,137). Patients with melanoma
in situ and very thin melanomas can probably safely undergo
transplantation after a 2-year waiting period (47,137).
Aggressive skin cancers, especially squamous cell carci-
nomas, can cause severe local tissue destruction, metastases
to distant sites and death (Table 23) (60). The high recur-
rence rate of nonmelanoma skin cancers occurs irrespective
of the time of removal of the lesions before (and in some
cases after) renal transplantation (47). Nevertheless, the ma-
jority of patients with recurrences of nonmelanoma skin can-
cers have been treated less than 2 years before transplan-
tation (47). A waiting period of 2 years may eliminate some
recurrent skin cancers, although the impact of this inter-
vention is not established. Some cancers, such as sebaceous
gland carcinomas and Merkel’s cell tumors require different
Lung cancer is the leading cause of death from cancer in the
US (Table 24) (140). The standardized incidence ratio of lung
cancer in the dialysis population was 1.4 (95% confidence
interval 1.1–1.8) in Australia and New Zealand, 0.9 (0.8–0.9)
in Europe and 1.1 (1.1–1.2) in the US (44). There is little ex-
perience with renal transplantation after treatment of lung
cancer. In a retrospective study, cigarette smoking at the time
of transplantation was found to be associated with posttrans-
plant malignancies in general, and lung cancer in particular
(141). Therefore, it is prudent to make every effort to encour-
age transplant candidates to quit smoking prior to transplan-
tation. Studies in the general population have failed to con-
firm the effectiveness of any screening strategy for reducing
the risk of lung cancer (106). Although low-dose computer-
ized tomography shows some promise, appropriate studies
have not yet been completed. There are no data addressing
the efficacy of screening for lung cancer prior to transplan-
tation.
Infections
Whenever possible, all treatable infections should be eradi-
cated prior to transplantation. One of the primary purposes

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 The Evaluation of Renal Transplant Candidates: Clinical Practice Guidelines

Table 24: Lung cancer

Possible screening Medical history and physical examination
Chest X-ray
Low-dose computerized tomography
Prophylaxis Smoking cessation
Incidence Lung cancer is 0.9–1.4 times as common (i.e. not significantly more common) in dialysis patients compared to the
general population. The rate of recurrence after transplantation is unknown.
Rationale Although there are few data available, immunosuppression associated with renal transplantation could increase the
risk of recurrence and diminish the chances of survival in patients with lung cancer. Therefore, it is reasonable to
screen for lung cancer and to wait for at least 2 years after successful treatment of lung cancer before renal
transplantation. Cigarette smoking is a strong risk factor for lung cancer and every effort should be made to encour-
age transplant candidates to quit smoking. Some argue that ongoing cigarette abuse should be considered a contra-
indication to transplantation.
Recommendations (A) Every effort should be made to encourage patients to quit smoking.
(C) Medical history, physical examination and chest X-ray should be part of the routine pretransplant evaluation.
(C) Patients with lung cancer that has been successfully treated should wait for at least 2 years before renal transplan-
tation.

Table 25: Human immunodeficiency virus (HIV)

Possible screening HIV antibody
Prevalence Estimates of the proportion of hemodialysis patients who are HIV positive range between ⬍0.5% to about 2.5%.
Rationale There are reasons to believe that outcomes may be either better or worse with renal transplantation and immunosup-
pression in patients who are HIV antibody positive.
Recommendations (A) All renal transplant candidates should be tested for HIVS.
(C) There are insufficient data on which to base a recommendation for or against renal transplantation in patients
who are HIV positive.

of the pretransplant evaluation is to eliminate infections that
may persist and become life-threatening after transplan-
tation. The number of different infections that should be con-
sidered when evaluating renal transplant candidates is rela-
tively large. It is not possible to consider the evaluation and
screening of all infections, and these guidelines instead focus
on the more commonly encountered infections. Infections
that are not otherwise covered include uncommon infections,
e.g. syphilis (142), strongyloidiasis (143–145), toxoplasmosis
(146), herpes type II infection (147–149), and/or infections for
which there is no known prevention or specific treatment,
e.g. polyoma virus (BK strain) infection (150–155). Whenever
possible, transplant candidates should receive immunizations
for infections that are prevalent (and potentially life-threaten-
ing) after renal transplantation. It is generally best to adminis-
ter immunizations before the development of ESRD, but if
this is not possible, immunizations should be administered
before transplantation.
A survey of 28 hemodialysis centers in the US (eight centers
and 29% of patients were from high incidence areas) found a
prevalence of human immunodeficiency virus (HIV) positivity
to be between 0.3 and 2.6% of dialysis patients (Table 25)
(156). This finding is similar to that reported recently from
Spain, where the prevalence of HIV positivity in patients on
hemodialysis was between 0.34 and 2.1%, and where 1% of
patients starting dialysis were HIV positive (157).
Every center responding to a recent US survey required testing
for HIV for renal transplant candidates, and 84% of these cen-
ters would not transplant an individual who refused HIV test-
ing. Furthermore, 88% would not transplant an asymptomatic
HIV-infected patient with a cadaveric donor kidney and 91%
would not transplant an HIV-positive recipient with a living kid-
ney donor. No transplant center that would consider trans-
planting an HIV-infected patient had performed such a trans-
plant in the year prior to the survey (158). The ethical issues in-
volved in the allocation of scarce medical resources, such as
organs for transplantation, are complex (159). Early reports de-
scribed the rapid onset of serious infection and death following
infection transmitted through a transplanted organ or inadver-
tent transplantation of HIV-infected patients (160–163). How-
ever, the issue of transplantation of HIV-infected patients has
changed with the advent of new combinations of anti-retroviral
agents, e.g. highly active antiretroviral therapies (HAART)
(164), and the recent case reports of prolonged survival of HIV-
positive patients after renal transplantation (165–169). In any
case, all renal transplant candidates should be tested for HIV
(166). Transplantation should be considered experimental at
this time in HIV-positive patients.
A center that wishes to undertake transplantation of HIV-in-
fected individuals should have extensive experience in both
transplantation and HIV management. The patient should
have a strong desire for transplantation and should under-

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Kasiske et al.

Table 26: Tuberculosis (TB)

Possible screening Exposure history or history of living in an endemic area
Purified protein derivative (PPD) skin test
Chest X-ray
Possible prophylaxis Isoniazid (with pyridoxine) for at least 6 months beginning before or at the time of transplantation
Prevalence About 9% of hemodialysis patients have a positive PPD and 16% have a history of exposure to TB.
Rationale TB is a relatively common, potentially life-threatening infection among patients with ESRD. Screening renal transplant
candidates with a PPD skin test is effective, although false negatives are probably more common among hemo-
dialysis patients than in the general population. Studies in the general population have shown prophylaxis with
isoniazid to be safe and effective. Studies have also documented the safety of prophylaxis among hemodialysis
patients and renal transplant recipients.
Recommendations (A) Renal transplant candidates who have not had a positive PPD skin test, a history of vaccination with bacille
Calmette Guérin (BCG), or a history of TB should be screened with a PPD skin test.
(B) The PPD skin test should preferably be applied with appropriate control antigens to screen for false-negatives
due to anergy.
(B) Renal transplant candidates should have a chest X-ray.
(A) Renal transplant candidates with active TB (positive sputum cultures, clinical signs and symptoms and/or chest
X-ray suggestive of active disease, or positive nasogastric aspirates in children) should receive adequate treatment
before transplantation.
(B) Renal transplant candidates with latent TB (positive PPD not induced by immunization and/or chest X-ray sugges-
tive of quiescent TB without positive sputum cultures or clinical signs and symptoms of active disease) and no
history of adequate treatment or prophylaxis should receive prophylaxis.
(B) Renal transplant candidates who are at high risk due to possible exposure to TB should receive prophylaxis.
(B) In the US, BCG is generally not recommended, except for infants and children who are at high risk for tuberculosis.

stand the potential risks. The HIV-positive transplant candi-
date should have:
O an undetectable HIV viral load
O demonstrated adherence to a HAART regimen
O no opportunistic infections
O a CD4 lymphocyte count that is greater than 300/mm3
There appears to be increased risk of mycobacterial disease
in the ESRD population, which is often asymptomatic (Table
26). A recent study reported that 32% of hemodialysis pa-
tients were anergic, 9% had a positive purified protein deriva-
tive (PPD) skin test, and 16% had a history of past or present
exposure to tuberculosis (TB) (170). The prevalence of TB in
renal transplant recipients is between 0.4 and 1.7% in the
Western world (171,172) and up to 11.8% in developing coun-
tries where there is a higher rate of endemic tuberculosis
(173–176). Immunosuppression can cause aggressive dis-
ease with wide dissemination (171,176–179). Evaluation of po-
tential renal transplant candidates should include a thorough
clinical history, as well as both chest X-ray and PPD skin test-
ing (if there is no history of a positive skin test or active TB).
If there is a history of TB, the duration and extent of therapy
should be noted. Abnormal radiographic findings require
further clinical investigation.
There is no clear evidence that prophylaxis reduces the inci-
dence of reactivation tuberculosis after renal transplantation.
For example, in one small study from a country where the inci-
dence of tuberculosis in the general population is high, the inci-
dence of posttransplant tuberculosis was 3/51 (6%) in patients
who received isoniazid prophylaxis and 13/223 (8.8%) in pa-
tients who did not (pΩ0.15) (175). Many US transplant centers
require pre- and/or posttransplant isoniazid prophylaxis for pa-
tients with a positive PPD skin test and no contraindications to
therapy (177,180,181). Others would argue that routine prophy-
laxis is unnecessary, and that only high-risk individuals should
be treated prophylactically, e.g. patients with a past history of
active disease, patients from high-risk populations, patients
with other immunocompromising conditions, or patients with
X-ray findings suggestive of active TB. Patients with a positive
PPD skin test who will receive antilymphocyte antibody treat-
ment may also merit prophylaxis (182). Isoniazid is the most
frequently used prophylactic agent, and it is given with pyridox-
ine. Isoniazid (and rifampin) may be poorly tolerated by pa-
tients with chronic hepatitis. In these instances, alternative
regimens such as ethambutol plus a fluoroquinolone can be
used.
Evidence-based guidelines for the use of bacille Calmette
Guérin (BCG) vaccination in the prevention of tuberculosis have
been developed (183–185). In the US, BCG is generally not rec-
ommended, except for infants and children who are at high risk
for tuberculosis, e.g. those residing in indigenous areas such
as Indian reservations, or for health care workers exposed to
tuberculosis. The BCG vaccine is not recommended for im-
munosuppressed patients due to the risk of adverse effects
(185).
The incidence of cytomegalovirus (CMV) disease is generally
less than 5% for recipients who do not have antibodies to

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 The Evaluation of Renal Transplant Candidates: Clinical Practice Guidelines

Table 27: Cytomegalovirus (CMV)

Possible screening Antibody to CMV
Possible prophylaxis None pretransplant
Incidence The proportion of transplant candidates who are CMV antibody positive (indicating prior CMV infection) varies by
age and geography, but is ⬎50% overall. The incidence of posttransplant CMV disease varies between ⬍5% for
low risk patients (both the donor and recipient are seronegative) to ⬎50% for high-risk patients (the donor is
seropositive and the recipient is seronegative). The intensity of immunosuppression increases the incidence of CMV,
and the use of posttransplant prophylaxis for CMV decreases the incidence and severity of CMVS.
Rationale The risk for CMV infection and its severity are influenced by whether the donor is seropositive (indicating risk of
transmission), the recipient is seropositive (indicating immunity) and the intensity of immunosuppression. Most
transplant centers tailor the use of posttransplant chemoprophylaxis to the risk of CMV based on these factors.
Therefore, it is useful to determine the CMV antibody status of potential transplant recipients and (living or cadaveric)
donors prior to transplantation.
Recommendations (A) Renal transplant candidates should have CMV antibody measured as part of the pretransplant evaluation.
(B) Patients should be informed of their risk for posttransplant CMV.

Table 28: Posttransplant infection in pretransplant peritoneal dialysis patients

Possible screening Medical history and physical examination
Possible prophylaxis None
Incidence Approximately 10% develop peritonitis early posttransplant.
Rationale Immunosuppression could exacerbate active or inadequately treated peritonitis.
Recommendations (C) In patients with active or recently treated peritonitis, eradication of the infection should be documented prior to
transplantation.

CMV and who receive kidneys from donors who are antibody
negative (Table 27) (186). The incidence of primary CMV dis-
ease among antibody negative recipients of antibody positive
donors is about 50–75% without specific prophylaxis
(186,187). The incidence among antibody positive recipients
of antibody positive or negative donors is about 25–40%
(186,187). The incidence and severity of CMV disease are also
influenced by the amount of immunosuppression used (188–
191). Chemoprophylaxis for CMV (with acyclovir, ganciclovir,
valacyclovir and/or intravenous immunoglobulin) has been
shown to be effective in large, randomized controlled trials
(192–198). A meta-analysis of controlled trials also con-
cluded that antiviral agents (acyclovir or ganciclovir) were ef-
fective in preventing CMV infection in solid-organ transplant
recipients (199). However, chemoprophylaxis can cause ad-
verse effects and it is expensive. Therefore, screening for
CMV antibody before transplantation helps to identify pa-
tients destined to develop symptomatic CMV infection, and
to limit the use of prophylactic antiviral agents to patients
who are at increased risk for CMV infection (200). This strat-
egy appears to be the most cost-effective (201,202). Evi-
dence-based guidelines that recommend posttransplant
prophylaxis according to the risk for CMV disease have been
developed (186). Although newer therapies have become
available since the publication of these guidelines, e.g. oral
ganciclovir and valacyclovir, the basic approach that is out-
lined in the guidelines remains valid. The recently reported
development of ganciclovir-resistant CMV strains in patients
treated with prophylaxis could ultimately undermine this
strategy, and therefore warrants close observation (203).
Transplant candidates should be informed of the risk of CMV
infection prior to transplantation. They can be told that CMV
can cause considerable morbidity, occasional loss of the graft
or even death, but that effective prophylaxis and treatment
are available. Candidates who are CMV antibody negative
can be told that they are at increased risk of developing CMV
infection posttransplant, and that the risk is also determined
by the antibody status of the donor. Candidates can be in-
formed of their specific risk for CMV infection based also on
the donor’s antibody status.
In a retrospective study, 30 (13%) of 233 peritoneal dialysis pa-
tients developed peritonitis within the first 90 days after trans-
plantation (Table 28) (204). Pretransplant risk factors included
the total number of peritonitis episodes, previous peritonitis
with Staphylococcus aureus and male gender. The authors
recommended early catheter removal after transplantation,
particularly in patients at high risk (204). A more recent retro-
spective study reported that patients on peritoneal dialysis at
the time of transplantation had a greater risk of developing in-
fections within the first 30 days posttransplant than patients
on hemodialysis (205). The infection sites were the abdominal
cavity, the surgical wound or peritoneal dialysis catheter site,
and the bloodstream. There was a 9-fold increased risk of in-
fection if the peritoneal dialysis catheters were not removed

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Kasiske et al.

Table 29: Dental infections and gingival hyperplasia

Possible screening Dental examination
Possible prophylaxis Intensive hygiene instruction, plaque removal and tooth extractions
Incidence The incidence of infections originating in the oral cavity is unknown. In some series as many as 33% of patients
treated with cyclosporine developed gingival hyperplasia.
Rationale The condition of the teeth and periodontal tissues pretransplant can theoretically influence the incidence and severity
of posttransplant infections (e.g. sinusitis, pneumonitis and bacteremia) and gingival hyperplasia. Recent observa-
tional studies in the general population have also linked chronic periodontal inflammation to cardiovascular disease.
Gingival hyperplasia is problematic in cyclosporine-treated renal transplant recipients.
Recommendations (C) Visual inspection of the oral cavity should be part of the pretransplant examination, and patients with damaged
teeth and/or periodontal disease should undergo further evaluation and treatment.

Table 30: Influenza A and B

Possible screening None
Possible prophylaxis Vaccination
Incidence Unknown, but likely to be at least as high as in the general population
Rationale Although the proportion that have an adequate antibody response to the influenza vaccine is lower compared to
normals, many patients respond, and vaccination is safe.
Recommendations (B) Annual influenza vaccination (October-November)

within 6 days of transplantation (205). In a study of 48 trans-
plants in children, posttransplant peritonitis developed in five
(10%) (206). Exit-site or tunnel infections occurred in nine
(19%). All infections were successfully treated, and graft sur-
vival was not affected (206). These and other data confirm that
transplantation in patients treated with peritoneal dialysis is
safe. It would seem prudent to delay transplantation for a pa-
tient with active or recent peritonitis. However, there are no
data to suggest what a safe interval between infection and
transplantation might be. Documentation of the eradication of
infection after the completion of antimicrobial therapy seems
appropriate. Early removal of dialysis catheters posttransplant
is generally recommended.
There are few data establishing the usefulness of prophylac-
tic dental evaluation and treatment prior to renal transplan-
tation (Table 29). Nevertheless, in an international survey
most (but not all) responding transplant centers indicated
that they include dental examination and treatment in their
pretransplant evaluation (207). There are anecdotal reports of
occult, posttransplant fevers caused by dental infections
(208). In each case the fever eventually responded to surgi-
cal extraction, and the authors concluded that these infec-
tions could have been prevented by careful pretransplant
evaluation and treatment (208). Although there is no evi-
dence that this is the case, it is certainly plausible. Similarly,
gingival hyperplasia is a common complication of posttrans-
plant medication regimens, especially when they include
cyclosporin A (CsA) and calcium channel blockers (209). In
a small, randomized, controlled trial, posttransplant plaque
control with intensive oral hygiene instruction, scaling and
root planing had a beneficial effect on CsA-associated gingi-
val hyperplasia (210). It has also been shown that pretrans-
plant gingival hyperplasia correlates with the severity of post-
transplant gingival disease (211). Thus, it is possible that initi-
ating evaluation and treatment prior to transplantation would
be beneficial. It is unclear whether antimicrobial therapy per
se can prevent or reduce gingival hyperplasia. A recent trial
found that metronidazole was ineffective (212). However, two
small studies reported that azithromycin reduced posttrans-
plant gingival hyperplasia (213, 214). Additional studies are
clearly needed to determine the role of antibiotics in trans-
plant candidates with periodontal disease. The potential im-
portance of this question has recently been underscored by
observational studies in the general population linking peri-
odontal inflammation to the development of cardiovascular
disease (CVD) (215–223) However, there are no controlled
studies showing that treatment of periodontal disease re-
duces the incidence of CVD.
It is likely that influenza is more severe when it occurs in
immunosuppressed renal transplant recipients (Table 30), al-
though systematic studies documenting this are lacking. In-
fluenza can be fatal, and bacterial super-infections are com-
mon in both immunosuppressed and non-immunosup-
pressed patients. In the general population, studies have
clearly shown that influenza vaccination reduces infection
and its consequences (224). The Advisory Committee on Im-
munization Practices and the American Academy of Pedi-
atrics recommend annual immunization with the trivalent in-
fluenza vaccine for all chronic dialysis patients (225). How-
ever, some studies have reported that the response to the
vaccine is reduced in hemodialysis patients (226–228). Ad-
ministering a second dose of vaccine during the same influ-
enza season has not increased the antibody response for
high-risk patients, e.g. the elderly (229, 230). Chemoprophyl-

26 2001; Suppl. 1: Vol. 2: 5–95

 The Evaluation of Renal Transplant Candidates: Clinical Practice Guidelines

Table 31: Pneumococcal (Streptococcus pneumoniae) infections

Possible screening None
Possible prophylaxis Vaccination
Incidence Approximately 1% of unvaccinated patients per year
Rationale Although the proportion that have an adequate antibody response to the pneumococcal vaccine is lower compared
to normals, many patients respond, and vaccination is safe
Recommendations (B) Polyvalent pneumococcal vaccine (capsular polysaccharides). Should be administered every 2 years.
(B) Infants and toddlers should be vaccinated at 2, 4, 6 and 12–15 months.

Table 32: Childhood infections/immunizations

Possible screening Antibody levels
Possible prophylaxis Vaccination
Incidence Measles, mumps, rubella, diphtheria, tetanus, pertussis and polio are very uncommon. Haemophilus influenzae is
a common pathogen in childhood, and is not unusual in immunocompromised adults. Varicella is very common. The
incidence of both Haemophilus influenzae and varicella is decreasing following widespread immunization programs.
Rationale Although immunity may be less regularly achieved, and may be of shorter duration in ESRD patients compared to
the general population, vaccination is effective enough to warrant routine use. Vaccination is also safe. Tetanus and
live vaccines should be avoided after transplantation.
Recommendations (B) Immunizations should be given according to existing guidelines.

axis with antiviral agents has not been well studied. An in-
creased incidence of adverse effects from amantadine and
rimantidine may be seen in patients with renal insufficiency,
and these agents are only active against influenza A. The
efficacy and safety of newer agents (zanamivir and oseltami-
vir) have not been well established in ESRD patients.
Very few studies have examined the incidence of pneumoc-
occal infections (Table 31). However, one study found that
14/197 (7%) of renal transplant recipients developed pneum-
ococcal infections over a 6-year period, or 1% per year (231).
Recently, there has been an increase in the incidence of peni-
cillin-resistant pneumococcus infection. Infections from
Streptococcus pneumoniae cause significant morbidity and
mortality. Although the vaccine is effective (232), antibody
levels may decline rapidly (233,234), and some suggest
monitoring antibody levels (234). Infants and toddlers should
be vaccinated at 2, 4, 6 and 12–15 months (235). The Advis-
ory Committee on Immunization Practices and the American
Academy of Pediatrics recommend pneumococcal immuniz-
ation for all chronic dialysis patients (225).
The incidence of measles, mumps, rubella, diphtheria, teta-
nus, pertussis and polio is very low, largely due to successful
vaccination campaigns (Table 32). However, some of these
rare diseases have recently become more common, and are
likely to be more severe in immunocompromised transplant
recipients compared to the general population (236–238).
The measles, mumps and rubella (MMR) vaccine is made
of live-attenuated viruses. Individuals born before 1957 are
advised to receive a 2-dose MMR vaccination (225,239).
The rate of serologic response to the MMR vaccine is re-
duced in patients on dialysis, and some have recommended
that antibody levels be tested, and that individuals with an
inadequate response be re-vaccinated (240). A series of im-
munizations with diphtheria and tetanus toxoids, and acellular
pertussis (DTaP) are recommended for infants (225,241). A
tetanus toxoid-diphtheria booster should be administered at
least every 10 years. In a study of 71 hemodialysis patients,
only 33 (44%) had sufficient antibodies against tetanus
(242). Furthermore, only 38% of the unprotected patients
seroconverted after immunization. Similar results were found
for diphtheria (242). The poor response rates to tetanus and
diphtheria have been confirmed by others (243,244), and it
has been suggested that antibody levels should be obtained
to confirm the efficacy of vaccination.
Until recently, the oral poliovirus vaccine, an attenuated virus,
was used almost exclusively. More recent recommendations
include the use of inactivated poliovirus vaccine, which is
somewhat less effective, but carries less risk of vaccine-as-
sociated poliomyelitis (245). This change in emphasis in the
US also reflects the fact that there have been no recent cases
of poliomyelitis in the Western Hemisphere. In the US, immu-
nization is recommended for all children and for adults who
missed immunization as a child.
The incidence of Haemophilus influenzae infection in children
has fallen dramatically following the introduction of a success-
ful vaccine. It is generally recommended that all children be im-
munized with inactivated Haemophilus influenzae type b.
Children with ESRD appear to respond to the vaccine, al-
though the rate of response may be reduced (246, 247).
Adults who may be susceptible to infection with encapsulated
organisms, such as asplenic individuals, should also be con-
sidered for immunization against Haemophilus influenzae.

2001; Suppl. 1: Vol. 2: 5–95 27

Kasiske et al.
Table 33: Consensus estimates of the rate of disease recurrence*
Disease
Focal segmental glomerulosclerosis
Immunoglobulin A nephropathy
Henoch-Schoenlein purpura
Membranoproliferative GN Type I
Membranoproliferative GN Type II
Membranous GN
Hemolytic uremic syndrome/thrombotic thrombocytopenic purpura
Antiglomerular basement membrane disease/Goodpasture’s
Wegener’s granulomatosus/vasculitis
Systemic lupus erythematosus
Oxalosis
Cystinosis
Fabry’s disease
Alport: de novo antiglomerular basement membrane disease
Sickle cell disease
Amyloidosis
Diabetic nephropathy Type 1
* Data represent a compilation from several reviews (257–269). Abbreviation: GN, glomerulonephritis.
Live-attenuated varicella zoster vaccine can be given to
children at 12–18 months. Children who do not have a reliable
history of varicella infection should be vaccinated once if 12
years old or less, twice 4–8 weeks apart if 13 or older. Varicella
zoster infections are very common in adults and children. In
one study the incidence of varicella was 22/49 (45%) in unim-
munized children and adolescents after renal transplantation
(248). However, successful vaccination with an attenuated,
live, varicella vaccine prior to transplant has led to a recent fall
in the incidence of varicella after transplantation (248). Trans-
plant recipients who are seronegative for varicella-zoster virus
are at risk for disseminated infection. These patients should be
vaccinated prior to transplantation (249).
If possible, patients should be immunized prior to ESRD,
according to guidelines for the general population
(239,241,245,250–252). Specific guidelines have been de-
veloped for the immunization of children with renal disease
(253,254). Children with renal disease should be vaccinated
according to the schedule recommended by the Advisory
Committee on Immunization Practices, the American Acad-
emy of Pediatrics and the American Academy of Family Phys-
icians (255,256). Children with chronic renal insufficiency,
and children on dialysis should receive varicella, hepatitis B
and MMR vaccines before transplantation, if unprotected.
Hepatitis A is recommended for patients with a high inci-
dence of hepatitis A.
Recurrent Disease
With notable exceptions, such as Alport syndrome, polycystic
kidney disease, chronic pyelonephritis and chronic interstitial
nephritis, virtually all diseases affecting the native kidney can
recur in the kidney transplant (Table 33). The risk of recur-
rence is generally small. For example, in an analysis of all
transplants performed between 1980 and 1991 in the Euro-
28
Recurrence (%)
20–30
40–50
10–20
20–30
80–90
10–20
10–25
10–25
15–50
∞1
90–100
0
⬍1
3–4
⬍1
33
100
pean Renal Association-European Dialysis and Transplant As-
sociation registry, only 3% of graft loss was attributable to
recurrent disease (270). However, there is substantial vari-
ation in the risk of recurrence between diseases, and it is
often difficult to predict the chances of recurrence for individ-
ual transplant candidates. For those who have recurrence, the
risk of graft failure has been estimated to be 1.9 times higher
than for patients without recurrent disease (271).
Studies assessing the risk of recurrence are difficult to inter-
pret for several reasons:
O Many patients do not have a histologic diagnosis of the
cause of ESRD prior to transplant. It is estimated that only
20% of ESRD patients have native kidney biopsy prior to
initiation of dialysis (Hariharan, unpublished observation).
This is because many patients present with bilateral con-
tracted kidneys and are not candidates for renal biopsy.
African-Americans are frequently labeled as having hyper-
tensive nephrosclerosis even though they may have glo-
merulonephritis. Posttransplant evaluation in many centers
does not include urinalysis, which could miss cases of re-
current and de novo disease. In addition, transplant biop-
sies are not routinely submitted for immunofluorescence
and electron microscopic examinations.
O The incidence of recurrent disease is dependent on the
length of follow-up. Many, if not most, observational
studies report the crude rate of recurrence rather than ac-
tuarial rates, which are censored for patients who die or
lose their grafts due to rejection. Thus, it is difficult to com-
pare the results from studies with different intervals of fol-
low-up.
O The diagnosis of recurrence is problematic. In some studies
most patients underwent biopsy and the rate of histologic
recurrence was reported. In others, only patients with clin-
2001; Suppl. 1: Vol. 2: 5–95
 The Evaluation of Renal Transplant Candidates: Clinical Practice Guidelines

Table 34: Focal segmental glomerulosclerosis (FSGS)

Possible screening Bioassay for a yet-to-be isolated serum protein
Possible prophylaxis Plasma exchange or adsorption
Incidence 20–40% recurrence, 40–50% graft failure
Rationale Although preliminary data suggest that some patients may have a serum protein that correlates with recurrent FSGS
after transplantation, no standardized assays are available clinically. Some investigators have suggested that the risk
for recurrent FSGS may be reduced with prophylactic plasma exchange.
Recommendations (A) Candidates with FSGS should be warned that there is a 20–40% risk of recurrence, and that 40–50% with
recurrence lose their grafts. However, the risk of recurrent FSGS need not preclude transplantation.
(B) A prior history of graft loss from recurrent FSGS should be considered at least a relative contraindication to living
donor transplantation, due to the likelihood of recurrence (up to 80%).
(C) Assays for a serum factor to predict recurrent FSGS have not been standardized or validated for clinical practice.
(C) There are not yet sufficient data for or against the use of prophylactic plasma exchange or other measures to
prevent recurrent FSGS.

ical presentations suggesting recurrence underwent biopsy
to diagnose recurrence. Obviously, the rate of recurrence
varies substantially depending on the definition.
O The incidence of most disease recurrence is very low. As
a result, most studies lack statistical power to accurately
assess the incidence and risk factors for recurrence. All
these factors make it difficult to estimate the true inci-
dence of recurrent diseases after renal transplantation, and
in the end only very crude estimates can be provided.
Patients with recurrent disease may progress to renal insuf-
ficiency and graft failure. Thus, informing potential renal
transplant candidates and their living donors of the risk of
recurrence and graft failure is an important part of the pre-
transplant evaluation. In addition, a specific diagnosis may
be useful for:
O planning the most appropriate posttransplant immunosup-
pression (although currently there are no data to support
altering immunosuppression practices for specific disease
types),
O suggesting whether monitoring one or more screening
tests may help to predict risk,
O suggesting whether the transplant should be delayed until
the disease is quiescent,
O determining the relative advisability of using a living donor.
Every effort should be made to obtain a report of the renal
biopsy results so that potential transplant recipients can
be adequately informed of the risk of disease recurrence.
Renal transplant candidates with focal, segmental, glomeru-
losclerosis (FSGS) should be told that FSGS recurs in approxi-
mately 20–40% of renal allografts (Table 34) (272–289). Fac-
tors that have been reported to increase the odds of recurrence
include time to development of ESRD (those with a more rapid
progression are more likely to have recurrence)
(281,282,284,286,288,290), race other than African Ameri-
can (285), younger age at onset of the nephrotic syndrome
(276,279) and diffuse mesangial proliferation on native kidney
biopsy (276,281,284). Possibly the strongest predictor of re-
currence is a history of recurrence in a previous transplant. In-
deed, the risk of recurrence when there has been a previous
allograft failure due to recurrent FSGS may be as high as 80%
(274,282,286,291). It has been shown by some investigators
that the presence of an abnormal serum protein correlates with
FSGS recurrence (286,292,293). However, standardized as-
says are not available for clinical use. There does not appear
to be any consistent effect of gender (282,286), the type of
prophylactic immunosuppression used (276,277,279) or the
time spent on renal replacement therapy before transplan-
tation (276). In one uncontrolled study the use of antibody in-
duction therapy was associated with a higher incidence of re-
current FSGS (287). There is also a hereditary form of FSGS
(294); in this form, FSGS does not appear to recur as often
after transplantation (294,295). There are isolated case reports
that the collapsing glomerulopathy variant of FSGS may also
recur after transplantation (296,297); however, collapsing glo-
merulopathy can also occur de novo (298,299).
Patients should be warned that graft loss may occur in 40–
50% with recurrent FSGS (282,283,286,300). If a living do-
nor is being considered, both the transplant candidate and
the potential donor should be aware of the risks. The very
high chance (up to 80%) of recurrence if a previous allograft
has been lost to recurrent FSGS should be taken into con-
sideration before proceeding with living donor transplan-
tation. In a recent study from the North American Pediatric
Renal Transplant Collaborative Study group, graft survival was
significantly worse for the 11.6% (752/6484) of patients with
renal disease due to FSGS (301). The 5-year graft survival for
living donor recipients was 69% vs. 82% (p0.001) for FSGS
vs. other renal disease. The 5-year graft survival for cadaveric
donor recipients was 60% vs. 67%, respectively. The authors
concluded that FSGS eliminated any survival advantage for
children receiving living donor transplants (301).
In general, the same risk factors for recurrence appear to
increase the odds that the recurrent disease will cause graft

2001; Suppl. 1: Vol. 2: 5–95 29

Kasiske et al.

Table 35: Immunoglobulin A (IgA) nephropathy

Possible screening None
Possible prophylaxis None
Incidence 20–40% recurrence, 6–33% graft failure
Rationale Most patients eventually develop histologic recurrence. As graft failure from rejection declines, improved graft survival
may increase the number of patients who develop clinically apparent recurrence and graft failure.
Recommendations (A) Patients should be counseled regarding the high incidence of recurrence, but relative benign (early) clinical
course for most recipients with IgA nephropathy.
(B) Recurrence is more common in recipients of living-related donor transplants, but this has yet to cause an increase
in graft failures. Hence living donor transplants need not be discouraged, unless there is evidence of familial IgA
nephropathy.
(B) Recurrent IgA in a transplant is not a contraindication to retransplantation.

Table 36: Henoch-Schoenlein purpura (HSP)

Possible screening None
Possible prophylaxis None
Incidence 15–35% recurrence by 5 years, 11% graft failure by 5 years
Rationale The rates of recurrence and graft failure due to recurrence are low enough to justify transplantation.
Recommendations Patients should be informed of the modestly increased risk of recurrence and the small risk of graft failure.

failure. The immediate onset of proteinuria after transplan-
tation has also been reported to be a negative prognostic
factor (286). Several small, uncontrolled reports suggest that
plasma exchange or protein adsorption may induce a re-
mission in some patients with recurrent FSGS (281,
289,292,293,302–304). Although a prolonged remission
could theoretically delay or prevent graft failure, there is a
paucity of long-term follow-up data examining outcomes of
patients treated with plasma exchange. Plasma exchange
has also been started before transplantation to prevent FSGS
from recurring (305). However, there are no controlled trials
to examine whether prophylactic plasma exchange is effec-
tive. Cyclosporine has been shown to inhibit the serum factor,
and CsA could theoretically play a role in the prevention and/
or management of posttransplant FSGS (306,307). On the
other hand, the incidence of recurrent FSGS does not appear
to be less in CsA-treated patients compared to historical con-
trols (276,277,279). Nevertheless, some have advocated
starting CsA pretransplant in recipients with FSGS to reduce
the chances of recurrence.
Most patients with immunoglobulin A (IgA) nephropathy
eventually develop IgA deposits, i.e. histological recurrence
(Table 35). The incidence of histologic recurrence has been
shown to increase with duration of follow-up after transplan-
tation (308). Clinical recurrence (variously defined) has been
reported in most studies to be 20–40% (273,275,278,
283,300,308–315). However, in the largest series (nΩ104,
median follow-up of 5 years) clinical recurrence occurred in
only 12.5% (315). Of those with recurrent disease, graft fail-
ure occurs in 6–33% (283,300,308,309,311–315). A shorter
interval between onset and ESRD appears to correlate with
recurrent disease (314,315). Recurrence is more common in
recipients of living-related transplants (309,315), but donor
source does not appear to affect graft survival in patients with
IgA nephropathy (314,315). Therefore, a living donor trans-
plant should not be discouraged. However, IgA nephropathy
may be familial in some cases and donors should be carefully
screened. It has been suggested that familial disease may in
part explain the higher rate or apparent recurrence in recipi-
ents of living donors. Furthermore, in a single-center study
there was a significant decrease in graft survival in IgA pa-
tients with better donor–recipient matching at the HLA DR
locus (314). Immunosuppression with CsA after transplant did
not influence the incidence of recurrent disease or the pro-
gression of recurrent disease to graft failure (314). Finally, un-
like the experience with recurrent FSGS, graft loss due to
recurrent IgA nephropathy is not a contraindication for re-
transplantation. Good long-term graft survival is observed
after both primary and secondary renal transplantation for IgA
nephropathy (314).
Henoch-Schoenlein purpura (HSP) recurs in 15–35%, but
does not often cause graft failure (Table 36)(309,310,316).
Clinical recurrence of HSP may be more likely in individuals
with evidence of active disease (including purpura) 8–18
months prior to transplantation (317,318). However, others
have reported recurrences in patients with quiescent disease
for at least 1 year (316). Nevertheless, patients should prob-
ably not undergo transplantation when systemic disease is
active. Some evidence suggests that a shorter duration of the
original disease, e.g. ⬍36 months, makes recurrence
more likely (316). Histologic evidence of recurrence may be
seen in 50–75% of patients. However, only about 35% will
manifest clinical evidence of recurrence by 5 years, and only

30 2001; Suppl. 1: Vol. 2: 5–95

 The Evaluation of Renal Transplant Candidates: Clinical Practice Guidelines

Table 37: Membranoproliferative glomerulonephritis (MPGN)

Possible screening Complements, C3 nephritic factor, hepatitis C virus ribonucleic acid (RNA) and rheumatoid factor
Possible prophylaxis None
Incidence Type I: 20–30% recurrence, 40% graft failure
Type II: 80–100% recurrence, 10–20% graft failure
Rationale The rate of recurrence and graft failure due to recurrence are low enough to justify transplantation in most cases.
Recommendations (A) Patients with MPGN should be informed of the risk of recurrence and the chance of graft failure from recurrent
disease.

Table 38: Idiopathic membranous glomerulonephritis

Possible screening None
Possible prophylaxis None
Incidence 10–20% recurrence, 50% graft failure by 10 years
Rationale The risk of recurrent idiopathic membranous nephropathy is probably not high enough to preclude transplantation
for most recipients.
Recommendations (A) Patients should be counseled regarding the relatively high incidence of recurrence, and moderately high risk of
graft failure should the disease recur.

in about 11% can graft failure be attributed to recurrent dis-
ease (316).
Patients with type I membranoproliferative glomerulonephritis
(MPGN) should be informed of the approximately 20–30%
risk of recurrence (Table 37) (273,275,278,300,310,319). Graft
loss may be seen in 40% of those patients with recurrence
(273,300). Patients with type II MPGN should be informed of
an approximately 80% risk of recurrence (273,275,
278,320,321). Graft loss is reported to be rare, occurring in
about 10–20% of patients with recurrence (321). With Type II
MPGN, progression towards ESRD is often slow compared to
Type I. Type III MPGN is unusual, but a case of recurrence has
been reported (322). It is important to differentiate these idio-
pathic MPGNs from those secondary to hepatitis C infection
(Table 58) (323, 324). Positive serology for hepatitis C should
increase the suspicion for secondary MPGN The transplant
glomerulopathy that resembles MPGN and is associated with
hepatitis C can occur with and without cryoglobulinemia, hy-
pocomplementemia and rheumatoid factor (325,326). It is
also important to differentiate MPGN from chronic rejection by
careful histological evaluation. Immunofluorescence and elec-
tron microscopy evaluations are useful to differentiate these
two entities, since immune deposits are not seen in MPGN as-
sociated with chronic rejection.
be as high as 50% in patients followed for 10 years (330). In
some series, a portion of patients with recurrent ‘‘idiopathic’’
membranous nephropathy may have hepatitis C (331). There
do not appear to be any readily identifiable risk factors for
recurrence (330).
A meta-analysis of the results of 10 observational studies pub-
lished between 1977–1997 has been reported (Table 39)
(332–341). In the meta-analysis there were 159 grafts in 127
patients with ESRD from hemolytic uremic syndrome (HUS),
although data on risk factors were available for only about half
of these patients (342). The overall rate of recurrence for HUS
was 28% (342). One-year graft survival was 33% compared to
77% in controls (342). Older age of onset of HUS, shorter inter-
val between HUS onset and transplantation, shorter interval
between HUS onset and ESRD, the use of living donors and
the use of calcineurin inhibitors were all associated with recur-
rence (342). There was no effect of gender or hemodialysis
duration prior to transplantation. There was no difference in the
rate of recurrence between first or second transplants. In
multivariate analysis, age at onset of HUS, interval between
HUS and ESRD, use of calcineurin inhibitors, and living-related
donors were statistically significant predictors of HUS (342).
The risk for graft failure in patients with posttransplant HUS/
thrombotic thrombocytopenic purpura (TTP) was reported to
be 5.4 higher than for patients without posttransplant HUS/
TTP (271).

The incidence of recurrent membranous nephropathy varies Cyclosporine (342), tacrolimus (343), anti-lymphocyte globu-
with duration of follow-up, but is probably around 10–20% lin (344) and OKT3 (345) have each been reported to be
(Table 38) (273,275,283,300,300,310,327–330). Graft loss associated with recurrence of HUS after transplantation in
from recurrence of idiopathic membranous nephropathy may case reports and small uncontrolled series. A recent multi-

2001; Suppl. 1: Vol. 2: 5–95 31

Kasiske et al.

Table 39: Hemolytic uremic syndrome/thrombotic thrombocytopenic purpura (HUS/TTP)

Possible screening None
Possible prophylaxis Antiplatelet agents
Incidence 28% recurrence, 50% graft failure
Rationale The chances of recurrence and risk factors for recurrence of HUS/TTP after renal transplantation are reasonably well
defined to allow patients and potential living donors to exercise informed consent.
Recommendations (A) Patients and living donors should be counseled regarding the risk of recurrent HUS and graft failure.
(B) In patients with a history of HUS, consideration should be given to avoiding calcineurin inhibitors and living
donors.
(B) Occurrence of HUS in a prior transplant should not be a contraindication to transplantation.
(C) The prophylactic use of antiplatelet agents may help to reduce the chances of recurrence after renal transplan-
tation.

Table 40: Antiglomerular basement membrane (anti-GBM)/Goodpasture’s disease

Possible screening Anti-GBM antibody titer
Possible prophylaxis None
Incidence Approximately 10%
Rationale Anti-GBM disease can recur in renal allografts, although the incidence of recurrence is not high enough to preclude
transplantation.
Recommendations (C) It is probably prudent to wait for circulating anti-GBM antibody levels to diminish before proceeding with trans-
plantation.

center study failed to find an association between the use of
CsA and the rate of recurrence (346). De novo HUS/TTP can
occur after exposure to CsA, and in this setting replacing CsA
with tacrolimus has been reported to be beneficial in some
cases (343,347,348) but not in others (349). Certainly de
novo HUS/TTP can also occur in patients being treated with
tacrolimus (343,350,351), and there is no evidence that the
incidence of HUS/TTP is different for CsA compared to tacrol-
imus (352). Although the evidence that CsA and/or tacrol-
imus causes de novo or recurrent posttransplant HUS/TTP is
not based on data from randomized, controlled trials, it may
nevertheless be prudent to avoid these agents in recipients
with HUS/TTP if possible.
Sporadic, epidemic HUS (often associated with toxigenic
strains of Escherichia coli) rarely recurs after transplantation. In
contrast, the rate of recurrence is very high in HUS inherited as
an autosomal recessive trait. In one report, six of seven patients
had recurrent HUS after transplantation, regardless of the
source of the kidney (living-related or cadaver) or the type of
immunosuppression (353). Another study found a recurrence
rate of 50% in those patients in whom HUS in the native kid-
neys was not associated with diarrhea (340). Autosomal domi-
nant HUS is relatively rare, but may also recur following trans-
plantation (354). Other familial conditions associated with
HUS include prostacyclin synthesis deficiency and Factor H
deficiency (355). Related donor transplantation should be
used with caution in these settings.
In the absence of sound clinical data, prudence would sug-
gest that individuals with active hemolysis should probably
forego transplantation until this is resolved. Similarly, due to
its association with oral contraceptives, patients with HUS/
TTP should probably avoid oral contraceptives. Prophylaxis
with antiplatelet agents, e.g. low dose aspirin, ticlopidine or
dipyridamole, may help to prevent recurrence. Indeed, there
is at least one multicenter, randomized, controlled trial in
non-transplant recipients suggesting that ticlopidine reduces
the incidence of recurrence in patients with TTP (356). On
the other hand, a recent report in non-transplant patients
suggested that clopidogrel bisulfate use is associated with
an increased incidence of TTP (357). Thus, the role of spe-
cific antiplatelet agents in the prevention of recurrent HUS/
TTP is unclear.
It is difficult to determine the incidence of recurrent anti-
glomerular basement membrane (anti-GBM) disease after
renal transplantation, since ESRD from this disorder is un-
common, and clinical recurrence is infrequent (Table 40)
(283, 310). Histologic recurrence may be seen in roughly
50% but clinical disease is reported to be present in only
10% of patients with anti-GBM disease. While successful
transplantation has been reported in a patient with circu-
lating anti-GBM antibodies at the time of transplantation
(358), it is recommended that circulating antibody should
be undetectable to minimize recurrence.

32 2001; Suppl. 1: Vol. 2: 5–95

 The Evaluation of Renal Transplant Candidates: Clinical Practice Guidelines

Table 41: Vasculitis including Wegener’s granulomatosus

Possible screening Antineutrophil cytoplasmic antibody (ANCA)
Possible prophylaxis Sulfamethoxazole-trimethoprim
Incidence 17% recurrence, ⬍10% graft failure
Rationale The risk of recurrence is moderately low and patients with recurrence usually respond to treatment.
Recommendations (A) Patients should be informed of the moderately increased risk of recurrence and small risk of graft failure due to
recurrence.
(B) Pretransplant ANCA does not appear to predict recurrence.
(C) The use of prophylactic CsA does not appear to reduce the risk of recurrence.

Table 42: Systemic lupus erythematosus (SLE)

Possible screening Clinical findings, e.g. skin rash, serositis or arthritis
Serum complements
Antinuclear antibody
AntiDNA antibody titer
Possible prophylaxis Immunosuppression, especially corticosteroids
Aspirin or other anticoagulant (if antiphospholipid antibody positive)
Incidence ⬍10% recurrence, graft failure is rare
Rationale It is theoretically possible that the activity of SLE reflected by clinical and serological parameters increases the risk
of recurrence after renal transplantation.
Recommendations (A) Patients can be told that SLE does not significantly reduce patient or graft survival.
(C) Patients with SLE should ideally be clinically and serologically quiescent at the time of transplantation.

Nachman and coworkers carried out a pooled analysis of pa-
tients with antineutrophil cytoplasmic antibody (ANCA)-as-
sociated vasculitis (Table 41) (359). They pooled results from
127 patients from the literature. The overall rate of recurrence
was 17% (359). The rate of recurrence was not statistically
different among patients treated with CsA (20%) or patients
with circulating ANCA at the time of transplantation (26%)
(359). The rate of recurrence was not different in patients
with Wegener’s granulomatosus, microscopic polyangiitis or
necrotizing crescentic glomerulonephritis. Data from small,
uncontrolled, retrospective studies suggest that the majority
of patients with recurrence can be treated successfully with
cyclophosphamide therapy (360–362). One report described
a successful outcome in 18 of 20 patients, six of whom
showed signs of active disease at the time of transplantation
(363). After 48 months of follow-up only one patient had
died and one had lost graft function due to chronic rejection
(363). Although successful transplantation has been reported
in active disease, it would probably be best to wait until the
disease is quiescent if possible. Sulfamethoxazole/trimetho-
prim combination has been shown to be useful in the treat-
ment of Wegener’s disease by some (364) but not others
(365).
Systemic lupus erythematosus (SLE) is the cause of renal
failure in approximately 5% of patients with ESRD (Table 42)
(310,366–377). While there are reports of successful trans-
plantation with active SLE (366–368,372), it is generally rec-
ommended that clinical manifestations (renal and extra-renal)
be quiescent on minimal doses of corticosteroids, e.g. no
more than 10 mg per day of prednisone, before transplan-
tation. Furthermore, it is suggested that serologic parameters
(complement, anti-nuclear antibody, anti-DNA antibody ti-
ters) should be normal, or at least stable before transplan-
tation (371), although clinical evidence supporting this recom-
mendation is lacking. Patients can be told that less than 10%
of transplant recipients with SLE have recurrence (310,366–
377). Clinical presentation may be extra-renal (rash, arthral-
gias, Raynaud’s phenomenon) or renal (proteinuria, graft dys-
function). The incidence of recurrence may be 35–45% if
protocol biopsies are performed (378). Recurrence that re-
sults in graft failure is rare, and virtually all studies using
matched or unselected controls have found no adverse effect
of SLE on patient or graft survival (368,373–376,379,380).
A few investigators have found that the incidence of acute
rejection appears to be increased (373,379), but in neither of
these studies was graft survival reduced in patients with SLE.
In the US, patients with SLE are transplanted at least as often
as patients with other causes of ESRD (381).
Primary oxalosis is very rare (Table 43). Among patients aged
20 or less, primary oxalosis was listed as the cause of ESRD
in 19/6230 (0.4%) in 1994–98 (63). Most cases of oxalosis
are due to primary hyperoxaluria type 1 (PH1), which is
caused by a rare, autosomal recessive deficiency of the he-
patic enzyme alanine:glycoxylate aminotransferase. This en-
zyme deficiency leads to an increase in urinary excretion of
calcium oxalate, recurrent urolithiasis and nephrocalcinosis.

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Kasiske et al.

Table 43: Primary oxalosis

Possible screening Urinary and plasma oxalate, and decreased alanine:glycoxylate aminotransferase on liver biopsy
Possible prophylaxis High fluid intake (3–6 liters/day), pyridoxine, orthophosphate, crystallization inhibitors (e.g. phosphate, magnesium
and citrate)
Incidence 90–100% recurrence in the absence of a liver transplant
Rationale Kidney transplantation can replace renal function, and aggressive medical management can prevent systemic oxalate
deposition if there is adequate renal function. However, only liver transplantation effectively restores the deficient
enzyme activity.
Recommendations (A) Intensive medical management with maintenance of a high fluid intake, pyridoxine, orthophosphate, and crystalli-
zation inhibitors is recommended for patients with renal function.
(B) Isolated kidney transplantation is an option for patients without severe systemic disease.
(B) Preemptive liver transplantation alone (before ESRD) is also a reasonable option for some patients.
(B) Simultaneous liver/kidney transplantation is the treatment of choice for patients with ESRD and severe systemic
oxalosis.

This, in turn, leads to renal failure, which impairs urinary ex-
cretion of oxalate and causes oxalate deposition throughout
the body (oxalosis). The diagnosis of PH1 is made by demon-
strating increased urinary and plasma oxalate, and decreased
alanine:glycoxylate aminotransferase on liver biopsy. Early in
the course, renal damage and systemic oxalate deposition
can be minimized by high fluid intake, pyridoxine and ortho-
phosphate (382). Oral orthophosphate reduces renal calcium
oxalate deposition, while pyridoxine is a coenzyme that func-
tions in the conversion of glyoxylate (the immediate precursor
to oxalate) to glycine. Urinary crystallization inhibitors such as
phosphate, magnesium and citrate may be useful. Despite
conservative management, ESRD is reached by age 15 in
50% (383). Although liver transplantation is potentially cura-
tive, there is no consensus regarding the timing of liver trans-
plantation and the role of isolated kidney transplantation in
treating patients with PH1 (384).
In patients without ESRD, early, preemptive liver transplan-
tation may be an option (385,386). Isolated kidney transplan-
tation may be considered for ESRD patients who are without
significant, systemic oxalosis, especially if there is evidence
for residual alanine:glycoxylate aminotransferase activity
(387,388). In a review 138 cases of renal transplantation from
the U.S. Renal Data System, there was no difference in 6-
year graft survival between isolated kidney vs. combined
liver/kidney transplantation (51% vs. 56%, respectively)
(389). Patient survival tended to be better for isolated kidney
vs. combined kidney/liver transplantation. Differences in pa-
tient selection and other factors make it difficult to interpret
the results of analysis of registry data. However, the authors
concluded that because kidney/liver transplantation can still
follow a failed kidney transplant, isolated, living-related donor,
kidney transplantation is a reasonable first option for patients
with PH1 (389). Aggressive hemodialysis should be used to
reduce the oxalate load pretransplant (383). Isolated kidney
transplant should also be accompanied by intensive medical
management to prevent recurrent renal disease (390,391).
Many argue that patients with ESRD should be considered
for combined liver/kidney transplantation. Between 1984 and
1987, 30 European centers reported 87 liver transplants
(most combined with kidney transplantation) (392). The 1-,
2-, and 5-year patient survival rates were 88%, 80%, and
72% (392). Graft survival rates were 82%, 78% and 62%,
respectively. Results were poor when transplantation was
delayed until advanced systemic oxalosis had developed
(392), and many have advocated early, preemptive liver
transplantation (393). Others have reported that growth im-
proves after combined liver/kidney transplantation (394). The
hyperoxaluria that occurs after combined liver/kidney trans-
plantation may threaten the renal allograft, and intensive
medical management to prevent nephrolithiasis should be
pursued (395,396).
Primary oxaluria type 2 (PH2) is extremely rare, with only a
handful of cases reported in the literature (397). It is caused
by a deficiency of hepatic D-glycerate dehydrogenase/gly-
coxylate reductase (397). Much less is known about the clin-
ical course and optimal management of PH2 compared to
PH1. Age of onset is greater, stone-forming activity less, and
incidence of ESRD less in PH2 compared to PH1 (398).
Among patients aged 20 or less, cystinosis was listed as the
cause of ESRD in 36/6230 (0.7%) in 1994–98 (Table 44)
(63). Early and adequate treatment of children with cystinosis
with oral analogues of cysteamine may delay onset of ESRD
(399,400). Recurrence per se does not occur since the trans-
planted kidney corrects the deficiency in the specific trans-
port system for lysosomal cystine efflux (401). However, cys-
tine crystals that do not seem to affect renal function have
been reported in the allograft (402). Morbidity due to con-
tinued accumulation of cystine in other organs is not pre-
vented by transplantation (403). Data from the U.S. Renal
Data System indicated that 15 (83%) of 18 patients with cys-
tinosis received renal transplants (2 living-related and 13 ca-
daveric), and the 3-year graft survival was over 75% (404).
Several single-center studies have also reported excellent
graft and patient survival (401,402,405,406). More recently,
the North American Renal Transplant Cooperative Study re-
ported that both cadaveric and living-related transplant out-
comes were excellent for children with cystinosis (407). In a

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 The Evaluation of Renal Transplant Candidates: Clinical Practice Guidelines

Table 44: Cystinosis

Possible screening None
Possible prophylaxis Oral analogs of cysteamine
Incidence Recurrence does not occur in the kidney, graft survival is excellent.
Rationale The transplanted kidney does not have the defect in lysosomal cystine efflux; however, the renal transplant does not
correct the systemic disease.
Recommendations (A) Renal transplantation is the treatment of choice for ESRD in children with cystinosis.

Table 45: Fabry’s disease

Possible screening None
Possible prophylaxis None
Incidence 100% histologic recurrence, rarely causes graft failure
Rationale Long-term graft survival appears to be the norm after renal transplantation in Fabry’s disease. Recurrence is very
slow and rarely leads to graft failure. Rather, graft failure is usually caused by death from sepsis or other systemic
complications.
Recommendations (B) Renal transplantation is the treatment of choice for patients with Fabry’s disease who do not have severe systemic
disease that would preclude transplantation.

Table 46: Alport syndrome and antiglomerular basement membrane disease

Possible screening None. (Measuring antiglomerular basement membrane antibodies does not predict disease or outcomes).
Possible prophylaxis None
Incidence Clinically significant antiglomerular basement disease is rare.
Rationale Alport syndrome does not recur in the allograft, and clinically significant antiglomerular basement membrane does
not occur frequently enough to influence the overall outcome after renal transplantation.
Recommendations (A) Renal transplantation is the treatment of choice for ESRD caused by Alport syndrome. Patients should be warned
of the small chance that clinically significant antiglomerular basement membrane disease may develop.

report of 30 adult cadaveric renal transplants, 1-year and 5-
year graft survival rates were 90% and 75%, respectively
(408). Finally, a recent report from the North American Renal
Transplant Cooperative Study dispelled concerns about
higher rates of graft thrombosis in patients with cystinosis
(409).
Fabry’s disease is due to a deficiency of alpha galactosidase
enzyme, which results in an accumulation of a glycosphingol-
ipid in the kidneys and other organs (Table 45). It was initially
hoped that kidney transplantation would provide sufficient
enzyme to prevent disease progression. However, this proved
not to be the case (410), and it is clear that the disease can
recur in the transplanted kidney (411–414). In addition, the
disease appears to progress in other organs as well (413,415).
However, histologic recurrences have mostly been docu-
mented several years after transplantation (411–414), and
long-term graft survival is common (416–418). Most recur-
rences have been associated with few renal manifestations,
e.g. microhematuria without renal functional impairment. In-
deed, 3-year graft survival of 80% has been noted by the
Collaborative Transplant Study (261). A more recent analysis
of data from the U.S. Renal Data System found that 5-year
patient and graft survival rates were 83% and 75%, respec-
tively, for 93 patients with Fabry’s disease, compared to 82%
and 67% for case-matched controls (418). Infectious compli-
cations are common and often life-threatening (413,419).
Bone marrow transplantation with genetically manipulated
cells may cure patients with this rare disorder in the future
(420).
Alport syndrome results from mutations in type IV collagen,
with X-linked (80% of patients), autosomal recessive (15%)
and autosomal dominant variants (5%) (Table 46). Recur-
rence is theoretically possible if a patient with Alport syn-
drome receives a kidney from a related affected individual,
but this has been reported only once (421). However, the
introduction of altered collagen in the basement membrane
of the transplanted kidney may induce the recipient to form
antibodies to the donor kidney collagen (422,423). Although
the true incidence of anti-GBM antibody formation is un-
known, clinically and histologically significant anti-GBM ne-
phritis is rare, occurring in 3–4% of transplanted males with
Alport syndrome. Rarely, it can cause nephrotic syndrome

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Kasiske et al.

Table 47: Sickle cell disease

Possible screening None
Possible prophylaxis None
Incidence Unknown rate of recurrence, long-term mortality is increased
Rationale Short-term patient and graft survival appear to be no different for patients with, compared to patients without, sickle
cell disease. However, long-term mortality appears to be increased about 2.5 fold. Nevertheless, preliminary analysis
comparing transplant recipients to patients left on the waiting list suggest that survival may be better after transplan-
tation.
Recommendations (B) Renal transplantation appears to be the treatment of choice for patients without severe systemic complications
that would preclude surgery and transplantation.
(C) While it may make intuitive sense to delay transplantation when patients are having frequent sickle cell crises,
there are no data to support this practice.

Table 48: Amyloidosis

Possible screening None
Possible prophylaxis Colchicine in familial Mediterranean fever
Incidence The overall rate of recurrence of amyloidosis in the transplanted kidney is 30–40%. Mortality in patients with recur-
rence is increased by about 20%.
Rationale Outcome after renal transplantation in amyloidosis is largely determined by the severity of the systemic disease. The
increased rate of graft failure is largely due to increased mortality.
Recommendations (B) Patients should probably not be transplanted if the systemic amyloidosis is severe.
(B) Outcomes after renal transplantation in patients with familial Mediterranean fever are good if systemic disease
is limited and colchicine prophylaxis is used.

and even graft failure (424–426). Anti-GBM nephritis occurs
even more rarely, if ever, in women transplanted for X-linked
Alport syndrome. Anti-GBM nephritis has occurred in both
males and females with autosomal recessive disease, but the
incidence in this subgroup is unknown. Recurrence of anti-
GBM nephritis in subsequent allografts is common. Only
rarely does anti-GBM nephritis cause nephrotic syndrome or
graft failure (424–426). A retrospective review of 30 trans-
plant recipients with Alport syndrome found that graft survival
was 75% and 42% at 5 and 10 years, while patient survival
was 96% and 77% at 5 and 10 years (427). The authors,
and others (407), concluded that patient and graft survival in
Alport syndrome were not different from that seen in other
renal transplant recipients.
Sickle cell disease often leads to ESRD, probably by causing
chronic interstitial fibrosis, but focal segmental glomerular
sclerosis and nephrotic syndrome also occur in some patients
(Table 47). Although renal changes consistent with recurrent
sickle cell disease have been reported in allografts (428), mor-
tality from systemic disease complications is the greatest
threat to graft survival. In a 1980 survey there were 34 trans-
plants in patients with sickle cell disease in whom the 1-year
graft survival was 67%, and the patient survival 87% (429). A
1999 study of U.S. Renal Data System data reported no differ-
ence in 1-year cadaveric graft survival between patients with
sickle cell disease (78%, nΩ85) and African Americans with
other renal diseases (77%, nΩ22,565) (430). However, the 3-
year graft survival was lower (48% vs. 60%, pΩ0.055) (430).
In multivariate analysis the adjusted 3-year relative risk for graft
failure was 1.60 (pΩ0.003), while the relative risk for death
was 2.95 (pΩ0.0001) at 1 year and 2.82 (pΩ0.0001) at 3
years. There was a trend toward improved survival for trans-
planted patients with sickle cell disease compared to sickle cell
disease patients left on the waiting list (relative risk 0.14, pΩ
0.056). In 1998 the North American Pediatric Renal Transplant
Cooperative Study registry reported the results of nine renal
transplants in children with sickle cell anemia (431). One and
2-year graft survival was 89% and 71% (431).
Anemia has been reported to improve following renal trans-
plantation (432,433). Ultimately, bone marrow transplan-
tation may offer a cure for patients with sickle cell disease
(434). However, this approach is still considered experimen-
tal (435,436). To date, there have been no reports of simul-
taneous kidney and bone marrow transplants for patients
with sickle cell disease.
Many patients with systemic amyloidosis (primary or second-
ary) succumb to cardiovascular disease, infections or pro-
gressive multi-organ involvement (Table 48). Transplantation
should generally be discouraged in patients with severe se-
quelae of amyloidosis. In a case control study of 45 patients
with amyloidosis, 3-year patient survival was only 59% com-
pared to 79% among controls (437). Graft failure censored
for death was similar in cases and controls. By 1 year after

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 The Evaluation of Renal Transplant Candidates: Clinical Practice Guidelines

Table 49: Mixed essential cryoglobulinemia

Possible screening Cryoglobulin, complement levels and hepatitis C virus (HCV), ribonucleic acid (RNA)
Possible prophylaxis None
Incidence 50% recurrence, frequent graft failure
Rationale Although the risks of recurrence and graft failure are high, outcomes are reasonable for at least some patients.
Recommendations (C) Patients should be informed of the increased risk of recurrence and graft failure. It may be prudent to wait until
the disease is relatively quiescent, clinically and serologically.
(C) Patients with mixed essential cryoglobulinemia should be screened for HCV RNA, and patients with high titers
should be considered for pretransplant, antiviral therapy.

Table 50: Waldenström’s macroglobulinemia

Possible screening None
Possible prophylaxis None
Incidence 10–25% recurrence, 50% graft failure
Rationale The rate of recurrence appears to be relatively low.
Recommendations (C) Patients should be informed of the increased risk of recurrence and graft failure.

Table 51: Immunoglobulin light chain deposition disease

Possible screening None
Possible prophylaxis None
Incidence 50% recurrence, 30% graft failure
Rationale Although recurrence is common, disease progression is slow and many patients do well for prolonged periods of
time following transplantation.
Recommendations (C) Patients should be informed of the increased risk of recurrence and graft failure.

transplantation, about 20% had evidence of recurrence of
amyloid in the allograft (437). Others have reported the rate
of recurrence of amyloidosis in the graft to be 30–40% (438,
439). In a recent analysis of the Collaborative Transplant
Study registry, 5-year survival for 413 patients with amyloid-
osis was 66% compared to 86% for patients with glomeru-
lonephritis and 84% for patients with polycystic kidney dis-
ease (440). The outcome of transplantation in amyloidosis
appears to be determined by the severity of the systemic
disease, rather than by recurrence in the allograft per se
(441). Retrospective studies suggest that recurrence of amyl-
oidosis associated with familial Mediterranean fever can be
prevented by colchicine (442,443). In a recent case report, a
patient with amyloidosis caused by a genetic mutation in the
fibrinogen gene was cured by combined liver and kidney
transplantation (444).
formed of an approximately 50% risk of recurrence, which is
often associated with graft dysfunction and graft loss (445,
446). Given the association between mixed essential cryo-
globulinemia and HCV, it is reasonable to screen for HCV
ribonucleic acid (RNA). It may also be reasonable to consider
pretransplant treatment in patients with replicative HCV dis-
ease and mixed essential cryoglobulinemia with antiviral ther-
apy (see Table 58).
Only a handful of cases of renal transplantation in patients
with Waldenström’s macroglobulinemia have been described
(Table 50). Recurrence can occur leading to graft dysfunc-
tion. Death due to sepsis is not uncommon (120, 447). Pa-
tients with Waldenström’s macroglobulinemia should be in-
formed that there is about a 10–25% risk of recurrence with
graft loss in up to 50% of these cases with recurrence (261).

There are very few data to guide the approach to patients
with mixed essential cryoglobulinemia (Table 49). Although
there is no evidence that transplantation during a clinically
and serologically active phase of mixed essential cryoglob-
ulinemia leads to recurrence, it is probably prudent to wait
until these parameters (including cryoimmunoglobulin and
complement levels) are quiescent. Patients should be in-
Of the few reported patients with light chain deposition dis-
ease, recurrence has been reported in roughly 50% (Table
51). Graft loss was seen in one-third of patients with recur-
rence that did not respond to aggressive therapy (including
plasmapheresis, melphalan and corticosteroids) (448–450).
There are two reported cases of recurrent fibrillary glomeru-
lonephritis (GN) among four (50%) individuals who received

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Kasiske et al.

Table 52: Progressive systemic sclerosis (scleroderma)

Possible screening None
Possible prophylaxis None
Incidence Approximately 20% recur, many with recurrence have graft failure
Rationale Outcomes after renal transplantation are generally good in patients with scleroderma.
Recommendations (B) Renal transplantation is the treatment of choice for ESRD caused by scleroderma, if systemic end-organ damage
is not too severe to preclude transplantation.

Table 53: Colonic diverticulae

Possible screening Medical history and physical examination
Barium enema
Colonoscopy
Stool occult blood
Incidence Colonic perforations occur in 0.5–2% of renal transplant recipients and can contribute to posttransplant morbidity
and mortality. Patients with autosomal dominant polycystic kidney disease (ADPKD) are at even greater risk (approxi-
mately 5%).
Rationale Chronic immunosuppression heightens the risks of colonic perforation after transplantation, because of immunosup-
pression and the masking of clinical signs and symptoms. Immunosuppression heightens the risk of sepsis from
colonic perforation. Patients with chronic renal failure have an increased tendency towards decreased gastrointestinal
motility and colonic dilatation from electrolyte abnormalities, the use of phosphate binders, potassium-absorbing
resins, iron supplementation and some antihypertensive medications.
Recommendations (D) There is no evidence to recommend screening, and some evidence to suggest that screening asymptomatic
patients prior to transplantation is ineffective.
(C) Although patients with ADPKD have a higher prevalence of diverticular disease, there is insufficient evidence to
recommend routine screening with barium enema or colonoscopy.
(C) Patients with a history of diverticulitis should have screening studies with consideration for elective partial colecto-
my prior to transplant.

kidney transplants. These patients presented with nephrotic
range proteinuria and the grafts were lost in both cases (451,
452). Immunoglobulin deposition disease may or may not
occur in multiple myeloma (see Table 19).
Progressive systemic sclerosis, or scleroderma, is an uncom-
mon cause of ESRD (Table 52). Occasional patients who
have severe cardiac, pulmonary or gastrointestinal involve-
ment may be at high risk for complications, severe gastroin-
testinal disease may interfere with drug absorption. Neverthe-
less, renal transplantation is the treatment of choice for most
patients with ESRD due to scleroderma. Although most pa-
tients with scleroderma and ESRD do well after renal trans-
plantation, approximately 20% may have a recurrence in the
allograft, and many of these will develop graft failure as a
result (453–455). In a report from the UNOS Scientific Regis-
try, 86 patients with scleroderma were transplanted over a
10-year period from 1987 to 1997 (456). One- and 5-year
graft survival rates were 62% and 47%, respectively. Among
the 14 known causes of graft failure, five had acute rejection,
four chronic rejection, three recurrent scleroderma, and one
each had infection and thrombosis (456). Outcomes did not
seem to be different in patients treated with or without CsA
(456).
The risk of recurrence is approximately 20%. Graft loss from
recurrence often occurred in patients in whom the time inter-
val from onset of the disease to transplantation was less than
1 year, but this experience accrued prior to the CsA era
(454). Patients who have undergone bilateral nephrectomy,
often to control severe hypertension, may have the best sur-
vival (261). Recently, autologous stem cell transplantation has
been used in patients with severe scleroderma but limited
target organ damage (457,458). Similarly, it has been pro-
posed that allogenic marrow transplantation may be benefi-
cial in selected patients (459). To date there have been no
reports of simultaneous bone marrow/kidney transplantation
for treatment of scleroderma and ESRD.
Gastrointestinal
Over the past 25 years the incidence of colonic perforation
after renal transplantation has remained remarkably stable at
0.5–2.0% (Table 53) (460–465). Mortality from colonic per-
foration is very high (17–43%) (464–466). Diverticulitis is the
most frequent cause of colon perforation in renal transplant
recipients. This may be related to the high prevalence of di-
verticulosis in patients on dialysis (467), and other predispos-
ing factors (468,469). In a retrospective study by Stelzner et
al., diverticular disease was found to be the cause of colonic
perforation in 36% of patients, whereas ischemic colitis ac-

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 The Evaluation of Renal Transplant Candidates: Clinical Practice Guidelines

Table 54: Peptic ulcer disease (PUD)

Possible screening Medical history and physical examination
Upper gastrointestinal endoscopy
Stool occult blood
Culture, 13C or 14C urea breath test, rapid urease test and serological tests for Helicobacter pylori
Incidence ⬍10% have symptomatic PUD posttransplant
Rationale PUD can cause significant morbidity and mortality following renal transplantation. Transplant recipients are at higher
risk for PUD from corticosteroids and infections such as herpes simplex virus, CMV, Candida species and Helicobact-
er pylori.
Recommendations (D) Routine examination of the upper gastrointestinal tract by endoscopy or X-rays is not recommended in asympto-
matic patients with no prior history of PUD.
(D) Routine screening for Helicobacter pylori in asymptomatic adults or children is not indicated.
(C) Upper gastrointestinal endoscopy should be considered for patients with a prior history of PUD.

Table 55: Cholelithiasis

Possible screening Medical history and physical examination
Ultrasound
Incidence 5–10%, but up to 25% among diabetics
Rationale There is increased risk of life-threatening cholecystitis after transplantation. Prophylactic cholecystectomy, especially
with laparoscopic surgery, is associated with low morbidity and mortality.
Recommendations (C) Patients with a history of cholecystitis should have an ultrasound to identify the presence of cholelithiasis, and
be considered for cholecystectomy.
(C) Diabetics should be screened by ultrasound for cholelithiasis and offered a pretransplant cholecystectomy if
gallstones are found.

counted for perforation in 24% of patients and colonic di-
lation in 12% of patients (465).
Although deaths from posttransplant colonic perforation are
not unusual, it is unclear how to prevent them. Retrospective
studies have suggested that early recognition and inter-
vention in cases of colonic perforation reduce mortality (464,
465). However, whether pretransplant screening and prophy-
lactic, partial colectomy in patients with severe diverticulosis
are effective is unknown. In one retrospective study, all trans-
plant candidates ⬎50 years old underwent screening, and
20 were found to have significant diverticular disease (463).
However, none of these patients had pretransplant colecto-
my, and none had symptomatic disease posttransplant
(463). Although most investigators have found that the inci-
dence of diverticulosis and colonic perforation (as well as
other gastrointestinal complications) is higher among pa-
tients with autosomal dominant polycystic kidney disease
(ADPKD) (470) there are no studies to suggest that screening
asymptomatic patients with ADPKD is effective in preventing
posttransplant colonic complications.
Finally, there are very few data to guide decision-making for
transplant candidates who have a history of symptomatic di-
verticular disease. However, it seems reasonable that patients
with a history of diverticulitis should be evaluated by barium
enema and/or colonoscopy, with consideration for resection
if extensive disease is present or symptomatic diverticulitis
persists (467,469,471).
Peptic ulcer disease (PUD) was once such a frequent (18–
40%) and potentially lethal posttransplant complication that
pretransplant screening and even surgery were often recom-
mended (Table 54) (472–486). With the increasing use of
prophylactic antacids, the incidence of symptomatic PUD has
declined. In patients receiving renal transplants between 1984
and 1989, the incidence of PUD complications was approxi-
mately 10% (487,488). More recently, prophylaxis with H2
blockers or proton pump inhibitors has reduced the risks of
serious complications (489). In 1995, Troppmann et al. re-
ported a 3.2% overall incidence of endoscopy proven ulcer-
ation of the upper gastrointestinal tract in patients in whom
antacids were the only ulcer prophylaxis (490). Patients with a
history of PUD disease demonstrated a 3-fold greater inci-
dence of posttransplant ulceration compared to patients with
no history of PUD disease, but there was no ulcer-related mor-
tality or graft loss. The authors concluded that renal transplan-
tation is safe, even in patients with a history of peptic ulcer dis-
ease (490). Recognition of the role of Heliobacter pylori and
its treatment have also helped reduce the morbidity associated
with peptic ulcer disease (491–494). However, routine screen-
ing for Heliobacter pylori is generally not recommended (495–
499).
There are insufficient data to determine which, if any,
asymptomatic patients should have routine, pretransplant
upper gastrointestinal evaluation. However, it seems reason-
able to recommend upper gastrointestinal endoscopy for
patients with a prior history of PUD. Patients found to have

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Kasiske et al.

Table 56: Liver disease

Possible screening Medical history and physical examination
Serum total bilirubin and serum transaminases
Viral hepatitis serologies (Tables 57 and 58)
Serum iron, iron binding capacity and ferritin
Incidence 8–28% of renal transplant recipients die of liver disease.
Rationale Liver disease is a common cause of morbidity and mortality posttransplant. Surgical risk, blood levels of medications,
and outcomes following transplantation may be affected by liver disease.
Recommendations (A) All transplant candidates should be screened with medical history, physical examination, serum total bilirubin,
serum transaminases, and serological tests for hepatitis B and hepatitis C (Tables 57 and 58).
(B) Patients with no evident cause of elevated serum transaminases should have serum iron, iron binding capacity
and ferritin levels.

active disease should be treated medically prior to trans-
plantation.
There is controversy surrounding the need for pretransplant
screening for cholelithiasis and cholecystectomy (Table 55)
(500–505). Some have advocated routine pretransplant
screening and prophylactic cholecystectomy (503), but
others have felt that this is unnecessary (504, 505). In a
cross-sectional study, 15 of 211 (7.1%) asymptomatic post-
transplant patients who underwent routine ultrasonography
were found to have cholelithiasis (504). On follow-up, 13
(87%) of the patients with cholelithiasis remained asympto-
matic, but two developed acute cholecystitis and under-
went uncomplicated laparoscopic surgery (504). The
authors concluded that pretransplant screening for choleli-
thiasis was not necessary (504). However, their results may
have been biased by the cross-sectional study design, and
the fact that longer follow-up may have increased the inci-
dence of cholecystitis and resulting complications. In an-
other retrospective study from a center where routine pre-
transplant screening was not carried out, patients who had
posttransplant cholecystectomies were located among ‘‘ac-
tive’’ renal transplant recipients (505). There were 52/662
(7.9%) who had undergone cholecystectomy for cholelithi-
asis. Since complications were seen in only 6/52 (11.5%),
and there was no mortality or graft loss, the authors argued
that prophylactic screening was probably not necessary
(505). However, the results of this study may have been
seriously biased by not including patients who had died or
lost their allografts.
In a retrospective study from a center where ultrasound and
prophylactic, laparoscopic cholecystectomy had become a
part of the routine pretransplant evaluation, 10% of 406 pa-
tients were found to have gallstones and 9% underwent un-
complicated, pretransplant cholecystectomy (503). Among
88 historical controls that did not undergo pretransplant
screening, 16 (18%). required surgery posttransplant for gall-
stones. There was significant operative morbidity in 2/16 (14%)
and mortality in 1/16 (9%) (503).These authors concluded that
screening and prophylactic, laparoscopic cholecystectomy
should be part of the pretransplant evaluation (503).
Unfortunately, there are no controlled trials comparing
prophylactic screening with no screening to determine which
approach is best. A screening program could target high-risk
patients, e.g. patients with diabetes (501). In the absence of
sound data, it may be most reasonable to include the patient
in the decision to screen or not to screen. Patients with chole-
lithiasis who do not have cholecystectomy should be caution-
ed about the increased risk of potentially life-threatening cho-
lecystitis after transplantation.
Liver disease is a significant cause of late morbidity and
mortality among renal allograft recipients (Table 56). Death
from liver failure has been reported in 8–28% of long-term
kidney recipients (114, 506). The most common cause of
chronic, posttransplant liver disease is viral hepatitis. There
are six principal hepatitis viruses: A, B, C, D (delta), E and
G. No evidence exists to suggest that hepatitis A virus
causes chronic liver disease in renal transplant recipients.
Hepatitis D virus is rare, but is associated with significant
progression of liver disease when co-infection with HBV in-
fection is present (507). Hepatitis E and G are not known
to cause chronic liver disease. Hepatitis B and C, however,
are the most common hepatotropic virus infections among
ESRD patients and each can have a significant impact on
the renal transplant recipient.
Patients with evidence of liver disease, e.g. signs, symp-
toms, or elevated serum transaminases, should be asked
about ingestion of alcohol and drugs that are known to
cause liver cell necrosis. Serum transaminases should be
reassessed after the patient has abstained from potential
toxins. With the widespread use of erythropoietin and the
resulting diminished need for blood transfusion, hepatic
dysfunction due to iron overload is becoming less common
in hemodialysis patients. Nevertheless, iron overload can
cause chronic liver disease after transplantation, and can
exacerbate liver damage in patients with viral hepatitis. Of
patients who underwent liver biopsy for chronic hepatic
dysfunction in the 1970’s and 1980’s, 12–44% had hemos-
iderosis (508, 509). Although the current prevalence of liver
disease from iron overload is much less, the exact preva-
lence is unclear.

40 2001; Suppl. 1: Vol. 2: 5–95

 The Evaluation of Renal Transplant Candidates: Clinical Practice Guidelines

Table 57: Hepatitis B virus

Possible screening Serum transaminases
Hepatitis B virus surface antigen (HBsAg)
Hepatitis B virus deoxyribonucleic acid (HBV DNA)
Hepatitis B virus e-antigen (HBeAg)
Liver biopsy
Possible prophylaxis Recombinant hepatitis B vaccine
Incidence The incidence of HBsAg positivity in the dialysis population has declined from 3% in 1976 to 0.2% in 1990, and
remains low.
Rationale HBsAg-positive patients with active viral replication (HBV DNA, HBeAg) are at increased risk for disease progression
following transplantation. Identifying patients with advanced disease will allow for informed decisions concerning
the advisability of proceeding with renal transplantation, remaining on maintenance dialysis or referral for evaluation
for combined liver-kidney transplantation. Some patients with HBV infection may benefit from initiation of lamivudine
(3Tc, Epivir) in the pre- or perioperative period.
Recommendations (A) All transplant candidates should be tested for HBsAg and serum transaminases. HBsAg-positive patients should
be tested for HBV DNA, HBeAg and delta virus infection.
(C) Given the poor sensitivity of serum transaminases and the risk of transplantation in patients with advanced
disease, liver biopsy should be strongly considered.
(C) Patients with cirrhosis may have an unacceptable risk of liver failure and should be advised to remain on dialysis,
or should be referred for combined liver-kidney transplant if appropriate.
(C) Consideration should be given to beginning lamivudine in the wait-listed patient with active viral replication or at
the time of transplantation in the HBsAg carrier.
(A) Patients who are HBsAg-negative should receive vaccination for HBV, if not already immunized. At least one
dose should be given prior to transplantation. HBV antibody status should be monitored annually, and booster doses
should be administered when antibody concentrations fall below protective levels.

The preponderance of data suggest that renal transplant re-
cipients who are hepatitis B surface antigen (HBsAg) positive
are at increased risk of dying after transplantation (Table 57)
(510–515). However, the exact risk cannot be determined for
an individual patient and many HBsAg-positive patients do
very well after transplantation (514,516,517). Moreover, many
of the early studies demonstrating poor results in HBsAg-
positive patients were performed prior to the identification of
hepatitis D (HBD) and hepatitis C virus (HCV). Recent data
suggest that patients who are co-infected with HBV and
either delta virus or HCV have more rapid progression of liver
disease and increased morbidity after transplantation (518,
519). In addition, there are no data to indicate whether
HBsAg-positive patients survive longer on dialysis or with a
renal allograft. Clearly, HBsAg positivity is not a contraindi-
cation to renal transplantation, but rather identifies a subset
of patients in whom a thorough pretransplant evaluation must
be done so that an informed decision concerning the advis-
ability of transplantation can be made.
Patients who are HBsAg positive and have circulating hepa-
titis B e-antigen (HBeAg) or serologic evidence of active viral
replication (i.e. HBV DNA) carry an increased risk of progress-
ive liver disease after transplantation (512, 520). Similarly,
HBD (delta)-positive patients, or those co-infected with HCV,
also have an increased risk (507, 518). These patients may
best be advised not to undergo renal transplantation, al-
though there are no data demonstrating whether the long-
term survival advantage of renal transplantation counterbal-
ances the increased risk associated with progression of liver
disease (521). Individual decisions in these cases should be
made. The role of lamivudine is not yet firmly established;
however, recent data suggests that it may be effective in con-
trolling viral replication in renal allograft recipients (522–525).
Drug resistance may limit the long-term effectiveness of lami-
vudine in some patients (526, 527).
The use of liver biopsy in the pretransplant evaluation of HBV-
infected patients is not based on firm evidence. Rather it is
based on an appreciation of the low sensitivity of serum
transaminases to identify significant liver disease in the ESRD
patient coupled with the often-unknown duration of infection.
Patients who are HBsAg negative should receive vaccinations
for HBV, if not already immunized, as part of the pretransplant
evaluation (225). At least one dose should be given prior to
transplantation since the antibody response to the vaccine is
better for hemodialysis patients compared to transplant re-
cipients (528–531). Nevertheless, the antibody response is
reduced in patients with ESRD, and a number of strategies
have been suggested to improve the rate of response. These
include doubling the dose (532), the use of intradermal injec-
tion (533–537), and the use of simultaneous granulocyte-
macrophage colony stimulating factor as an adjunct
(227,538,539). The response rate to vaccination is also better
if given before ESRD develops (539). Antibody levels should
be monitored annually, and booster doses administered
when concentrations fall below protective levels (225).
Our knowledge of the natural history of HCV-associated liver
disease in renal transplant recipients remains incomplete
(Table 58). Pretransplant anti-HCV antibody is associated
with an increased risk of posttransplant liver disease. In one
study, pretransplant anti-HCV positive recipients had a rela-
tive risk of 5.0 (95% confidence interval (CI) 2.4–10.5) for

2001; Suppl. 1: Vol. 2: 5–95 41

Kasiske et al.

Table 58: Hepatitis C virus (HCV)

Possible screening Serum transaminases
Enzyme linked immunosorbent assay (ELISA) for HCV antibodies
Recombinant immunoblot assay (RIBA) for HCV antibodies
Polymerase chain reaction (PCR) for HCV ribonucleic acid (RNA)
Incidence Roughly 10–20% of hemodialysis patients have HCV antibodies. Biochemical abnormalities of liver function are seen
in 7–24% of transplant recipients, and about 50% of the cases of liver disease can be attributable to HCV infection.
Anti-HCV is present in 11–49% of renal transplant recipients.
Rationale Liver failure is the cause of death in 8–24% of long-term renal transplant survivors. Identification of patients with
advanced histologic disease prior to transplantation would allow for an informed decision concerning the advisability
of proceeding with transplant or remaining on dialysis.
Recommendations (A) All transplant candidates should be tested for anti-HCV by ELISA with confirmatory testing by RIBA.
(C) Patients with positive anti-HCV serology should have serum tested for HCV RNA to confirm current HCV infection.
(C) Given the poor sensitivity of serum transaminases and the risk of transplantation in patients with advanced
disease, liver biopsy should be strongly considered.
(C) Patients with cirrhosis may have an unacceptable risk of liver failure and should be advised to remain on dialysis,
or should be referred for combined liver-kidney transplant if appropriate.
(B) Candidates who are positive for HCV RNA may benefit from a course of interferon-alpha prior to transplantation.

posttransplant liver dysfunction (541). The introduction of im-
munosuppression was accompanied by a 1.8–30.3-fold in-
crease in circulating viral titer (541). Hepatitis C is also associ-
ated with an increased incidence of proteinuria and glomeru-
lar disease posttransplant (542, 543). Despite these findings,
there is no consensus on the long-term impact of HCV infec-
tion on patient or graft survival. Some studies have noted
an adverse impact on patient outcomes (515,541,544–549),
while others have not (172,550–558). Differences in patient
populations, duration of follow-up and study design (most
are retrospective) may explain differences in results. The type
or number of HCV genotypes does not appear to affect out-
comes (559). Likewise, superinfection with hepatitis G does
not seem to affect outcome (560). Mortality associated with
HCV appears to be increased in hemodialysis patients (561),
and recent studies found that HCV-infected allograft recipi-
ents had better long-term survival than wait-listed dialysis
controls (562,563). Thus, the presence of HCV antibody per
se is not a contraindication to renal transplantation.
It is probably reasonable to follow a strategy similar to that
described for HBsAg-positive patients, whereby HCV-positive
patients should be considered for a liver biopsy as part of
the pretransplant evaluation (564,565). Although there are
no prospective studies demonstrating that pretransplant liver
histology predicts posttransplant outcomes, some retrospec-
tive observational studies have found that posttransplant his-
tology correlates with outcome (508,515). Transplant candi-
dates with advanced liver disease, i.e. cirrhosis, may be coun-
seled to remain on dialysis, although there is insufficient data
to state that transplantation is absolutely contraindicated in
this situation. Patients should be informed of the risks of im-
munosuppression on worsening liver disease; however, the
exact risk is unknown.
One promising approach is to eliminate HCV viral replication
prior to transplantation. Several small trials have examined
the safety and efficacy of interferon alpha-2a treatment of
hemodialysis patients (566–575). Two of the trials were ran-
domized and controlled (569,574). Overall, 50–75% became
HCV RNA negative by the end of therapy, and 25–50% had
a sustained remission (Table 58A). The incidence of adverse
effects, especially fever and flu-like symptoms, was high, and
many patients were unable to complete therapy. On the other
hand, these adverse effects generally disappeared com-
pletely with cessation of treatment. Among patients who had
pre- and posttreatment liver biopsies, there was usually histo-
logical improvement as well (568,573,575). Thus, these re-
sults suggest that HCV-infected candidates with active HCV
(indicated by RNA levels on polymerase chain reaction assay)
should consider treatment with interferon alpha-2a. Pharma-
cokinetic studies have indicated that levels of interferon al-
pha-2a tend to be higher in hemodialysis patients compared
to controls with normal renal function (572,576). A reason-
able dose is 3 million IU, given 3 times per week subcutane-
ously for 6 months. Recent studies in patients from the gen-
eral population have suggested that peginterferon alpha-2a
administered once weekly is more effective than interferon
alpha-2a administered thrice weekly (577,578), and studies
with this agent are warranted in hemodialysis patients. Pa-
tients who relapse can be offered a second course of inter-
feron alpha-2a with ribavirin.
Recently, a number of randomized, controlled trials have
examined the efficacy of ribavirin in non-ESRD patients with
hepatitis due to HCV. Ribavirin alone does not appear to be
effective (579,580). However, the combination of interferon-
alpha and ribavirin is superior to interferon alpha alone in in-
ducing sustained remission from HCV in patients who have
not previously been treated with interferon alpha (581–586).
Similarly, the combination appears to be superior to alpha-
interferon alone in patients who have previously been treated
with interferon alpha, but have relapsed (585,589–591). The
incidence of adverse effects of combination therapy is

42 2001; Suppl. 1: Vol. 2: 5–95

 The Evaluation of Renal Transplant Candidates: Clinical Practice Guidelines

Table 58A: Clinical trials of interferon-alpha in hemodialysis patients with active hepatitis C virus replication (HCV ribonucleic acid measured
by polymerase chain reaction)
Year Dose Rx Completed Stopped Follow-up Response Sustained
(3/wk) (months) Rx (n) Rx (n) (months) n (%) n (%)
94 (567) 5¿106 4 23 14 5 15 (41) 10 (27)
95 (568) 3–1¿106 6 13 6 14 10 (53) 12 (63)
95 (569) 3¿106 6 18 1 18 10 (53) 3 (16)
97 (570) 1.5–3¿106 6 14 3 12 4 (29) 2 (14)
97 (570) Control 0 9 3 12 0 (0) 0 (0)
97 (571) 3¿106 6 11 0 18 11 (100) 3 (27)
97 (572) 3¿106 6 12 0 19 11 (92) 5 (42)
97 (572) 3¿106 12 8 3 19 10 (91) 7 (64)
98 (573) 3–6¿106* 6 6 3 6 n.a. 3 (33)
98 (574) 1¿106 12 9 1 6 6 (67) 2 (20)
99 (575) 3¿106 6 9 10 27 mean 14 (74) 8 (42)
99 (575) Control 0 17 0 27 mean 1 (6) 1 (6)
99 (576) 3¿106 12 16 1 6 15 (88) 12 (71)
Rx, treatment.
Two trials were randomized and controlled (570,575), the rest were uncontrolled. Control groups are in italics. Response is based on conver-
sion of HCV RNA from positive to negative.
* Six of 9 patients were initially treated daily for 2 weeks.

Table 59: Postoperative atelectasis, pneumonia, and respiratory failure

Possible screening Medical history, physical examination, chest X-ray
Possible prophylaxis Smoking cessation
Incidence 5–22% develop postoperative pulmonary complications
Rationale Pulmonary complications are a common cause of morbidity and occasionally mortality after major surgery. Pulmonary
complications can also prolong the hospital stay. Smoking cessation may help prevent these complications. Rarely,
severe chronic obstructive lung disease or other chronic lung disease may preclude transplantation.
Recommendations (C) All patients should be screened with history, physical examination, and chest X-ray to identify lung disease that
may increase the risk for major postoperative pulmonary complications.
(B) Measurement of forced expiratory volume may be useful in assessing surgical risk in patients with known lung
disease and patients with signs or symptoms suggesting lung disease.
(A) Patients should be strongly encouraged to stop smoking prior to transplantation, and should be offered a smoking
cessation program and/or pharmacological aids to smoking cessation.

increased, especially hemolytic anemia (580,583,584,587,
592,596). Unfortunately, there are few studies examining
ribavirin in patients with ESRD. The dose of ribavirin should
be reduced in ESRD patients (598).
Finally, it has been suggested that HCV-positive transplant
candidates may be reasonable recipients for kidneys har-
vested from HCV-infected organ donors (598, 599). What
little data exist suggest that there is no increased risk to the
recipient in the short term (599, 600), and that waiting times
are reduced (599). However, the long-term consequences of
transmitting a new HCV strain or co-infecting the recipient
with two strains (donor and recipient) are unknown. There-
fore, such a strategy should be used only with adequate in-
formed consent.
Pulmonary
Currently, most define a postoperative pulmonary compli-
cation as one that prolongs the hospital stay or results in
morbidity and mortality, e.g. pneumonia, respiratory failure
and atelectasis (Table 59) (601). Little information is available
to guide the pretransplant evaluation of patients with respir-
atory disease. However, the preoperative assessment of risk
for postoperative pulmonary complications in the general
population has recently been reviewed (601, 602). Except for
issues pertaining to the increased risk of opportunistic pul-
monary infections, the preoperative evaluation of renal trans-
plant candidates should be similar to that for patients facing
other types of surgery (603–612). The highest risk of respir-
atory complications is in patients undergoing thoracic or
upper abdominal operations (603–606,608), and the risk
might be expected to be lower in the patient having a kidney
transplant. By multivariate analysis, risk factors for postopera-
tive pulmonary complications that developed in 11.8% of
adult, male recipients undergoing elective abdominal surgery,
were postoperative nasogastric suction, preoperative sputum
production and longer duration of anesthesia (613). In an-
other multivariate analysis (after controlling for type of
surgery, duration of anesthesia and other risk factors) current
cigarette smokers were 5.5 times more likely to develop pul-

2001; Suppl. 1: Vol. 2: 5–95 43

Kasiske et al.

Table 60: Ischemic heart disease (IHD)

Possible screening Medical history and physical examination
Fasting lipid profile
Fasting blood glucose (if not diabetic)
Electrocardiogram
Noninvasive cardiac stress test
Coronary angiography
Possible prophylaxis Risk factor modification
Coronary revascularization
Incidence The prevalence of IHD is very high in patients with ESRD, and almost half of the deaths that occur during the first
30 days posttransplant are due to IHD.
Rationale Identifying transplant candidates with IHD disease allows i) patients and clinicians to better understand the risk of
transplantation, ii) pretransplant revascularization that may reduce the risk of transplantation, and iii) aggressive risk
factor modification.
Recommendations (A) Assess IHD risk factors: a prior history of IHD, men Ø45 or women Ø55 years, IHD in a first degree relative,
current cigarette smoking, diabetes, hypertension, fasting total cholesterol ⬎200 mg/dl, high density lipoprotein
cholesterol ⬍35 mg/dl and left ventricular hypertrophy.
(A) Risk factor modification should be aggressively pursued.
(B) Patients at high risk, e.g. renal disease from diabetes, prior history of IHD, or Ø2 risk factors, should have a
cardiac stress test.
(B) Patients with a positive cardiac stress test should undergo coronary angiography for possible revascularization
prior to transplantation.
(B) Patients with critical coronary lesions should undergo revascularization prior to transplantation.

monary complications compared to those who didn’t smoke
(614). Thus, patients who smoke should be offered a smoking
cessation program and/or pharmacological aids to smoking
cessation (nicotine patches, nicotine gum, oral bupropion),
and should be strongly encouraged to stop smoking before
transplantation. The risk of pulmonary complications in obese
patients has been reported to not be increased over that of
non-obese patients (601). However, obesity, at least among
women, was found to be an independent risk factor for hos-
pital length of stay and cost following renal transplantation
(615). Some have suggested that the forced expiratory vol-
ume is the best predictor of postoperative respiratory compli-
cations (604), and this test may be useful for selected pa-
tients with known pulmonary disease. The ‘‘prohibitive’’ risk
group can successfully undergo surgery with careful prepara-
tion (603,608, 609). Patients with asthma that is under con-
trol can generally undergo transplantation without undue risk
(608).
Cardiovascular Disease
Cardiovascular disease (CVD) is the leading cause of death
after renal transplantation (Table 60) (616–620). In a cohort
of 7040 patients who died with a functioning graft after re-
ceiving a kidney transplant between 1988 and 1997, 36.1%
of deaths were attributed to IHD and another 6.1% to stroke
(620). Almost half (47.1%) of deaths with graft function oc-
curring within 30 days after transplantation were due to CVD,
primarily acute myocardial infarction (620). Determining the
presence and severity of IHD prior to transplantation may
provide the patient and physician with useful information re-
garding the risk of surgery and the risk of long-term morbidity
and mortality. Indeed, the presence of severe IHD could play
a major role in the decision to undergo transplantation or not.
Knowing the extent of IHD at the time of transplant surgery
may also allow physicians to take extra precautions, e.g. in-
vasive hemodynamic monitoring during the perioperative
period. In at least some patients, the medical and/or surgical
treatment of IHD before rather than after transplant surgery
may improve the outcome (621). Finally, identifying patients
with IHD is important in targeting patients for aggressive risk
factor modification before and after transplantation.
A large number of studies in non-transplant populations have
attempted to define the cardiovascular risk of non-cardiac
surgery. Goldman et al. developed a Cardiac Risk Index for
assessing the cardiovascular risk of major surgery (622).
Points are assigned based on age, history of myocardial in-
farction, physical findings of heart failure, arrhythmias, rou-
tine laboratory tests (including potassium, bicarbonate, urea
nitrogen and creatinine) and the type of surgery. While some
have found that this index predicts major cardiac compli-
cations from surgery (623, 624), others have not (625–627).
A number of easily detectable risk factors such as malnu-
trition (628,629), poorly controlled BP (630) and diabetes
(631) are associated with a greater surgical risk. Detsky and
colleagues modified the Goldman Cardiac Risk Index to in-
clude significant new angina and remote myocardial infarc-
tion (632). The Modified Cardiac Risk Index improved the
predictive accuracy among higher-risk, class III patients
(632).
The 1997 American College of Physicians guidelines adopted
the Modified Cardiac Risk Index of Detsky et al. (632,633)
but recommended that additional information on ‘‘low risk

44 2001; Suppl. 1: Vol. 2: 5–95

 The Evaluation of Renal Transplant Candidates: Clinical Practice Guidelines
variables’’ should be collected (634). The Modified Cardiac
Risk Index adopted by the American College of Physicians’
guidelines assigns points for:
O myocardial infarction ⬍6 months earlier (10 points),
O myocardial infarction ⬎6 months earlier (5 points),
O angina with walking 1 to 2 blocks or climbing 1 flight of
stairs or less at a normal pace (10 points),
O inability to perform any physical activity without develop-
ment of angina (20 points),
O alveolar pulmonary edema with 1 week (10 points) or ever
(5 points),
O suspected critical aortic stenosis (20 points),
O rhythm other than sinus or sinus plus atrial premature be-
ats on electrocardiogram (5 points),
O ⬎5 ventricular premature contractions on electrocardio-
gram (5 points),
O poor general medical status defined as PO2 ⬍60 mm Hg,
PCO2 ⬎50 mm Hg, potassium level ⬍3 mmol/l, blood
urea nitrogen ⬎50 mmol/l, creatinine ⬎260 mmol/l (2.9
mg/dl), bedridden (5 points).
O age ⬎70 years (5 points),
O emergency surgery (10 points).
Class IΩ0–15 points, Class IIΩ20–30 points, Class IIIΩmore
than 30 points. There is strong evidence that Class II or III
patients have a ⬎15% likelihood of developing a periopera-
tive cardiac event. For patients who were Class I, it was
recommended to collect low risk variables: age ⬎70 years,
history of angina, diabetes, Q waves on electrocardiogram,
history of myocardial infarction, history of ventricular ectopy,
ST-segment ischemic abnormalities during resting electrocar-
diography, hypertension with severe left ventricular hyper-
trophy, or history of congestive heart failure. Patients with 0–
1 low risk variables were felt to be at low risk (⬍3% peri-
operative cardiac events), those with 2 or more low risk vari-
ables were felt to be at intermediate risk (3–15% risk of peri-
operative cardiac event) (635).
Other risk prediction algorithms for non-cardiac surgery in-
clude those of the American College of Cardiology and the
American Heart Association (635), the Physiological and Op-
erative Severity Score for the enUmeration of Mortality and
Morbidity (POSSUM) (636,637), and the Portsmouth modi-
fication (P-POSSUM) (638–641). Few studies have simul-
taneously compared several different risk prediction methods.
However, one study found that four different methods pro-
duced similar results (642). There are no studies comparing
2001; Suppl. 1: Vol. 2: 5–95
the ability of these methods to predict the cardiovascular risk
of renal transplant surgery.
A potentially useful approach is to select patients who are
at increased risk (based on medical history) for non-invasive
cardiac stress testing, and those with a positive stress test
for coronary angiography (643). Because a prior history of
IHD has been found to be a major risk factor for posttrans-
plant IHD events (616,617,643–646), all patients with a his-
tory of myocardial infarction, angina pectoris or congestive
heart failure should probably undergo cardiac stress testing
and angiography if the stress test is positive. Because the
prevalence of IHD is very high in diabetic patients referred for
transplant evaluation, some have advocated that all diabetic
patients should undergo coronary angiography. Several in-
vestigators have performed coronary angiograms in consecu-
tive diabetic patients, whether or not symptoms of IHD were
present (647–652). The results of these studies have been
remarkably consistent: 59/198 had one or more lesions with
greater than 75% stenosis (652), 25/100 had lesions greater
than 70% (649), 4/11 had lesions greater than 70% (648)
(647), 9/21 had lesions greater than 50% (648) and 25/77
had ‘‘serious coronary artery disease’’ (650). Thus, less than
one half of the patients in any of these studies had angiogra-
phically severe coronary artery disease, and in the largest
study 93/198 (47%) had no lesions with greater than 50%
stenosis (652).
In general, patients who do not have a history of IHD can
be selected for non-invasive cardiac stress testing based on
clinical criteria. Clinical parameters linked to posttransplant
IHD include age ⬎50 years, diabetes mellitus, and an abnor-
mal electrocardiogram (643,653). Accepted risk factors for
IHD in the general population include:
O diabetes,
O men Ø45 years,
O women Ø55 years (or women with premature menopause
but no estrogen replacement therapy),
O a family history of premature IHD (definite myocardial in-
farction or sudden death before age 55 in a male first-
degree relative or before age 65 in a female first-degree
relative),
O current cigarette smoking,
O hypertension (blood pressure Ø140/90 mm Hg or taking
antihypertensive medications),
O total cholesterol Ø200 mg/dl,
O high density lipoprotein cholesterol ⬍35 mg/dl (654).
For asymptomatic patients who have a history of IHD or who
have multiple risk factors for IHD, a non-invasive test may
45
Kasiske et al.
help to determine the risk for posttransplant IHD. The ideal
test would determine who should undergo angiography, who
should be advised of an increased risk, who should be moni-
tored more closely during surgery, and who could proceed
without further concern. Such a test should be of high
enough sensitivity (proportion of positive results in patients
with disease) and specificity (proportion of negative results
in patients without disease) to ensure that the positive predic-
tive value (proportion of all positive tests that are in patients
with disease) and negative predictive value (proportion of all
negative tests that are in patients without disease) are both
sufficiently high. A high positive predictive value will prevent
patients being subjected to angiography unnecessarily, while
a high negative predictive value will ensure that high-risk pa-
tients are not missed.
A number of non-invasive cardiac screening tests to identify
patients at high risk for cardiac events have been described.
These include exercise electrocardiogram testing
(626,627,655), ambulatory electrocardiogram monitoring
(656,657), measurement of left ventricular ejection fraction
(658,659), magnetic resonance imaging (660), exercise or
dipyridamole single-photon emission computed tomography
(SPECT) (658, 661), positron emission tomography (PET)
(662), electron beam computed tomography (663–668) and
thallium/sestamibi scintigraphy (with exercise or dipyridamo-
le) (669–674) echocardiography (with exercise or dobuta-
mine) (675,676). Few studies have assessed exercise electro-
cardiogram testing in patients with ESRD. It has been used
infrequently because of the inability of many ESRD patients
to reach target heart rate levels. Data from elderly non-ESRD
patients demonstrating that failure to reach a target heart rate
predicted postsurgical IHD events can probably not be ex-
trapolated to patients with ESRD (627). Although ambulatory
electrocardiographic monitoring has been shown to identify
non-ESRD patients at increased risk for vascular surgery
(656,657), few data are available to assess this approach in
patients with ESRD. Radionuclide imaging and echocardiog-
raphy have been used to estimate ejection fraction to predict
risk in patients undergoing major surgery (658, 659), but few
data are available to critically assess the ability of ejection
fraction alone to predict cardiac risk in renal transplant candi-
dates (677–679). Similarly, few studies have assessed the
potential usefulness of recently described techniques such as
magnetic resonance imaging, SPECT and PET for screening
patients with ESRD. In one study, dipyridamole SPECT was
judged to be ineffective (sensitivity 37%, specificity 73%) in
screening for angiographic coronary artery disease in 45 pa-
tients with ESRD (680).
Recently, results of electron beam computed tomography
have been shown to correlate with both angiographic coro-
nary artery disease and IHD events (663–668). However, a
study of 1196 high-risk patients found no difference be-
tween electron beam computed tomography and traditional
risk-factor assessment in predicting coronary events (681).
Although the incidence of coronary calcifications is high in
patients with ESRD (682,683), the usefulness of this test
46
in assessing the potential risk of surgery in patients with
ESRD has not been evaluated. The relative cost-effective-
ness of electron beam computed tomography, compared to
other screening tests, is also unknown.
Most data on the effectiveness of non-invasive screening
techniques are from studies examining either dipyridamole
thallium/sestamibi scintigraphy or dobutamine echocardiog-
raphy. In non-ESRD patients, dipyridamole thallium/sestamibi
scintigraphy has been reported to be useful in assessing car-
diac risk before major surgery (669–672,684). More recent
data indicate that the routine use of thallium scintigraphy
adds little to clinical data in defining surgical cardiac risk
(658,674,685). Differences in the results of these studies
have been attributed to differences in study design (686).
However, study results suggesting the lack of usefulness of
thallium/sestamibi scintigraphy in non-ESRD patients may
not invalidate the usefulness of the test in ESRD patients who
may have a higher pretest probability of disease.
In one well designed, prospective study, dipyridamole thal-
lium scintigraphy was performed in 80 diabetic patients
being evaluated for renal transplantation (687). Results were
compared to quantitative angiography using lesions of at
least 70% occlusion to define coronary artery disease. With
an incidence of angiographic coronary artery disease of 53%,
the sensitivity of the test was 86%, specificity 79%, positive
predictive value 82% and negative predictive value 83%. In
another study of 176 consecutive diabetic kidney or kidney-
pancreas transplant recipients who had undergone pretrans-
plant dipyridamole thallium scintigraphy, only one of 111
(0.9%) patients without fixed or reversible defects had car-
diac events within 6 weeks after transplantation (688).
Several other studies have examined how well exercise and/
or dipyridamole thallium scintigraphy predicted cardiac
events in ESRD patients (673,689–697). In studies where
the incidence of IHD events was 9–20%, the positive and
negative predictive values of thallium scintigraphy were, re-
spectively: 7 and 84% (680), 23 and 89% (673), 38 and
96% (696), 47 and 91% (697), 67 and 100% (692), and 100
and 95% (690). In studies where the incidence of events was
21–51%, the positive and negative predictive values were 75
and 86% (693), 83 and 89% (694), 68 and 71% (695), 23
and 79% (689), 60 and 81 (689), and 31 and 88% (691).
Some of the variability in the results of these studies is likely
due to differences in study design, the definition of positive
test results (fixed vs. reversible lesions), duration of follow-
up, the proportion of patients who underwent transplantation
during the follow-up period, the definition of endpoints and
patient population characteristics. Most of these studies suf-
fer from the fact that patients were pre-selected by referral.
Dobutamine echocardiography has shown promise as a
screening test for coronary artery disease in a number of in-
vestigations of non-ESRD patients (675,676) and ESRD pa-
tients being considered for renal transplantation (698–701).
Results of dobutamine echocardiography have been com-
2001; Suppl. 1: Vol. 2: 5–95
 The Evaluation of Renal Transplant Candidates: Clinical Practice Guidelines
pared to angiography. In one study the incidence of coronary
artery disease (lesions of at least 50% occlusion) was 47%,
the sensitivity 86%, the specificity 94%, the positive predic-
tive value 92% and the negative predictive value 88% (698).
In a study using 50% occlusion to define coronary artery
disease (assessed by quantitative angiography) the sensitivity
was 52% and the specificity 74% (701). Using a 70% oc-
clusion cutpoint the sensitivity was 75% and the specificity
71% (701). For a 75% cutpoint by visual estimation, the sensi-
tivity and specificity were 75% and 76%, respectively (701).
After an average follow-up of 22.5 months, 20% of patients
with a negative test and 55% of those with a positive test
had a cardiac death, myocardial infarction or coronary re-
vascularization, suggesting that dobutamine echocardiogra-
phy is a useful but imperfect screening test for angiogra-
phically defined coronary disease in renal transplant candi-
dates. Dobutamine echocardiography is less expensive than
thallium scintigraphy. Direct comparisons of these two
screening modalities in dialysis patients are lacking. However,
Smart et al. directly compared dobutamine-atropine stress
echocardiography with dipyridamole sestamibi scintigraphy
in 183 patients from the general population (coronary angio-
graphy was the ‘‘gold standard’’) (702). Dobutamine-atropine
echocardiography was more specific for detecting coronary
artery disease than dipyridamole sestamibi (91% vs. 73%,
p⬍0.01), while the sensitivities of the two tests were similar
(87% vs. 80%, respectively) (702).
In summary, non-invasive tests play an important role in as-
sessing IHD risk in renal transplant candidates, although
these tests are less than perfect in predicting angiogra-
phically documented coronary disease or IHD events. The
most extensively studied test, thallium/sestamibi scinti-
graphy, has recently been shown to add little to other clinical
information in the evaluation of surgical risk in non-ESRD pa-
tients (658,685,686). However, a high pretest likelihood of
cardiac events in ESRD patients with indicators of IHD, dia-
betes and/or multiple CVD risk factors could make the use of
thallium scintigraphy reasonable in this setting. Dobutamine
echocardiography may be an acceptable and more cost-ef-
fective alternative to thallium scintigraphy. Fewer data are
available to judge the effectiveness of more expensive
screening techniques using SPECT, PET or electron beam
computed tomography. Almost no data are available to judge
strategies that may combine more than one noninvasive test.
Combined imaging using both dobutamine echocardiogra-
phy and nuclear scintigraphy has been reported in patients
from the general population, for example, but not in hemo-
dialysis patients (676). Finally, the expertise of the center in
performing a noninvasive test and patient preference should
also be taken into account when selecting test modalities.
Patients who appear to have critical lesions should probably
undergo revascularization (coronary artery by-pass surgery,
angioplasty, atherectomy, stent placement, etc.) prior to
transplantation. In patients who have less severe disease the
optimal timing of invasive intervention is unclear. Manske et
al. conducted a randomized, controlled study of 26 asympto-
2001; Suppl. 1: Vol. 2: 5–95
matic diabetic patients who were found to have stenoses of
greater than 75% (621). Patients randomized to revasculariza-
tion prior to transplantation had fewer posttransplant cardio-
vascular disease events than patients managed medically.
These findings suggest that diabetic patients with severe
coronary artery disease should undergo surgery before,
rather than after, renal transplantation. However, there are
some important limitations of this study.
O Patients in the medical treatment arm received short-
acting nifedipine, which has recently been suggested to
cause an increase in ischemic heart disease events. If the
study were repeated today, optimal medical management
would probably include a beta-blocker instead.
O Another weakness of the study is that bypass grafting and
angioplasty were treated as equivalent revascularization
therapies. This assumption is not supported by current
clinical evidence.
O The very small sample size makes it possible that the ob-
served differences were due to chance. Unfortunately,
there are no other randomized, controlled trials examining
the timing of invasive intervention in diabetic or non-dia-
betic patients with coronary artery disease. It may not be
valid to extrapolate the findings in diabetic patients to non-
diabetic patients.
Several studies have reported the results of coronary artery by-
pass surgery in hemodialysis patients (621,703–717). In gen-
eral, morbidity and mortality were increased in dialysis patients
compared to comparable diabetic and non-diabetic patients
without ESRD (711,716–721). In one large observational study,
adjusted, in-hospital mortality was 3.1 times higher for dialysis
compared to non-dialysis patients (717). Major infections
(710,722), bleeding (713, 722), (717) and mediastinitis (717)
have been reported to occur more often in dialysis vs. non-di-
alysis patients who undergo open heart surgery (711,718–721).
In a study of 30 consecutive diabetic patients who had pre-
transplant coronary artery bypass surgery, perioperative mor-
tality was 3%(723). During follow-up, five patients experi-
enced six myocardial infarctions, the majority within 6 months
of transplantation (723). In an analysis of data from the U.S. Re-
nal Data System, the in-hospital mortality from 7419 bypass
graft procedures in hemodialysis patients (who were not
necessarily transplant candidates) was 12.5% (714). Whether
the risk of surgery is greater before, rather than after, renal
transplantation is unclear. Most reported studies of bypass
surgery in renal transplant patients have been limited to small
numbers of patients (703,704,706,724–726). In one study,
perioperative complications were less frequent in transplant re-
cipients compared to dialysis patients (706). In a preliminary
study of patients from the U.S. Renal Data System, the in-hos-
pital death rate associated with bypass grafting for renal trans-
plant recipients was 4.9% (727). However, this figure cannot
be directly compared to the mortality of bypass grafting for
hemodialysis patients above, since the latter included patients
who were not transplant candidates.
47
Kasiske et al.

Table 61: Left ventricular hypertrophy (LVH)

Possible screening Medical history and physical examination
Electrocardiogram
Chest X-ray
Echocardiogram
Possible prophylaxis Correction of underlying ischemic heart disease (IHD), anemia and hypertension
Prevalence Approximately 75% of unselected hemodialysis patients have evidence of LVH on echocardiogram when initiating
hemodialysis.
Rationale The prevalence of LVH is high among hemodialysis patients, and LVH in hemodialysis patients is associated with
increased mortality both before and after renal transplantation. Effective management of IHD, anemia and hyperten-
sion may reduce LVH and prevent its complications. Therefore, it is reasonable to screen for LVH as part of the
pretransplant evaluation.
Recommendations (A) Patients should be evaluated for possible LVH with medical history, physical examination, electrocardiogram and
chest X-ray.
(B) Patients with evidence of LVH should undergo an echocardiogram to confirm its presence and screen for possible
underlying causes.
(A) Anemia, hypertension and IHD should be treated to reduce LVH and its associated complications.

Available data suggest that percutaneous balloon angioplasty
may be safe and effective in hemodialysis patients (713,728–
731). The rate of restenosis was higher in dialysis vs. non-
ESRD patients in some (728,730), The rate of restenosis may
be reduced with coronary stenting (730). Nevertheless, major
cardiac events are more frequent in dialysis vs. non-ESRD
patients after balloon angioplasty (731). A large proportion of
transplant candidates are diabetic and a recent study in non-
ESRD diabetic patients with symptomatic IHD found that
outcomes after myocardial infarction were superior for those
who had undergone coronary artery bypass surgery com-
pared to angioplasty (732). In a large study comparing out-
comes of bypass grafting vs. angioplasty in dialysis patients
from the U.S. Renal Data System, the in-hospital mortality
was 12.5% for 7419 bypass procedures and 5.4% for 6887
angioplasty procedures (714). After comorbidity adjustment,
there was 9% (95% C.I. 3–14%) less risk for all-cause mor-
tality for bypass grafting compared to angioplasty over a 2-
year follow-up period. There was 15% (8–22%) less risk of
cardiac death and 63% (57–68%) less risk of myocardial in-
farction (714). Of course, comorbidity adjustment may not ac-
count for differences in coronary anatomy and other risk fac-
tors, and at least some of these differences could due to
selection bias rather than differences in the risk of the pro-
cedures per se.
Finally, patients with known IHD, and patients who are at
high risk for IHD, should probably be periodically re-screened
with a non-invasive stress test while they are waiting for a
cadaveric transplant. Unfortunately, there are very few data
to suggest how often this should be done. In a study of 193
patients with serum creatinine ⬎2.5 mg/dl (which included
10 hemodialysis and 31 transplant recipients), the cardiac
event rate among patients with dobutamine echocardio-
grams showing nonischemic responses increased from 8%
to 16% between 24 and 40 months (735). Given the high
rate of IHD events in ESRD patients, it may be reasonable to
screen patients every 1–2 years. However, additional studies
are clearly needed to address this important issue.
Approximately 75–85% of adult and pediatric patients on
hemodialysis have left ventricular hypertrophy (LVH) on echo-
cardiography (736, 737). LVH is associated with increased
mortality on hemodialysis (736) and peritoneal dialysis (738).
Although LVH often improves after renal transplantation
(739–742), it nevertheless predicts a worse posttransplant
outcome (741, 742). Even in the absence of randomized con-
trolled trials it is reasonable to conclude that correcting LVH
in hemodialysis patients may reduce risk and improve out-
comes while on the waiting list and after renal transplan-
tation.

It is reasonable to proceed with renal transplantation in
asymptomatic patients who have successfully undergone re-
vascularization. However, all patients with IHD or multiple car-
diac risk factors should receive aggressive risk factor man-
agement (654, 733). Although there are no clinical trials as-
sessing the efficacy of risk factor intervention in ESRD, it is
reasonable to consider measures to treat cigarette smoking,
hyperlipidemia and hypertension. The National Kidney Found-
ation Task Force on CVD recently made recommendations on
the evaluation and management of CVD risk in patients with
ESRD (734).
Potentially reversible risk factors for LVH in hemodialysis pa-
tients include anemia hypertension and IHD (Table 61)
(737,743,744). An approach to IHD has been outlined above.
There is reasonably good evidence that partial correction of
anemia improves LVH and reduces mortality among hemo-
dialysis patients (745,746). Similarly, some small studies sug-
gest that partially correcting anemia in patients with renal in-
sufficiency helps to reduce LVH (747). However, the results
of a large, randomized, controlled trial in hemodialysis pa-
tients with congestive heart failure or IHD suggested that nor-
malizing the hematocrit (42%) increased the risk of death

48 2001; Suppl. 1: Vol. 2: 5–95

 The Evaluation of Renal Transplant Candidates: Clinical Practice Guidelines

Table 62: Congestive heart failure (CHF)

Possible screening Medical history and physical examination
Electrocardiogram
Chest X-ray
Echocardiogram
Possible prophylaxis Risk factor management
Prevalence Approximately 45% of unselected hemodialysis patients have a history of fluid overload, and 20% have decreased
systolic function on echocardiogram.
Rationale Although patients with myocardial dysfunction are undoubtedly at increased risk for surgery, in at least some patients
CHF may improve after transplantation. CHF is often a manifestation of ischemic heart disease.
Recommendations (A) Patients should be evaluated for signs and symptoms of myocardial dysfunction.
(B) Patients with signs and symptoms of CHF should have an echocardiogram or other suitable test to assess
myocardial function.
(B) Unless it is severe, myocardial dysfunction per se should not be a contraindication to transplantation.
(B) Patients with severe myocardial dysfunction may be candidates for combined heart and kidney transplantation.

(748). Therefore, it appears to be most reasonable to partially
correct anemia, e.g. target hematocrit 33–36%, in patients
with renal insufficiency and hemodialysis. Guidelines exist for
the management of anemia in hemodialysis patients (749).
Hypertension is clearly associated with LVH, and effectively
treating hypertension may reduce LVH in hemodialysis pa-
tients (744,750). Similarly, antihypertensive therapy appears
to reduce LVH in patients with renal insufficiency who do not
yet require hemodialysis (751). Some uncontrolled data even
suggest that converting enzyme inhibitors may improve LVH
independent of its effect on blood pressure (752). Although
there are no randomized, controlled trials testing the long-
term efficacy of blood pressure reduction, it seems reason-
able to optimize blood pressure control in patients with LVH.
In the studies that have defined congestive heart failure
(CHF). as a fluid-overload condition the cross-sectional
prevalence of a history of CHF among hemodialysis patients
has been 42–47% (Table 62) (748, 753, 754). In an echo-
cardiographic study, however, 19% of hemodialysis patients
(surviving at least 6 months on dialysis) had systolic dysfunc-
tion at the time of dialysis initiation (743). On a second echo-
cardiographic examination 18∫10 months later, 20% of this
cohort had diastolic dysfunction (743). After 4 years, the
cumulative (actuarial) incidence of CHF, defined as volume
overload, was approximately 70% among those with systolic
dysfunction at baseline, 45% among those with left ventricu-
lar hypertrophy or dilatation on baseline examination, and
about 20% among those with a normal baseline echocardi-
ogram (743). This same group earlier reported the prevalence
of echocardiographic left ventricular failure to be 2% in renal
transplant recipients, compared to 18% among hemodialysis
patients (755). Regression of left ventricular abnormalities is
associated with an improved cardiac outcome among hemo-
dialysis patients (756).
The usual signs and symptoms of CHF may be difficult to
distinguish from noncardiogenic volume overload often seen
in patients with ESRD. On the other hand, volume overload
often indicates underlying IHD in patients with ESRD. In ad-
dition, the hypotension that often occurs during hemodialysis
treatments and makes it difficult to remove excess extracellu-
lar fluid may also be a clinical indicator of CHF and underlying
IHD in this population. In any case, all patients should be
assessed clinically to determine whether myocardial dysfunc-
tion may be present at the time of transplant evaluation. It is
also important to perform an echocardiogram in these pa-
tients, because the configuration of the LVH and whether the
patient has systolic or diastolic dysfunction have important
prognostic implications (743). A cardiac stress test may also
be important to screen for IHD. Patients without significant
coronary artery disease may have decreased myocardial
function for several reasons. Clinical findings consistent with
thyroid dysfunction, systemic amyloidosis, valvular heart dis-
ease, hypertrophic cardiomyopathy or constrictive pericarditis
should be sought. Occasionally, a large arteriovenous shunt
may cause or contribute to CHF. An echocardiogram is es-
sential to fully discern possible causes and to assess the se-
verity of myocardial dysfunction in patients with ESRD.
Reversible causes of myocardial dysfunction should be
treated. Severe, irreversible heart failure should probably pre-
clude renal transplantation unless heart transplantation is also
considered. However, many patients with mild or moderate
(idiopathic) cardiac dysfunction may respond to renal trans-
plantation with an improvement in myocardial function
(742,757–765). Indeed, most investigators have reported that
echocardiographic or radionuclide-determined ejection frac-
tion increases and left ventricular mass decreases after renal
transplantation. Some of this improvement may be due to
changes in intravascular volume and preload, and/or im-
provement in hematocrit, rather than improvement in myo-
cardial function per se. In any case, these data should be
taken into consideration before refusing renal transplantation
to a patient who has decreased myocardial function and idio-
pathic cardiomyopathy.
Available data suggest that there is an increased incidence of
atherosclerotic cerebral vascular disease following renal trans-

2001; Suppl. 1: Vol. 2: 5–95 49

Kasiske et al.

Table 63: Cerebral vascular disease

Possible screening Medical history and physical examination
Carotid ultrasound in high-risk patients
Computed tomography or magnetic resonance imaging in high-risk autosomal dominant polycystic kidney disease
(ADPKD) patients
Possible prophylaxis Carotid endarterectomy
Anticoagulation in patients with chronic atrial fibrillation
Surgical ligation of intracranial aneurysms
Incidence The cumulative incidence of cerebral vascular disease (thrombotic strokes and transient ischemic attacks) is about
15% by 15 years posttransplant.
Rationale Cerebral vascular disease events are common after renal transplantation and data from studies in the general popula-
tion suggest that prophylactic surgery may be effective in selected patients. Patients with ADPKD have an increased
risk of intracranial aneurysms that can rupture and cause fatal intracerebral bleeding. High-risk ADPKD patients can
be identified for screening and prophylactic surgical intervention.
Recommendations (C) Consider screening asymptomatic patients who are at high risk for cerebral vascular disease with carotid ultra-
sound.
(B) Consider carotid endarterectomy for asymptomatic patients with surgical risk of ⬍3% and Ø60% diameter
reduction on ultrasound (American Heart Association Guidelines).
(C) Consider carotid endarterectomy for asymptomatic patients whose surgical risk is 3–5%, and who have Ø75%
stenosis in the presence of contralateral internal carotid artery stenosis Ø75% (American Heart Association Guide-
lines).
(B) Patients with symptomatic cerebral vascular disease should have optimal medical and surgical management,
and should be symptom free for at least 6 months before transplantation.
(A) Patients with chronic, nonvalvular, atrial fibrillation should generally be treated with anticoagulation following
guidelines developed for the general population.
(B) ADPKD patients with a family history of intracranial aneurysms or with a previous episode of subarachnoid
bleeding should undergo computerized tomography or magnetic resonance imaging every 5 years.
(B) ADPKD patients with intracranial aneurysms ⬎10 mm should be considered candidates for prophylactic surgical
ablation.

plantation (616,617,619,766,767). In a single-center, retrospec-
tive study, the cumulative incidence of cerebral vascular dis-
ease was 15% by 15 years (619). In another study of 406 stable
renal transplant patients, the prevalence of peripheral vascular
disease at 4 years posttransplant was 3% (767).
A number of risk factors have been identified for posttrans-
plant cerebral vascular disease including a history of pretrans-
plant cerebral vascular disease, age, cigarette smoking, dia-
betes, hypertension and hyperlipidemia (Table 63)
(616,619,766,768,769). Clearly, patients with a history of cer-
ebral vascular disease and/or multiple risk factors should be
warned of their increased risk and should be counseled re-
garding risk factor intervention. Prophylactic therapy with
low-dose aspirin may be prudent, although there are no con-
trolled trials assessing the risks and benefits of aspirin
prophylaxis in renal transplant recipients.
There is no direct evidence that screening asymptomatic re-
nal transplant candidates for the cerebral vascular disease is
beneficial. In the general population, asymptomatic carotid
bruits do not appear to greatly increase the risk of cerebral
vascular disease (770,771). Although asymptomatic carotid
bruits increase the risk of stroke after coronary artery bypass
surgery, the increase in risk is probably small (772). In add-
ition, carotid bruits may be associated with atherosclerotic
disease of the ascending aorta that may cause a relatively
greater increase in risk for cardiac surgery than for renal
transplantation.
There are no studies in renal transplant candidates to suggest
that screening high-risk, asymptomatic patients with carotid
ultrasound is beneficial. The frequency of carotid plaques de-
termined by ultrasonography is not a strong predictor of cer-
ebral vascular disease events after renal transplantation (768).
For years there has been controversy over whether carotid en-
darterectomy benefits patients with asymptomatic carotid ste-
nosis. However, the results of recent, randomized, controlled
trials led the American Heart Association to recommend that
for patients with surgical risk of ⬍3% and life expectancy of
Ø5 years, ipsilateral carotid endarterectomy is acceptable for
stenosis Ø60% diameter reduction (grade A recommenda-
tion). They suggested that unilateral carotid endarterectomy
simultaneous with coronary artery bypass graft for carotid
stenosis Ø60% diameter reduction was acceptable (grade C
recommendation) (773). For patients with surgical risk 3–5%,
ipsilateral endarterectomy for stenosis Ø75% in the presence
of contralateral internal carotid artery stenosis Ø75% was
deemed acceptable (773). These guidelines were heavily in-
fluenced by the results of the Asymptomatic Carotid Athero-
sclerosis Study (774). A recent meta-analysis of five ran-
domized, controlled trials also concluded that carotid endart-
erectomy was superior to medical management in selected
patients with asymptomatic disease (775). The applicability of

50 2001; Suppl. 1: Vol. 2: 5–95

 The Evaluation of Renal Transplant Candidates: Clinical Practice Guidelines

Table 64: Peripheral vascular disease (PVD)

Possible screening Medical history and physical examination
Radiographic imaging (e.g. Doppler ultrasound, helical computerized tomography and angiography)
Possible prophylaxis Risk factor modification
Bypass surgery or angioplasty
Incidence The rate of lower extremity amputation in patients with ESRD is 5–10 per 100 patient years. The incidence of PVD
is much higher in patients with diabetes.
Rationale PVD is common in patients with ESRD and its detection may help identify patients for intensive risk factor modifi-
cation and possible revascularization (if symptomatic). In addition, patients with PVD are also at high risk for other
cardiovascular disease complications. Occasionally, severe aortoiliac disease may require reconstructive surgery be-
fore or after renal transplantation.
Recommendations (C) Medical history and physical examination should be used to screen for PVD.
(C) Angioplasty or surgical intervention for PVD should be reserved for patients with symptomatic disease.
(D) Routine aortoiliac angiography is not warranted, given the low incidence of disease severe enough to require
vascular reconstructive surgery.
(C) Consider radiographic imaging in patients with signs or symptoms of aortoiliac disease.
(B) Aortoiliac reconstruction can be carried out successfully before, at the time of, or after renal transplantation.
(D) Anastomosis of a transplant into a vascular prosthesis should be considered only as a last resort, and patients
should be informed of the rate of failure of this procedure.

the results of these studies to clinical practice depends on
whether the patient populations and surgical expertise in the
studies and in community practice are comparable. The results
of at least one study suggested that this may not be the case
(776). It is likely that the surgical risk of endarterectomy is
higher in most renal transplant candidates than in the general
population.
Patients with transient ischemic attacks or other evidence of
cerebral vascular disease within the previous 6 months
should be referred to a neurologist to evaluate for possible
treatment. Such treatment could include carotid surgery
(777,778). Indeed, large, randomized, controlled trials have
demonstrated benefit from carotid surgery in appropriately
selected, symptomatic patients (779–780). Transplantation
should be considered only after medical and surgical man-
agement has been maximized and patients have been symp-
tom-free for at least 6 months.
Patients with chronic, nonvalvular, atrial fibrillation are at
increased risk for stroke. A number of large, randomized,
controlled trials have examined the risks and benefits of anti-
coagulation with aspirin and/or warfarin in the general popu-
lation with atrial fibrillation (783–790). Meta-analyses of
these trials have generally (791–794), but not always (795),
concluded that therapy is beneficial. Guidelines are available
for management (796–798). A detailed discussion of the in-
dications for anticoagulation to prevent stroke in patients with
nonvalvular atrial fibrillation is beyond the scope of the cur-
rent guidelines. However, there are few reasons not to follow
existing guidelines that target patients in the general popula-
tion. This is especially true for patients with living donors,
when anticoagulation can easily be reversed before elective
surgery. It is usually not difficult to manage anticoagulation
even for patients undergoing cadaveric renal transplantation.
Patients with ADPKD have an increased incidence of ruptured
intracranial aneurysms (799). Although it is unclear how renal
transplantation affects the risk of subarachnoid hemorrhage
in ADPKD, it is possible that surgery, hypertension and other
factors may increase the risk. In the absence of more specific
data, transplant candidates with ADPKD should probably be
managed like others with ADPKD. Since there is risk associ-
ated with cerebral angiography, noninvasive screening tests
should be used to screen high-risk patients. High-resolution
computerized tomography or magnetic resonance imaging
appear to be reasonably effective in this setting (800,801).
Studies have shown that patients with a family history of in-
tracranial aneurysms and patients with a previous episode of
subarachnoid bleeding are at greatest risk for hemorrhage
(801–803). Decision analysis has suggested that such pa-
tients should probably be screened periodically, e.g. every 5
years (802, 804). The benefit of screening is age-related,
with individuals less than 35 years of age likely to see the
most benefit (802). Patients with aneurysms ⬎7 mm in di-
ameter are at greatest risk of subarachnoid bleeding and
would be most likely to benefit from prophylactic surgery
(801,802,805). In a recent retrospective study, the rate of
rupture was ⬍0.05% per year among 727 patients with no
history of ruptured aneurysms and diameter ⬍10 mm (806).
The risk of surgery greatly exceeded the risk of rupture in this
population (806).
Peripheral vascular disease (PVD) is important both as a
cause of limb ischemia and amputations, and as a cause of
allograft ischemia (Table 64). Few studies have examined the
incidence and clinical correlates of PVD in patients with
ESRD, before or after renal transplantation. However, existing
data suggest that the incidence is high (616,617,619,767,807–
810). In a recent retrospective study of 664 adult kidney
transplant recipients, the cumulative incidence of PVD

2001; Suppl. 1: Vol. 2: 5–95 51

Kasiske et al.

Table 65: Cognitive dysfunction and the ability to give informed consent
Possible screening Medical history and physical examination
Neuropsychiatric testing
Prevalence The prevalence of cognitive dysfunction and/or other psychosocial problems that may interfere with a potential
transplant recipient’s ability to give informed consent is not known. Approximately 30% of unselected hemodialysis
patients have evidence for some cognitive dysfunction.
Rationale Ethical and legal considerations demand that a patient or legal surrogate must be able to give informed consent
before elective surgery. In addition, the potential impact of cognitive dysfunction on graft survival must be considered.
Recommendations (A) The ability of renal transplant candidates to give informed consent should be determined.
(B) Renal transplant candidates who cannot give informed consent must have a support system that will ensure
compliance with medication and posttransplant follow-up.
(B) Cognitive dysfunction should not automatically preclude renal transplant candidates from transplantation.

(claudication, amputation or revascularization) was 4.2% at 5
years and 5.9% at 10 years (810). Among Medicare ESRD
patients, the rate of lower extremity amputations was 6.2 per
100 patient years in 1994 (809). The rate among diabetics
was 13.8 per 100 patient years (809). Two-thirds of patients
with lower extremity amputations died within 2 years (809).
Gender, diabetes, hypertension, lipid abnormalities and ciga-
rette smoking appear to be risk factors for PVD in patients
with ESRD (619,767,808,810). Among 129 diabetic (nΩ34)
and nondiabetic (nΩ95) patients undergoing renal transplan-
tation, preexisting PVD was associated with a shortened pa-
tient survival (811). Thus, although there are few data to guide
evaluation therapy, it would seem prudent to evaluate and
treat patients with symptomatic PVD prior to renal transplan-
tation. In particular, patients with diabetes and history of is-
chemic ulceration in a lower extremity, and/or patients with
claudication should have at least a noninvasive evaluation.
Angiography should be considered if noninvasive studies
suggest the presence of large-vessel disease.
Although atherosclerotic aortoiliac disease can pose a sig-
nificant technical challenge to renal transplantation, sub-
jecting asymptomatic patients to routine angiography is prob-
ably not warranted. In one report, 1400 Norwegian patients
underwent abdominal aortic angiography as part of a routine
pretransplant work-up (812). Only 26 (less than 2%) were
found to have aortoiliac disease severe enough to require sur-
gical reconstruction (501). Thus, a large number of patients
who did not require intervention were subjected to the risk of
angiography. Some centers routinely perform duplex ultra-
sonography of the aortoiliac system to ascertain the integrity
of the iliac vessels used for vascular anastomosis of the trans-
planted kidney. However, the cost-effectiveness of this
screening test has not been scrutinized. In patients with signs
or symptoms of aortoiliac disease, pretransplant angiography
can be useful. Surgical reconstruction can be successfully
carried out either before or at the time of renal transplantation
(813–821).
In a multicenter study, 13 cases (0.2% of transplants) of allo-
graft arterial anastomosis to a vascular prosthesis were iden-
tified (817). In six cases the reconstruction was performed at
the same time as the transplant. There were three immediate
graft losses due to hemorrhage and thrombosis and two peri-
operative deaths (total 38%) (817). Patient survival was only
37% after 5 years. The authors concluded that this was a haz-
ardous procedure (817). In contrast, aortoiliac reconstruction
per se does not appear to be as hazardous. In a retrospective
study, 1-year graft survival with aortoiliac reconstruction per-
formed before or at the time of transplant (nΩ36) was 86%
compared to 85% for aortoiliac reconstruction performed after
renal transplantation (820). The authors concluded that out-
comes of aortoiliac surgery before or after kidney transplan-
tation were similar to those of non-transplant patients.
Psychosocial
A psychosocial evaluation should investigate all aspects of a
potential recipient’s behavior or social condition that might
adversely affect the outcome of transplantation (Table 65).
Transplant centers vary widely in their approach to the psy-
chosocial evaluation. A survey found that only 7% of trans-
plant centers have formal, pretransplant psychosocial evalu-
ation criteria (822). The transplant evaluation is often compli-
cated by moral, ethical and legal considerations. In addition,
the psychosocial assessment has a potential for bias, and
should therefore be conducted by a professional who is
knowledgeable and experienced in the evaluation of trans-
plant candidates. Many programs rely on a social worker with
experience and expertise in evaluating transplant candidates
to screen for possible psychosocial barriers to transplan-
tation. Patients with potential problems are then referred to a
psychologist or psychiatrist with experience in the evaluating
transplant candidates.
The potential recipient should have sufficient cognitive ability
to weigh risks and benefits of the surgical procedure and
understand the need for life-long immunosuppression. Indi-
viduals who demonstrate difficulty with attention, assimi-
lation or memory should be referred for a formal neuropsychi-
atric assessment of cognitive function. Reversible medical
causes of cognitive impairment should be screened by
checking thyroid function tests, thiamin, vitamin B12, etc., as
well as baseline measurements of anemia, acidosis, uremia
and hepatic function.

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 The Evaluation of Renal Transplant Candidates: Clinical Practice Guidelines

Table 66: Chemical dependency

Possible screening Medical history (with a focus on health behaviors) and review of medical records
Prevalence The prevalence of past or present chemical dependency among renal transplant candidates may be 25% or higher.
Rationale Chemical dependency is a threat to health and longevity, and may interfere with a patient’s ability to adhere to
therapies and follow-up after transplantation.
Recommendations (B) Renal transplant candidates with a history of chemical dependency should undergo evaluation, counseling, and
treatment by appropriate professionals prior to transplantation.
(B) Chemical dependency in the custodial parent(s) of a potential pediatric renal transplant candidate should prompt
referral to appropriate professionals and (legal) child-protection measures should be considered.
(C) A documented drug- and/or alcohol-free period Ω6 months prior to transplantation may help ensure adherence
to posttransplant medications and follow-up.

A cognitive deficit should not automatically exclude a patient
from transplantation. The severity of the deficit must be con-
sidered for its effect on the potential recipient’s ability to con-
sent to the procedure and to comply with the need for life-
long immunosuppression and medical follow-up. The impact
of renal transplantation on the cognitive deficit itself will de-
pend on the cause and reversibility of the deficit. Sehgal et
al. demonstrated a high prevalence of unrecognized mental
impairment among hemodialysis patients (823), but it re-
mains controversial whether or not well dialyzed ESRD pa-
tients manifest marked neuro-cognitive deficits (824). In
adult patients, P300 cognitive evoked potentials, a highly
sensitive, objective measure of subclinical brain dysfunction
measured during electroencephalogram époques, improve
after successful transplantation (825).
In children, successful renal transplantation and posttrans-
plant medical compliance are intimately linked to the family’s
coping skills, socioeconomic status and their adjustment to
the diagnosis of renal failure. Thus, pretransplant evaluation
should include an assessment of the strengths and stresses
of the parents with particular attention to who serves as pri-
mary caretaker. Families with many other young children,
those with limited social support, single-parent families and
those of lower socioeconomic status may require additional
assistance as they attempt to balance the demands of com-
plex posttransplant care with the needs of other family mem-
bers (828). The child’s intelligence, level of schooling, psy-
chomotor and emotional development also have a major im-
pact on renal graft survival and should be assessed at the
time of pretransplant evaluation (829).

Some individuals with irreversible cognitive impairment, al-

though unable to give informed consent, may nevertheless
benefit from transplantation. Transplanting patients with
mental retardation has led to concern that the recipient’s
compliance with therapy and quality of life will be inad-
equate to warrant allocation of a scarce medical resource.
However, in one study, eight mentally retarded patients who
were able to take medications under supervision had excel-
lent outcomes after renal transplantation, and caregivers
agreed that transplantation had improved the quality of life
and health of these individuals (826). Careful evaluation of
the support system available to the potential recipient is im-
perative. The presence of a reliable primary support person
who will take charge of administering immunosuppressive
medications and monitor compliance with medical follow-
up is essential.
Children are unable to give informed consent. The role of the
pediatric patient in shared decision-making varies with age
and maturity. School-aged children should agree to the trans-
plant even though their parents or legal guardians must con-
sent to surgery and immunosuppressive medications. Ado-
lescents should be actively involved in the transplant decision
process. Because of the high risk of noncompliance, trans-
planting an adolescent who does not desire it should be post-
poned until he/she agrees to cooperate with posttransplant
follow-up and immunosuppression therapy (827).
Renal failure in children is associated with deficits in cognitive
function that improve after transplantation (830). However,
children with irreversible cognitive impairment may also do
well after transplantation. Children with Down syndrome, for
example, have had good outcomes following renal transplan-
tation (831).
Alcohol and drug abuse can interfere with a patient’s ability to
adhere to therapy after renal transplantation (Table 66) (822).
There are few data, however, documenting the prevalence of
chemical dependency among hemodialysis patients and re-
nal transplant candidates. In one study 25% of patients
evaluated for a renal transplant reported a history of sub-
stance abuse (832). Because of under-reporting by individ-
uals anxious to be approved for transplantation, independent
sources of information should probably also be used to dis-
cover whether there may be a chemical dependency problem
(832). Every effort should be made to ensure that chemical
dependency is adequately treated prior to transplantation. It
is reasonable to insist that renal transplant candidates with
a history of chemical dependency undergo counseling and
treatment, and that caregivers document a drug- or alcohol-
free period of at least 6 months. Periodic screening for con-
tinued abstinence during wait-listed time may be advisable
as relapse may occur. All patients should be strongly encour-
aged to quit smoking.

2001; Suppl. 1: Vol. 2: 5–95 53

Kasiske et al.

Table 67: Mental illness

Possible screening Medical history (with a focus on the social history) and review of medical records
Prevalence The prevalence of mental illness among renal transplant candidates is difficult to assess precisely, but more than
30% have a history of mental illness and/or chemical dependency and approximately 20% suffer from depression.
Rationale Mental illness may interfere with a patient’s ability to adhere to therapies and follow-up after transplantation. Im-
munosuppressive medications, particularly corticosteroids, have been reported to exacerbate some mental illnesses.
Recommendations (B) Mental illness is not an absolute contraindication to transplantation.
(B) Renal transplant candidates with a history of mental illness should undergo evaluation, counseling and, if neces-
sary, treatment by appropriate mental health professionals prior to transplantation.

Table 68: Noncompliance

Possible screening Medical history (with a focus on health behaviors) and review of medical records
Incidence It is difficult to precisely estimate how often renal transplant recipients fail to adhere with therapy and follow-up after
transplantation, but a consensus estimate would probably be around 20%.
Rationale Noncompliance is an important cause of graft failure after renal transplantation. It may be possible to reduce the
risk of noncompliance by identifying the patients who are most at risk and by carefully instructing renal transplant
candidates on the importance of adhering to medication regimens and posttransplant follow-up visits.
Recommendations (C) Although it is often difficult to predict noncompliance, it is reasonable to delay transplantation for patients who,
despite interventions, are not able to improve life-threatening, noncompliant behaviors.
(B) Renal transplant candidates should be informed of the importance of adherence to medications and follow-up
visits after transplantation.
(B) Renal transplant candidates should be informed of the number of medications and clinic visits that are often
required posttransplant.
(B) The potential cost to the patient of posttransplant medication and care should be carefully reviewed, and attempts
should be made to remove any financial barriers to optimal posttransplant care.

Mental illness is common in ESRD (Table 67). Over 30% of
66 consecutive renal transplant candidates reported a history
of mental health or substance abuse treatment (832).
Twenty-three percent described a history of substance
abuse, while 17% reported a history of outpatient or inpatient
mental health treatment. Since under-reporting is probably
common, the true incidence may be much higher. Up to 20%
of patients on hemodialysis have depression (833). Among
renal transplant candidates 16% are depressed and 9% have
major depression (832).
The evaluator should ask not only about the patient’s history
of mental illness, but also about the family history of mental
illness and substance abuse. Attempts should be made to
understand how the patient copes with illness. Inquiries
should be made about the patient’s mood, and individuals
should be screened for neuro-vegetative signs and symp-
toms. Patients should be asked about sleep disorders such
as insomnia and hypersomnia, lack of interest in pleasurable
activities or work, symptoms of poor energy and chronic fa-
tigue, lack of concentration, decreased appetite, feelings of
worthlessness, guilt and suicidal ideation (834).
Defining absolute psychiatric contraindications to transplan-
tation is difficult at best (835–838). However, most would
agree that caregivers should attempt to reduce psychiatric
barriers to successful transplantation. Individuals with a sig-
nificant mood or anxiety disorder, psychosis, substance
abuse or a severe personality disorder should be referred for
psychiatric diagnoses, treatment and follow-up to reduce
barriers to transplantation.
While 30% of renal transplant programs have indicated that
active affective disorders are contraindications to transplan-
tation, depression in ESRD can be readily treated (822, 834).
Because depression has been identified as a predictor of
poor survival in ESRD, prompt referral to a mental health pro-
fessional is indicated (839). Active schizophrenia is regarded
as an absolute contraindication to renal transplantation by
70% of transplant centers (822). However, schizophrenia that
is well controlled is not generally considered a contraindi-
cation (822). Case reports demonstrate the potential for suc-
cessful transplantation for individuals with major psychoses,
if adequate support and supervision is provided (840,841).
Noncompliance with immunosuppressive medications may
be the third leading cause of graft failure after renal transplan-
tation (Table 68) (842). Studies report rates of noncompli-
ance to range from 5 to 55%, and differences probably re-
flect differences in definition and methods of ascertainment
(843, 844). Except possibly a history of substance abuse
and/or a previous graft loss due to noncompliance, few pre-
transplant characteristics reliably predict posttransplant non-
compliance (843–845). As part of the pretransplant evalu-
ation, patients should be informed of the need to take medi-
cations after transplantation, and the importance of

54 2001; Suppl. 1: Vol. 2: 5–95

 The Evaluation of Renal Transplant Candidates: Clinical Practice Guidelines

Table 69: Ensuring adequate urinary drainage posttransplant

Possible screening Medical history and physical examination
Voiding cystourethrogram (VCUG)
Incidence 2.5–25% of pretransplant VCUGs are abnormal, but most abnormalities are too minor to require pretransplant
intervention.
Rationale Genitourinary abnormalities are common in patients undergoing renal transplantation. In some patients pretransplant
intervention may be needed to minimize the risk of infection and to ensure that urinary drainage is adequate after
renal transplantation.
Recommendations (B) Patients with a history of genitourinary abnormalities may require a complete evaluation, including a VCUG,
cystoscopy and/or retrograde pyelogram.
(E) In adults it is not necessary to obtain a VCUG unless the medical history suggests that there may be genitourinary
abnormalities.
(C) Due to the high incidence ESRD from congenital, genitourinary abnormalities in children, VCUG should be
included in the pretransplant evaluation of most children.

adherence to medication schedules and follow-up visits. The
number of medications that are often required should not be
underestimated.
The potential cost to the patient of posttransplant medication
and care should also be carefully reviewed, so that both the
transplant center and the patient understand the financial
barriers to posttransplant care (846,847). The cost of main-
tenance immunosuppression often exceeds $10,000 per
year. Even with Medicare or other insurance coverage, pa-
tients frequently face co-payments that can divert a substan-
tial portion of their family’s income from food, housing and
other expenses. Patients are sometimes faced with having to
choose between buying food and paying the rent, or taking
medication. Other costs may include travel to and from the
transplant center, time off work, etc.
Good communication between the transplant physician and
the patient is important if compliance and long-term graft
survival are to be achieved. Barriers to effective communi-
cation include lack of a common language as well as more
subtle cultural factors. In such cases, a family member or
ethnically matched professional translator should be iden-
tified pretransplant and should agree to accompany the pa-
tient to posttransplant clinic appointments (847).
Genitourinary
Increasingly, evidence suggests that a voiding cystourethro-
gram (VCUG) or other urologic procedure is not necessary un-
less there is a history of bladder dysfunction (Table 69). Among
112 adult patients evaluated with VCUG, cystoscopy and retro-
grade pyelograms, abnormalities of the upper or lower tract
were documented in 25% of patients (848). However, it is un-
clear how many of these abnormalities would have been
missed if only patients with a history of problems had been
studied (848). In a more recent retrospective study, 51 genito-
urinary abnormalities were found in 333 patients undergoing
routine VCUG pretransplant (850). However, all abnormalities
were either suspected beforehand or were not severe enough
to require correction pretransplant. These same authors re-
viewed their results after adopting a strategy of limiting VCUG
to patients with a history of urinary problems. After 493 trans-
plants (51% had a VCUG), only one urological complication
was encountered (acute urinary retention) (850). The authors
concluded that routine VCUG was not necessary (850). In an-
other retrospective review of 517 routine VCUG studies, only
2.5% were felt to be abnormal, and each abnormality occurred
in a patient with a history of urological problems (851). These
authors also concluded that a VCUG was only necessary in pa-
tients with a history of urological abnormalities (851). Others
have reported similar findings (852,853). Based on these data,
it seems reasonable to reserve VCUG for patients in whom an
abnormality is suspected. In children there is very high inci-
dence ESRD from congenital, genitourinary abnormalities.
Among individuals less than 20 years of age, cystic, hereditary
and/or congenital disease accounted for 31.1% of ESRD in
1994–98 (63). Congenital obstructive uropathy accounted for
8.9%, while renal hypoplasia or dysplasia accounted for 10.2%
of ESRD in this age group (63).
Causes of bladder dysfunction are neurogenic, malformations
and chronic infection. Most patients can be managed without
pretransplant, urinary diversion or bladder augmentation
(854). A retrospective study compared results of reimplan-
tation into a defunctionalized bladder (nΩ7) with mainten-
ance of urinary diversions (nΩ10) (855). The reimplantation
group had no major complications, while in the group with
urinary diversions there were eight major complications (ana-
stomic leaks, ureteroileal stenosis, calculus formation, uro-
sepsis, metabolic acidosis and wound dehiscence/infection)
(854). Others have also reported good results with excision
of urinary diversions and reimplantation into a defunctional-
ized bladder in highly selected patients (855).
Intermittent self-catheterization may be an option for some, if
not most, patients with defunctionalized bladders. Infection is
the major complication. In a small, retrospective comparison of
intermittent self-catheterization (nΩ6) with pretransplant uri-
nary diversion (nΩ7), only two patients in each group had feb-
rile urinary tract infections requiring hospitalization over mean

2001; Suppl. 1: Vol. 2: 5–95 55

Kasiske et al.

Table 70: Approach to patients with a dysfunctional urinary excretory system

Possible screening Medical history and physical examination
Voiding cystourethrogram (VCUG)
Cystoscopy
Retrograde pyelography
Incidence 0.5–1.1% require bladder augmentation or urinary diversion.
Rationale Inadequate urinary drainage posttransplant can lead to obstruction, calculus formation and serious infections. Every
effort should be made prior to transplantation to ensure that there will be adequate urinary drainage posttransplant.
Recommendations (B) Patients with a history suggestive of urological abnormalities should undergo a complete evaluation that may
include VCUG, cystoscopy and retrograde pyelography.
(B) Most patients with a dysfunctional bladder can be managed without urinary diversion or bladder augmentation,
using reimplantation into the dysfunctional bladder, and if necessary, intermittent self-catheterization.
(C) Which, if any, surgical approach should be used to ensure adequate urinary drainage must be individualized in
the absence of data from clinical trials.

Table 71: Native kidney nephrectomy

Possible screening Radiographic imaging, e.g. ultrasound of the native kidneys.
Prevalence Probably ⬍5% of patients require removal of one or both native kidneys prior to transplantation, although the exact
frequency is unknown.
Rationale Pretransplant nephrectomy may prevent potentially life-threatening, posttransplant complications, and may reduce
morbidity.
Recommendations (C) In some patients, the morbidity of large and/or frequently painful polycystic kidneys may be reduced by pretrans-
plant nephrectomy.
(C) Pretransplant nephrectomy may be indicated in some patients with chronic renal parenchymal infection, infec-
tious renal stones and/or obstructive uropathy complicated by chronic infections.
(D) Patients with uncomplicated vesicoureteral reflux do not usually require pretransplant nephrectomy.
(D) Nephrectomy is not generally needed to reduce the risk of recurrent glomerulonephritis in the allograft.
(C) Whether to screen asymptomatic transplant candidates for renal carcinoma is unclear, and when to perform
nephrectomies for suspicious lesions should be individualized.
(B) Bilateral nephrectomy may be indicated in children with congenital syndromes associated with a high risk for
Wilm’s tumors (Table 7).
(B) Consider bilateral nephrectomy for renal transplant candidates who have poorly controlled hypertension, espe-
cially if appropriate medical therapy has been ineffective.
(B) Bilateral nephrectomy is recommended in patients with Congenital Nephrotic Syndrome.
(C) Bilateral nephrectomy may be indicated in patients with persistent nephrotic syndrome despite optimal medical
management.

follow-up periods of 3.7 and 5.7 years, respectively (857).
Overall, the authors felt that the morbidity and quality of life
with intermittent self-catheterization was superior compared
to that associated with the use of surgical approaches (857).
Others have reported similar results in adults (858–860) and
children (861). Although infections are common, long-term,
prophylactic antibiotics are probably not necessary (862).
For patients in whom simple reimplantation into a dysfunc-
tional bladder is not felt to be an option, surgical augmentation
of the bladder prior to reimplantation may be possible (863–
866). Alternatively, using a preexisting urinary diversion obvi-
ates the need for additional surgery and may be an option for
some (867,868). The last resort in the management of dys-
functional bladders is the creation of a new urinary diversion
(867,869,870). Unfortunately, there are no randomized trials
comparing different approaches to the pretransplant manage-
ment of patients with defunctionalized bladders. In most small,
observational studies, patients with pretransplant ileal con-
duits, augmented bladders, or continent reservoirs have had
similar graft and patient survival rates compared to patients
with normally functioning collecting systems (863–866,871–
876). Renal function has generally not been compromised
(865,866,875,876). The major complication is infection. Most
patients with urinary diversions have asymptomatic bacteruria,
although symptomatic infections are undoubtedly more com-
mon as well (871,874,875). In one retrospective case control
study, urosepsis occurred in 1/22 cases compared to 1/54
controls (875). The authors of this study concluded that
prophylactic antibiotic treatment is probably not warranted
(875). In all of these studies, the small numbers of patients and
the lack of suitable controls make it difficult to draw firm con-
clusions. This is understandable, since the number of patients
who require pretransplant urinary diversion or bladder aug-
mentation has generally been reported to be only 0.5–1.1%
(866,875).

56 2001; Suppl. 1: Vol. 2: 5–95

 The Evaluation of Renal Transplant Candidates: Clinical Practice Guidelines
Patients with ADPKD may theoretically benefit from unilateral
or bilateral nephrectomy to reduce symptomatic bleeding, pre-
vent recurrent infection, control blood pressure (see below), al-
leviate adverse effects of the large size of the kidneys (877), or
to create enough space for the allograft (Table 71). However,
there are few studies documenting the benefits of pretrans-
plant nephrectomy in patients with ADPKD. In one retrospec-
tive, uncontrolled study, 25/99 transplant recipients with
ADPKD had pretransplant unilateral (nΩ19) or bilateral (nΩ6)
nephrectomy (878). An additional 10 patients had at least one
native kidney removed posttransplant. Graft survival was sig-
nificantly better among ADPKD patients who had pretrans-
plant nephrectomy compared to those who did not (p⬍0.05)
(878). In contrast, posttransplant nephrectomy (required for
cyst-related complications) was associated with worse graft
survival compared to patients who did not require posttrans-
plant nephrectomy. These authors concluded kidneys should
be removed prior to transplantation in patients who have
symptomatic, cyst-related complications (878). A recent re-
port described a low rate of complications from bilateral neph-
rectomy with concomitant transplantation in 10 ADPKD (879).
On the other hand, outcomes among 47 consecutive ADPKD
patients without pretransplant nephrectomy were compared
to those of 47 matched, non-ADPKD controls (880). There
were no differences in 1- and 5-year graft survival rates. Only
three ADPKD patients had cyst infections and two had epi-
sodes of hematuria, but in neither case was invasive inter-
vention required. These authors concluded that routine pre-
transplant nephrectomy is not required for most patients with
ADPKD (880). In the absence of data to the contrary, it seems
reasonable to reserve pretransplant nephrectomy for ADPKD
patients who have recurrent, symptomatic, cyst-related com-
plications.
Few studies have examined the risks and benefits of native
kidney nephrectomy in patients with chronic, renal paren-
chymal infection, infectious renal stones (e.g. staghorn cal-
culi) and/or obstructive uropathy with chronic infection. How-
ever, it seems reasonable that pretransplant nephrectomy in
such patients may help to prevent serious infections after
transplantation. Vesicoureteral reflux has also been con-
sidered to be an indication for pretransplant nephrectomy
(881). In a retrospective study, 36/820 (4%) of transplants
were in patients who had documented vesicoureteral reflux
(882). Ten patients had pretransplant ureteral reimplantation,
eight bilateral nephrectomy, and 18 persistent reflux. Graft
survival at 3 years was lower in patients with reflux (with
or without pretransplant intervention), but the incidence of
infection was similar in patients with bilateral nephrectomy or
persistent reflux (882). Thus, there is currently little evidence
to suggest that bilateral nephrectomy is indicated in patients
with vesicoureteral reflux and recurrent urinary tract infec-
tions.
The risk of renal cell carcinoma has also been given as a
reason to recommend pretransplant, bilateral nephrectomy.
In one study, ultrasound examination of the native kidneys
was used to screen 129 patients for possible malignancy
2001; Suppl. 1: Vol. 2: 5–95
prior to transplantation (56). Suspicious lesions were treated
by nephrectomy, and renal cell carcinoma was found in 5/
129 (3.9%) (56). The malignancies were all limited to the
kidney. The authors recommended ultrasound to identify pa-
tients who might be candidates for pretransplant nephrec-
tomy to prevent renal cell carcinoma (56). However, it is un-
clear how many of these patients would have developed clin-
ically significant, invasive carcinomas had pretransplant
screening not been carried out. On the other hand, carci-
noma of the native kidneys is common after transplantation,
and is associated with considerable morbidity and mortality
(883). Thus, it seems reasonable to screen transplant candi-
dates with radiographic imaging, e.g. ultrasound of the native
kidneys, and to consider nephrectomy for patients with sus-
picious lesions. Preemptive bilateral nephrectomy may be in-
dicated in some patients with congenital syndromes associ-
ated with a high risk of Wilm’s tumor (Table 7).
Bilateral pretransplant nephrectomy has been advocated as
a means to prevent recurrence of the original kidney disease
in the allograft. However, there are very few data suggesting
that this strategy is effective. In a recent study of 319 trans-
plants in patients with glomerulonephritis, bilateral nephrec-
tomy (nΩ61) did not prevent or delay the onset of recurrent
glomerulonephritis (283). In fact, the rate of recurrence was
significantly greater for patients who had undergone pre-
transplant bilateral nephrectomy. Both FSGS and membra-
nous nephropathy recurred more often among patients sub-
jected to pretransplant nephrectomy (283). Although this
propensity for a higher incidence of recurrence could reflect
selection bias (patients with more severe disease more often
getting nephrectomy), these data nevertheless suggest that
there may be little benefit of bilateral nephrectomy to prevent
recurrence of most glomerulonephritis (283). Whether there
may be some benefit for specific diseases remains to be
established. Occasionally, pretransplant bilateral native kidney
nephrectomy may necessary to treat severe, debilitating pro-
teinuria (884).
Poorly controlled blood pressure is often used as an indi-
cation for pre- or posttransplant nephrectomy. Hypertension
is associated with CVD in renal transplant recipients (885),
and CVD is the most important cause of death after trans-
plantation (886). Hypertension accounted for 25.4% of all
new cases of ESRD in the U.S. Renal Data System registry
in 1998 (886). The prevalence of hypertension in patients
with chronic renal disease ranges from 60 to 100% (885).
The causes of hypertension after renal transplantation are
multiple and include renal function impairment, chronic rejec-
tion, volume overload, toxicity from immunosuppressive
drugs and other secondary causes such as renal artery ste-
nosis (885,887). Hypertension can also be transmitted in
some cases with the renal allograft (888). Pretransplant hy-
pertension is associated with posttransplant hypertension
(889). Retrospective studies have suggested that hyperten-
sion before transplantation is also associated with poor out-
comes after renal transplantation (890,891). Poorly controlled
blood pressure appears to be a strong risk factor for allograft
57
Kasiske et al.

Table 72: Obesity

Possible screening Medical history and physical examination, height, weight, and body mass index (BMI)
Prevalence In some centers, 10–18% of renal transplant recipients have a pretransplant BMI Ø30 kg/m2.
Rationale Obese renal transplant recipients have an increased risk for CVD and surgical complications. Some renal transplant
centers have reported lower graft survival rates and increased mortality for renal transplant recipients with a BMI
⬎25–30 kg/m2. Obesity has been associated with a higher incidence of posttransplant diabetes and CVD. However,
there are no data comparing outcomes of obese patients with those of comparable patients treated with dialysis.
Recommendations (B) Appropriately supervised weight loss therapy, combining low calorie diet, increased physical activity, and behavior
therapy, is recommended for obese renal transplant candidates with a goal weight BMI ⬍ 30 kg/m2 prior to renal
transplantation.
(C) There are few data to suggest which if any obese patients should be denied transplantation based on obesity
per se.

failure in African American transplant recipients, and the level
of pretransplant blood pressure identifies those patients at
the highest risk for renal allograft failure (891,892).
It has long been appreciated that bilateral nephrectomy can
improve blood pressure control, whether performed before
(893,894) or after transplantation (895,896). However, many
of these data were generated in the pre-CsA era. A more
recent review of renal transplant recipients undergoing bilat-
eral nephrectomies at the time of living donor kidney trans-
plantation, reported no differences in blood pressure control
or number of antihypertensive agents required when com-
pared to patients not undergoing bilateral nephrectomies
(897). Bilateral laparoscopic nephrectomy has been effective
in patients with poorly controlled hypertension after success-
ful renal transplantation (898, 899). It has been suggested
that, with the availability of synthetic erythropoietin as well
as 1,25 vitamin D preparations, pretransplant nephrectomy
should be performed more frequently to reduce the number
of antihypertensive medications patients must take (900).
This would both reduce cost of medical care posttransplant
and obviate the need for strict patient compliance with
multiple antihypertensive medications. On the other hand, bi-
lateral nephrectomy is not without morbidity and mortality.
For some patients the loss of residual renal function may be
detrimental. In general, it seems prudent to consider bilateral
nephrectomy for renal transplant candidates who have poorly
controlled hypertension after correction of extracellular vol-
ume and appropriate medical therapy.
Bilateral nephrectomy has been recommended for patients
with Congenital Nephrotic Syndrome (901, 902). Some other
patients with nephrotic syndrome that cannot be optimally
managed by medical therapy may benefit from pretransplant
bilateral nephrectomy as well, although evidence demon-
strating the effectiveness of this approach for specific dis-
eases is often lacking (903).
and women in all age groups (Table 72) (904,905). The body
mass index (BMI) is calculated as an individual’s weight in
kilograms divided by the square of their height in meters (kg/
m2) and provides an acceptable approximation of total body
fat for the majority of patients (904,906). Individuals with a
BMI of 25–29.9 kg/m2 are considered overweight, and indi-
viduals with a BMI Ø30 kg/m2 are considered obese. Among
301,614 patients initiating renal replacement therapy between
1995 and 1999 in the U.S. Renal Data System Registry, the
mean BMI was 26.0 kg/m2 (27.0 kg/m2 for 133,379 diabetics
and 24.7 kg/m2 for 168,235 non-diabetics) (886).
In the ESRD population, malnutrition at the time of initiation
of dialysis is a strong predictor of mortality, both short-term
and long-term (906). Probably as a result of this, a higher
BMI has been associated with a reduced mortality among
hemodialysis patients (906). In contrast, obesity is an import-
ant risk factor for renal transplant recipients and is considered
by many transplant centers one of the exclusion criteria for
renal transplantation for at least some individuals (907–909).
Approximately 10–18% of transplant recipients have a pre-
transplant BMI Ø30 kg/m2 (910, 911). Obese renal transplant
recipients (BMI Ø30 kg/m2) have higher rates of delayed
graft function and suffer from more surgical complications,
including wound infections, than non-obese renal transplant
recipients (910–914). Obesity is also associated with a pro-
longed posttransplant hospital length of stay and increased
cost of transplantation (615). The incidence of posttransplant
diabetes mellitus is also higher in obese renal transplant re-
cipients (909, 911). Several transplant centers have reported
increased immunological graft losses and decreased graft
survival associated with higher mortality rates in obese renal
transplant recipients (908–910, 915). Other transplant cen-
ters, however, have not observed significant correlations be-
tween obesity and graft survival rates (911). Obese recipients
of combined kidney-pancreas transplantation have been re-
ported to have decreased pancreas and renal graft survival
rates (916).

Endocrine It is prudent to recommend weight reduction to a BMI ⬍30

kg/m2 for renal transplant candidates. Each transplant center
Studies in the general population have shown that obesity is should determine whether obesity should serve as a sole cri-
associated with increased morbidity and mortality for men terion for exclusion of individual patients from consideration

58 2001; Suppl. 1: Vol. 2: 5–95

 The Evaluation of Renal Transplant Candidates: Clinical Practice Guidelines

Table 73: Diabetes

Prevalence Diabetes is the most common cause of end-stage renal disease (ESRD) and 32% of first, cadaveric renal transplant
recipients have ESRD caused by diabetes.
Rationale Renal transplantation improves the survival of patients with ESRD caused by diabetes. Pancreas transplantation
improves glycemic control, reduces the frequency of hypoglycemic episodes and improves the quality of life of renal
transplant recipients. Although pancreas transplantation can retard and even reverse lesions of recurrent diabetic
nephropathy, the clinical relevance of this is unclear. It is also unclear whether pancreas transplantation improves
other microvascular or macrovascular complications compared to kidney transplantation alone.
Recommendations (B) Pancreas transplantation should be considered as an alternative to insulin therapy for ESRD patients with Type
1 diabetes who have undergone, or plan to undergo, renal transplantation.
(C) Patients who have a living kidney donor should consider undergoing renal transplantation before considering
subsequent, cadaveric, pancreas transplantation.

for renal transplantation. Given the increased cardiovascular
mortality for obese renal transplant recipients, special atten-
tion to the cardiac evaluation of obese renal transplant candi-
dates is recommended (909). Weight loss therapy in the
general population is most successful when it combines low
calorie diets, increased physical activity and behavior therapy
(904). A similar approach is recommended for renal trans-
plant candidates. There are too few data to make recommen-
dations regarding pharmacological therapy or surgery to treat
obesity in renal transplant candidates.
Diabetes mellitus is the leading cause of ESRD in most indus-
trialized nations (Table 73) (917). The proportion of ESRD
caused by diabetes continues to increase. In the U.S. Renal
Data System registry, 48.4% of the 72 000 new cases of
ESRD was attributed to diabetes in 1998 (886). Among ca-
daveric and living donor transplants with identifiable causes
of ESRD, 29.1% had ESRD from diabetes (886). Patients
with ESRD from diabetes have higher mortality rates
from multiple causes, including CVD, sepsis, and withdrawal
from treatment compared to non-diabetic patients (917). Reti-
nopathy, coronary artery disease, cardiomyopathy, PVD,
neuropathy, autonomic dysfunction, myopathy and other
complications associated with diabetes persist and/or pro-
gress during ESRD (917). However, survival of patients with
ESRD caused by diabetes is better after renal transplantation
than survival of comparable patients who remain on dialysis,
and the incremental survival advantage for diabetic transplant
recipients is greater than the survival advantage for nondia-
betics (521,918). Nevertheless, renal transplant recipients
with diabetes have increased mortality compared to non-dia-
betic renal transplant recipients (43).
Pancreas transplantation has become an accepted therapy
for patients with Type 1 diabetes mellitus who require renal
replacement therapy (919,920). The American Diabetes As-
sociation has recommended pancreas transplantation as an
acceptable alternative to insulin therapy for diabetic patients
with ESRD who have, or plan to have, a kidney transplant
(920). Pancreas transplantation can improve the quality of
life of renal transplant recipients by eliminating the need for
exogenous insulin, and by eliminating or reducing the num-
ber and severity of acute hypoglycemic episodes (921,922).
Although tight control of blood glucose helps prevent compli-
cations of diabetes (923), there have been no randomized
controlled trials to determine whether pancreas transplan-
tation ameliorates the long-term complications of diabetes or
prolongs the life of kidney transplant recipients compared to
kidney transplantation alone.
The outcomes of kidney-pancreas transplantation continue to
improve. The 1-year patient survival rates in the International
Pancreas Transplant Registry now exceed 90–96% (924). In-
sulin independence is achieved by more than 70% of pan-
creas after kidney transplant recipients and by more than
80% of simultaneous kidney-pancreas transplant recipients
(919,924). Recent observational studies have reported a sur-
vival advantage for diabetic ESRD patients with simultaneous
kidney-pancreas transplantation compared to renal transplan-
tation alone (925–927).
The Diabetes Control and Complications Trial (DCCT) showed
the benefits of tight glycemic control in several microvascular
disease complications of diabetes, including diabetic nephro-
pathy (923). Tight control of blood sugar retards the develop-
ment of diabetic glomerular lesions in renal transplant recipi-
ents with Type 1 diabetes mellitus (928). The importance of
normoglycemia in preventing the development of diabetic
nephropathy has been recently underscored by the demon-
stration that pancreas transplantation, with restoration of
normoglycemia for at least 10 years, can reverse lesions of
diabetic nephropathy in native kidneys (929).
Diabetic renal transplant recipients can develop histological
changes of diabetic nephropathy in the allograft as early as
3 years after transplantation (930). This is no longer a disease
of the second decade as some recipients can develop symp-
tomatic disease and graft failure due to recurrent diabetic
nephropathy within 10 years (931). Although diabetes often
develops in the allograft after kidney transplantation (931–
933), recurrent diabetic nephropathy is still an uncommon
cause of graft failure (930,931,934). The proportion of dia-
betic renal transplant recipients who lose their grafts due to
recurrent diabetes is poorly documented. Successful com-
bined kidney-pancreas transplantation can prevent the devel-
opment or reduce the progression of recurrent diabetic

2001; Suppl. 1: Vol. 2: 5–95 59

Kasiske et al.
nephropathy (935,936). Nevertheless, it is still unclear
whether pancreas transplantation has any effects on the renal
allograft that are clinically relevant. Therefore, preventing the
development of diabetes in the renal allograft is, by itself, not
a convincing reason to carry out pancreas transplantation.
The effects of pancreas transplantation upon other diabetic
complications have been more difficult to demonstrate. Res-
toration of normoglycemia with combined kidney-pancreas
transplantation did not influence the progression of advanced
diabetic retinopathy in two observational studies (937,938).
However, a more recent uncontrolled series of 20 patients
noted stabilization of advanced diabetic retinopathy following
simultaneous kidney-pancreas transplantation (939). The
lack of a suitable control group makes interpretation of these
studies problematic, since retinopathy may stabilize in some
patients after kidney transplantation alone. Improvements in
diabetic microangiopathy in the conjunctival microcirculation
have been reported for patients with Type 1 diabetes mellitus
after simultaneous kidney-pancreas transplantation (940).
Pancreas transplantation has been associated with some im-
provements in diabetic neuropathy (941–944), but the fact
that neuropathy may also improve after kidney transplan-
tation alone makes it difficult to quantitate improvements due
to pancreas transplantation without controlled trials (945). No
benefits in macrovascular complications have been demon-
strated when comparing recipients of combined kidney-pan-
creas transplants and kidney transplants alone (946, 947).
Pancreas transplantation has been associated with increased
surgical and medical complications compared to kidney
transplantation alone (948,949), although it appears that im-
provements in surgical techniques and medical care have re-
duced the frequency of adverse events (919,950,951). Infec-
tions are more common in kidney-pancreas transplant recipi-
ents compared to kidney transplantation alone (950,952,
953). Simultaneous kidney-pancreas transplantation has
been associated with a higher incidence of acute renal allo-
graft rejection (954,955). Nevertheless, newer immunosup-
pressive regimens have been associated with significant de-
creases in the reported rates of renal allograft rejection in
patients undergoing simultaneous kidney-pancreas trans-
plantation (956,957). Successful kidney-pancreas transplan-
tation is associated with improvements in quality of life (958).
It is reasonable to recommend pancreas transplantation to
ESRD patients with Type 1 diabetes mellitus who have un-
dergone, or are planning to undergo, renal transplantation.
There has been more experience with simultaneous kidney-
pancreas transplantation than with other types of pancreatic
transplantation. In a recent retrospective comparison of simul-
taneous kidney-pancreas transplantation with kidney trans-
plant alone (transplanted between 1986 and 1996), there
were similar patient and graft survival rates, but lower
discharge renal function and a higher rate of acute rejection
with simultaneous kidney-pancreas transplantation (955). In-
formation such as this should be part of the shared decision
making process for patients and physicians contemplating
60
simultaneous kidney-pancreas versus living-related kidney
followed later by a possible cadaveric pancreas transplant. Fi-
nally, in a recent report, seven consecutive Type 1 diabetic pa-
tients became insulin independent after pancreatic islet trans-
plantation (810). Efforts are currently underway to reproduce
this remarkable achievement in other patients and transplant
centers. If these efforts are successful, islet transplantation
may move from the experimental arena into mainstream clin-
ical practice.
Patients with ESRD can suffer from multiple bone disorders,
included high-turnover bone disease (secondary hyperpara-
thyroidism), low-turnover bone disease (osteomalacia) and
dialysis-related amyloid bone disease (Table 74) (959,960).
Successful renal transplantation is the best treatment for
most causes of low-turnover bone disease (including de-
ranged calcium and vitamin D metabolism and aluminum in-
toxication) and for dialysis-related amyloid bone disease
(959,960). Renal transplantation also corrects the negative
calcium and positive phosphorus balance present in patients
with ESRD. Nevertheless, persistence of hyperparathyroidism
after renal transplantation is common (960–962). Almost
90% of renal transplant recipients have elevated parathyroid
hormone (PTH) at the time of transplantation and more than
30% of these patients persist with elevated PTH up to 3 years
after transplantation (963). The duration of time on dialysis
and the intensity of hyperparathyroidism prior to transplan-
tation correlate with the severity of posttransplant hyperpara-
thyroidism (962–965). Hypercalcemia is the most common
biochemical marker of hyperparathyroidism and has been re-
ported in 10–22% of renal transplant recipients
(964,966,967). Normocalcemic, long-term renal transplant
recipients can have inappropriately high PTH levels even in
the setting of preserved renal function (961). Several cases of
malignant calcinosis (968), pseudoclubbing (969) and pri-
mary adenomas have been reported (967). Stones have been
noted rarely (970). Hyperparathyroidism has also been linked
to posttransplant renal dysfunction (971–975). Stability and
improvement in posttransplant aluminum bone disease have
also been noted after pretransplant parathyroidectomy (976).
The prevention and management of renal osteodystrophy in-
cludes dietary phosphorus restriction, phosphorus-binding
agents, vitamin D metabolites, vitamin D analogues and di-
alysis (959). For most patients with ESRD, parathyroidecto-
my is reserved as a last step after failure of medical treatment
in the treatment of secondary hyperparathyroidism and after
exclusion of aluminum-induced bone disease. Indications for
parathyroidectomy for ESRD patients on dialysis include re-
fractory and/or symptomatic hypercalcemia (after exclusion
of other causes of hypercalcemia), refractory hyperphos-
phatemia, severe intractable pruritus, serum calcium x phos-
phorus product that persistently exceeds 70–80 mg/dl with
progressive extraskeletal calcifications and calciphylaxis
(959,977). Subtotal parathyroidectomy, total parathyroidecto-
my with autotransplantation, and total parathyroidectomy
without autotransplantation have been advocated by different
transplant centers with excellent results (978–981).
2001; Suppl. 1: Vol. 2: 5–95
 The Evaluation of Renal Transplant Candidates: Clinical Practice Guidelines

Table 74: Hyperparathyroidism

Possible screening Serum calcium, phosphorous, and parathyroid hormone (PTH)
Prevalence Hyperparathyroidism is common in patients with ESRD and has been reported in almost 90% at the time of trans-
plantation. At least 30% of renal transplant recipients have persistent hyperparathyroidism and 10–20% have hyper-
calcemia.
Rationale Persistent hyperparathyroidism after renal transplantation is associated with hypercalcemia, bone disease, and poss-
ibly hypertension and renal dysfunction. Hyperparathyroidism can be prevented or effectively treated with dietary
measures, phosphorus binders, vitamin D metabolites/analogues and in some cases surgery.
Recommendations (A) Calcium, phosphorous, and PTH should be measured as part of the pretransplant evaluation, and should be
repeated periodically while patients are on the transplant waiting list.
(B) Parathyroidectomy should considered for renal transplant candidates who have failed medical management and/
or have severe, persistent, complications of hyperparathyroidism, e.g. refractory hypercalcemia, refractory hyperphos-
phatemia, severe intractable pruritus, serum calcium-phosphorus products that persistently exceed 70–80 mg/dl
with progressive extraskeletal calcifications, and calciphylaxis.

Table 75: Preventing posttransplant graft thrombosis

Possible screening Medical history (focusing on a history of thrombotic events)
Antiphospholipid antibodies
Hemoglobin and platelet count
Prothrombin time and activated partial thromboplastin time
Factor V Leiden
Protein C and protein S
Homocysteine
Possible prophylaxis Anticoagulation
Incidence The incidence of early posttransplant (arterial and/or venous) allograft thrombosis is approximately 2–6%.
Prevalence The prevalence of specific coagulation abnormalities among renal transplant candidates is poorly defined, but there
appears to be an increased prevalence of several pro-thrombotic factors.
Rationale The incidence of graft thrombosis is high enough to warrant screening patients who may be at increased risk for graft
thrombosis due to coagulation abnormalities. Patients who have abnormalities can be treated with anticoagulation to
prevent allograft thrombosis posttransplant.
Recommendations (B) All renal transplant candidates with systemic lupus erythematosus should have antiphospholipid antibodies meas-
ured.
(B) Patients with antiphospholipid antibodies should receive prophylactic aspirin and/or other anticoagulation in the
perioperative period, especially if there is a history of thrombosis (e.g. pulmonary embolus, deep vein thrombosis,
recurrent hemodialysis access clotting, or thrombosis of a previous allograft) or spontaneous abortion.
(C) Patients who have had a history of thrombosis should have a coagulation profile that includes antiphospholipid
antibodies, hemoglobin, platelet count, prothrombin time, activated partial thromboplastin time, factor V Leiden,
protein C, protein S, and homocysteine.
(C) Patients who have had a history of thrombosis and have one or more abnormalities in the coagulation profile
should receive prophylactic aspirin and/or other anticoagulation in the perioperative period.

The extent of secondary hyperparathyroidism that is accept-
able in the patient prior to renal transplantation is unknown
(967,968,971,976,982). Some identify length of time on dialy-
sis and pretransplant hypercalcemia as being predictive of
the need for parathyroidectomy (971). The percent of trans-
plant recipients requiring posttransplant parathyroidectomy
has varied from 1.5 to 5.9% (967,971). The rate of recurrent
hyperparathyroidism in patients on dialysis is quite high and
some suggest that patients who are unlikely to be trans-
planted should have a total parathyroidectomy and that renal
transplant candidates should have sub-total parathyroidecto-
my with autotransplant (983). Based on available data, we
recommend pretransplant parathyroidectomy for patients
with symptomatic secondary hyperparathyroidism and for
patients with hypercalcemia (in the absence of exogenous
calcium supplementation) and marked elevations of PTH.
Coagulopathies
The incidence of early posttransplant renal allograft throm-
bosis has been reported to be 1.9% (984), 2.6% (27/1045)
(985), 3.2% (138/4394) (986), 4.0% (7/176) (987), 4.8%
(44/915) (988), 6.1% (34/558) (989), and even 12% (12/
100) (990) among adults and children (Table 75). Pretrans-
plant risk factors may include recipient age⬍6 (985), young

2001; Suppl. 1: Vol. 2: 5–95 61

Kasiske et al.
donor age (984,986,990), transplant before starting main-
tenance dialysis (985,991), prolonged cold ischemia time
(984,986), female donor (984), cadaveric vs. living-related
donor (in children) (986), peritoneal dialysis vs. hemodialysis
(988), diabetes (984) and prior history of venous thrombosis
in the recipient (984).
Few studies have attempted to determine the prevalence of
coagulation abnormalities among renal transplant candidates.
Approximately 40% of patients with SLE have an antiphospho-
lipid (anticardiolipin) antibody (lupus anticoagulant). The pres-
ence of an antiphospholipid antibody is associated with throm-
bocytopenia, in vitro coagulation abnormalities, thrombotic
events, and fetal abortion. This antiphospholipid antibody syn-
drome (APAS) syndrome is encountered in patients with and
without SLE. In one study of 85 renal transplant patients with
SLE, antiphospholipid antibody was detected in 25/85 (29%)
and clinical events occurred in 60% compared to 8% without
antiphospholipid antibody (992). In another study of eight pa-
tients with SLE and an antiphospholipid antibody, there were
four thrombotic episodes compared to none in five SLE pa-
tients without antiphospholipid antibody (993). In a study of
non-SLE transplant recipients, 50/178 (28%) had pre- or post-
transplant antiphospholipid antibodies, and pretransplant anti-
phospholipid antibodies were associated with posttransplant
venous thrombosis (994). In addition, anticardiolipin anti-
bodies have been linked to chronic HCV infection, and anti-
cardiolipin antibodies were recently associated with throm-
botic microangiopathy in transplant recipients with HCV(995).
The presence of antiphospholipid antibodies has been associ-
ated with early graft failure and graft thrombosis
(991,996,997). In a recent study, 19% of 502 patients awaiting
renal transplantation had antiphospholipid antibodies (998).
There were 23 patients with APAS (998). All seven with APAS
who underwent transplantation without anticoagulation had
graft thrombosis, while grafts survived in three of four with
APAS who received anticoagulation (998). None of the 37 pa-
tients with high antiphospholipid antibody titers without APAS
lost their allografts as a result of thrombosis (998).
Other coagulation abnormalities reported to be associated
with allograft thrombosis include factor V Leiden (999),
shortened activated partial thromboplastin time (1000), a het-
erozygous prothrombin gene mutation at position 20210
(1001), protein S and/or C deficiency (1002) and thrombocyt-
osis (1003). The prevalence of these and other coagulation
abnormalities among renal transplant candidates has not
been well defined. In one study of renal transplant recipients,
protein S deficiency was found in 1.5% (2/132) and factor V
Leiden in 7.6% (10/132) (1004). Among 17 children on peri-
toneal dialysis there were significant increases in factor VII,
factor VIII, von Willebrand factor and antithrombin III, while
there was a decrease in plasminogen (1005).
Data from case-controlled studies indicate that there may be
an increased risk of venous thrombosis in patients from the
general population who have elevated (greater than 95th per-
centile) plasma homocysteine levels (1006–1008). Some
62
studies have also reported that the C677T polymorphism of
the methylenetetrahydrofolate reductase gene (associated
with high homocysteine levels) increases the risk of venous
thrombosis for some patients in the general population
(1009–1011). Although hemodialysis and renal transplant pa-
tients have increased homocysteine levels, the potential role
of homocysteine in graft thrombosis is unclear. Folic or folinic
acid supplements can safely reduce homocysteine levels in
hemodialysis patients (1012–1014) and it may be reasonable
to attempt to lower homocysteine prior to transplantation.
In summary, all of the studies linking coagulation abnormali-
ties to allograft thrombosis are retrospective. Whether coagu-
lation abnormalities measured before transplantation predict
posttransplant events needs to be confirmed in prospective
studies. Whether the beneficial effects of anticoagulation
outweigh the risk of bleeding (particularly in the perioperative
period) needs to be addressed in clinical trials. In the mean-
time, a reasonable strategy may be to screen high-risk pa-
tients for coagulation abnormalities, and to prophylactically
treat those who have both a prior history of thrombosis and
demonstrable coagulation abnormalities.
Age
In 1998, 48.2% of all patients beginning renal replacement
therapy in the U.S. Renal Data System registry were over the
age of 65 (Table 76) (886). As the prevalence of the two
major causes of ESRD (diabetes mellitus and hypertension)
increases with age, it is anticipated that the age of patients
with ESRD will continue to increase (1015). The last 10 years
have seen a marked increase in the number of renal trans-
plants performed in older patients (1016). According to UNOS
data, about 9% of all patients in the waiting list for renal trans-
plantation are 65 years or older (1016).
Patients 60 years and older with ESRD and who receive a
kidney transplant survive longer than dialysis patients with
the same number of comorbid conditions (1017,1018). A re-
cent analysis of registry data indicated that transplant recipi-
ents 60–74 years old had better survival compared to simi-
larly aged dialysis patients on the transplant waiting list (521).
Although patient survival declines with increasing age, graft
survival censored for death is better with increasing age
(1019,1020). The net result is that there is similar overall graft
survival for older compared to younger renal transplant recipi-
ents (1019,1020). Older renal transplant recipients have an in-
creased risk of death due to cardiovascular disease
(1021,1022). Infections in the first few months after transplan-
tation are also an important cause of death in older renal
transplant recipients (1021). A recent analysis of data from
U.S. Renal Data System and UNOS showed that the relative
risk of death from infection after transplantation rises with
increasing age of the transplant recipients (1023). Similarly,
among Caucasian renal transplant recipients, the relative risk
for chronic renal allograft failure was noted to rise with in-
creasing recipient age (441).
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 The Evaluation of Renal Transplant Candidates: Clinical Practice Guidelines

Table 76: Advanced age

Prevalence Almost 50% of all patients with end-stage renal disease are 50 years or older. More than 9% of patients on the
United Network for Organ sharing waiting list are 65 years or older.
Rationale Cardiovascular disease and malignancies are more prevalent in older renal transplant recipients, and older recipients
have higher mortality than younger recipients. Nevertheless, older renal transplant recipients survive longer than
similar patients who remain on dialysis.
Recommendations (B) There should be no absolute upper age limit for excluding patients whose overall health and life situation suggest
that transplantation will be beneficial.
(B) Advancing age increases the need to screen for CVD and most malignancies.
(C) Advancing age increases the need to periodically reevaluate patients on the waiting list.

Table 77: Anticipating posttransplant drug interactions

Incidence Although renal transplant candidates typically take multiple medications that may interfere with immunosuppression
after renal transplantation, there are few data on the incidence of adverse drug reactions after renal transplantation.
Rationale Avoiding critical drug interactions in the early posttransplant period can prevent over-immunosuppression (increased
risk of infections and cancer), under-immunosuppression (increased risk of rejection), nephrotoxicity and other ad-
verse events.
Recommendations (B) Medications that renal transplant candidates require should be carefully reviewed in anticipation of possible drug
interactions if they are continued posttransplant. Patients and caregivers should be made aware of potential problems
so that they can be prevented after transplantation.

Patients 60 years of age and older have longer initial hospital-
izations posttransplant, but fewer acute rejection episodes,
and their self-reported quality of life appears to be similar
to that of age-matched, non-transplant controls (1024). The
improvements in renal transplant results for older patients in-
clude those treated with cyclosporine or tacrolimus
(1019,1020,1024,1025).
candidates should be carefully reviewed prior to renal trans-
plantation to anticipate and if possible avoid potentially
dangerous drug interactions in the posttransplant period. Ap-
propriate drug adjustments in the setting of impaired renal
function and in many patients for possible liver disease and
advanced age are also important considerations before and
after renal transplantation.

Given the excellent results of renal transplantation, older renal
transplant candidates who have no medical contraindications
should be considered for renal transplantation. A detailed
evaluation, with special emphasis on CVD risk and screening
for malignancy, is especially important in this group of pa-
tients. Older renal transplant candidates who are on the wait-
ing list for transplantation should probably be reevaluated
more often than comparable younger individuals, because
their medical status may change quickly.
Medications
Renal transplant recipients require multiple drugs as part of
their immunosuppressive regimen, for prophylaxis against
posttransplant complications, for treatment of underlying
medical conditions and for the treatment of new compli-
cations that arise after transplantation (Table 77). Drug inter-
actions of particular relevance for renal transplant recipients
include alterations in the pharmacokinetics of immunosup-
pressive drugs (which can lead to over-immunosuppression
or under-immunosuppression) and toxicities from potenti-
ation of physiological and pharmacological actions of drugs
(1026,1027). The medication regimens of renal transplant
Many drugs can interact with cyclosporin A (CsA) and affect
its absorption, distribution, metabolism and/or excretion,
possibly resulting in renal and/or extrarenal toxicities
(1026,1028–1030). CsA is largely metabolized by the hepatic
monoxygenase system, in particular cytochrome P450
(1026,1029). Many drugs decrease CsA metabolism and
cause increased CsA concentrations, e.g. nondihydropyridine
calcium channel blockers, imidazole antifungal compounds
and macrolide antibiotics. Drugs that increase CsA met-
abolism and result in decreased CsA concentrations include
phenobarbital, phenytoin, carbamazepine and rifampicin. In-
creased risks of nephrotoxicity for patients on CsA have been
noted with nonsteroidal anti-inflammatory drugs, amino-
glycosides, amphotericin B, and other agents. Finally, CsA
blocks the metabolism of 3-hydroxy-3-methylglutaryl-coen-
zyme A (HMG-CoA) reductase inhibitors, and the dosage of
HMG-CoA reductase inhibitors will need to be reduced by
50% or more if CsA is administered to patients (1026,1031).
Tacrolimus differs in its absorption from CsA in that it does
not require the presence of bile (1026,1031). Tacrolimus is
metabolized by the cytochrome P450 system and similar
drug interactions to those previously described for CsA have
been described (1026,1031).

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Kasiske et al.

Table 78: Blood group

Rationale Antibodies to major blood group antigens can cause hyperacute rejection and graft failure. The current practice is
to transplant ABO blood group donors into identical ABO blood group recipients.
Recommendations (A) The blood group of the recipient should be compatible with that of the donor.
(C) Efforts to transplant kidneys from donors whose blood group is incompatible with the recipient should be con-
sidered experimental.

Table 79: Tissue typing

Rationale Matching for human leukocyte antigens (HLA) improves long-term outcomes after renal transplantation.
Recommendations (A) Donors and recipients should be matched as closely as possible for HLA-A, -B, and -DR antigens.
(B) HLA-A, -B, and -DR antigens should be determined by using standard serological and/or molecular (low to
intermediate resolution) procedures.
(B) Molecular genotyping of HLA antigens should be strongly considered for African American renal transplant
candidates.

Serious interactions can also occur with other immunosup-
pressive drugs used in renal transplantation. Azathioprine is
partly metabolized by xanthine oxidase. Allopurinol (a potent
inhibitor of xanthine oxidase) can cause marked increases in
azathioprine metabolites and potentially fatal bone marrow
suppression (1026). It is best to avoid the combined use of
azathioprine and allopurinol. However, if both drugs are
necessary, very low doses must be used (1032,1033). Myco-
phenolate mofetil can be associated with bone marrow sup-
pression, especially when administered with other myelosup-
pressive drugs (1031). The bioavailability of mycophenolic
acid, the active metabolite of mycophenolate mofetil, may be
reduced by aluminum/magnesium hydroxide containing anti-
acids and cholestyramine (1031).
In summary, renal transplant candidates and renal transplant
recipients frequently require multiple pharmacological agents
as part of their medical treatment. It is important to anticipate
potentially dangerous drug interactions prior to transplan-
tation and to take appropriate steps to prevent posttransplant
complications.
Histocompatibility
Histocompatibility testing seeks to identify donor-recipient
combinations likely to yield successful transplants utilizing
three principles: ABO blood group compatibility, HLA
matching and donor-specific crossmatching. The cross-
matching excludes donor organs from recipients who have
preexisting anti-donor immunity likely to cause graft failure.
After ABO compatibility, the pretransplant crossmatch may
represent the most important procedure performed in the
histocompatibility laboratory.
To increase the efficient use of donor organs, kidneys that
cross blood types are being used for transplantation (Table
78). Specifically, the A2 blood type has a lower blood group
antigen expression, behaves like an O blood type, and there-
fore may be successfully transplanted into O recipients
(1034–1036). In addition, a number of groups have
attempted to use different antibody removal strategies to re-
duce the risk of accelerated acute rejection and to improve
the success of ABO incompatible transplants (1037–1042).
Optimum matching of donor and recipient HLA antigens can
reduce the incidence of acute rejection episodes and improve
long-term graft survival (Table 79) (1043–1053). Recent im-
provements in the techniques used to determine histocom-
patibility include the use of molecular genotyping. Molecu-
larly defined alleles or subtypes may be the best strategy to
eliminate inconsistencies (1054). Comparisons of serological
and molecularly defined HLA class typing have demon-
strated that mistyping occurs (1055,1056). The more accu-
rate molecular typing may be necessary to distinguish be-
tween a zero mismatch and true 6-antigen matched grafts.
In a large study of kidney donors and recipients, there was
evidence of serotyping discrepancy of HLA-A (18.0%) and
HLA-B (25.4%) demonstrated by molecular genotype of
African Americans (1056). Overall, 36.3% of African Ameri-
cans showed either an HLA-A or HLA-B discrepancy (1056).
In the same study, only 8.5% of Caucasian kidney donors
and recipients were mistyped. The high tissue typing discrep-
ancy rate in African Americans provides a strong argument
for using molecular techniques for genotyping this popula-
tion. This substantial discrepancy may also help to explain the
historically inferior graft survival rates for African American
recipients receiving primarily kidneys from non-African
American donors.
Matching donor-recipient HLA antigens is particularly import-
ant for patients who have had a prior transplant. It is strongly
recommended not to re-expose a recipient to an HLA class
II antigen of a previously rejected allograft (1057–1062).
Moreover, it is critical to test highly reactive sera (sera with
high titers of pre-formed antibodies reflecting immune mem-
ory) in a recipient-donor crossmatch to assess recipient-do-
nor compatibility.

64 2001; Suppl. 1: Vol. 2: 5–95

 The Evaluation of Renal Transplant Candidates: Clinical Practice Guidelines

Table 80: Crossmatch

Rationale To avoid hyperacute and/or accelerated rejection, a crossmatch is performed testing informative recipient sera
(highest PRA, current and immediately pretransplant sera) against donor lymphoid target cells to identify the pres-
ence of IgG antibodies to (donor) HLA antigens.
Recommendations (A) Flow cytometry or a complement-dependent cytotoxicity (CDC) assay that is more sensitive than the NIH-CDC
or Amos-modified NIH-CDC assays, e.g. the anti-human globulin (AHG) enhanced CDC assay, should be used for
all patients.
(A) Since the AHG-CDC and flow cytometry crossmatches are membrane-dependent assays, it is important to know
whether tested sera contain IgG antibodies to HLA antigens to correctly interpret crossmatch results. A positive flow
cytometry or AHG-CDC crossmatch against either T cell or B cell donor targets, using sera with IgG antibodies to
HLA antigens is a contraindication to transplantation. A positive flow cytometry or IgG AHG-CDC crossmatch against
donor targets using sera without HLA antibodies, is not a contraindication to transplantation, since the positive
crossmatch may be directed against non-HLA antigens, e.g. autoreactive antibodies.
(B) Since the flow cytometry crossmatch is more sensitive than the AHG-CDC crossmatch, it is incumbent upon
each transplant center to decide (using their own clinical data) how to include or exclude a donor-recipient pairing
when presented with AHG negative, flow cytometry positive crossmatch results.
(B) It is necessary to determine whether a positive crossmatch is due to IgG or IgM, since IgM-positive AHG or flow
cytometry crossmatches are not contraindications to transplantation. IgM reactivity should therefore be eliminated
by heat or chemical treatment.

The primary goal of donor-recipient HLA matching is to mini-
mize positive crossmatches and to reduce posttransplant im-
mune activation, which could lead to rejection and/or graft
loss. Although substantial efforts have been made to improve
serological and/or molecular identification of HLA antigen,
rejections still occur. Efforts to use cross-reactive antigen
groups (CREGS) have yielded minimum benefit (although
improvement in CREG-matched transplants for African
Americans have been reported) (1063–1065). Non-HLA anti-
gens, such as endothelial specific antigens, may also play a
role in antibody-mediated rejection (1066).
While refinements in DNA molecular technology may more
precisely discriminate the degree of donor-recipient mis-
matches, any advances from HLA matching may be difficult
to ascertain because of new immunosuppressive agents that
are likely to achieve 1-year graft survival rates of 85–90% for
primary recipients of cadaveric donor renal allografts (1067).
The crossmatch identifies recipient anti-donor reactivity that is
associated with a poor clinical outcome (Table 80) (1068). The
original standard, the National Institutes of Health (NIH) – com-
plement-dependent cytotoxicity (CDC) crossmatch, has been
altered by longer incubation times, Amos-modified washes
and the use of anti-human globulin (AHG) to enhance the sen-
sitivity for detecting anti-HLA antibodies (1069,1070). Both im-
munoglobulin M (IgM) and immunoglobulin G (IgG) antibodies
can cause a positive CDC crossmatch. However, IgM anti-
bodies, whether they are auto-antibodies or antibodies di-
rected at HLA class I antigens, are not a contraindication to
transplantation (1071–1073). Anti-donor antibodies detected
by the AHG-enhanced CDC crossmatch (when the same sera
was thought to be non-reactive by the NIH-CDC) have been
found to increase the incidence of accelerated and acute rejec-
tions. A negative AHG (no reactive IgG antibodies) or a positive
IgM AHG (not clinically relevant) crossmatch is acceptable for
primary renal transplantation. It was once thought that primary
recipients with a positive crossmatch from historical, high
panel reactive antibody (PRA) sera could be successfully trans-
planted. It is now believed that if the past-positive serum con-
tains IgG anti-donor antibody, the allograft is at risk to reject
due to reactivation of immune memory. However, if the past-
positive crossmatch is due to an IgM antibody, rejection is less
likely to occur (1074, 1075). Similarly, recipients with a prior
transplant can be successfully re-transplanted if negative AHG
crossmatches are obtained from testing the historically highest
PRA and the pretransplant sera (1059).
There has been disagreement as to the relevance of a posi-
tive B cell target crossmatch. A positive T cell crossmatch
was thought to be an absolute contraindication to transplan-
tation, whereas a positive B cell crossmatch may or may not
have been a contraindication (1075). More recently, a number
of retrospective studies have shown that positive B-cell cross-
matches are associated with poorer outcomes (1076–1079).
Positive B-cell crossmatches associated with poor outcomes
appear to be due to IgG antibodies.
Flow cytometry crossmatching is a more sensitive method
than AHG-CDC for detecting small quantities of alloantibod-
ies in recipient sera (1080,1081). Flow cytometry has been
used to crossmatch highly sensitized or retransplant candi-
dates (1059,1061,1081–1088). There is considerable debate
about its relevance for primary recipients (1059,1089–1091).
However, many of the studies showing the relevance of flow
cytometry crossmatching were performed using the NIH-
CDC as a screening crossmatch and then subsequently
tested by flow cytometry. No AHG-CDC tests were per-
formed. It is still uncertain whether an antibody identified only
by flow cytometry (in the absence of AHG-CDC reactivity)
should be a contraindication to transplantation. While it is
clear that anti-HLA class I antibodies are clinically relevant,
the relevance of anti-HLA class II antibodies is less clear
(1079,1081,1082).

2001; Suppl. 1: Vol. 2: 5–95 65

Kasiske et al.

Table 81: Pretransplant antibodies to HLA antigens

Rationale Patients may be exposed to HLA antigens before transplantation. It is therefore necessary to test patient sera for the
presence of antibodies to HLA antigens and use these reactive sera in the recipient-donor crossmatch to prevent
hyperacute and/or accelerated rejection.
Recommendations (A) The presence and quantity of antibodies to HLA antigens can fluctuate with time. Also, patients may display an
anamnestic (memory) immune response leading to accelerated rejection despite a negative pretransplant cross-
match with current or pretransplant sera. Therefore, it is necessary to test patient sera on a regular basis, e.g.
monthly, bimonthly, or quarterly. When performing a donor-specific crossmatch, historically reactive (immune mem-
ory), current and immediately pretransplant sera should all be used.
(A) Methods used to test for the presence of alloantibodies should be sensitive and identify clinically relevant IgG
antibodies to HLA antigens.
(B) In highly cytotoxic patients, e.g. panel reactive antibodies (PRA), ±50%, avoiding blood transfusions will help to
reduce the level of PRA. If transfusion is necessary, then leukocyte-poor blood should be used.

It has recently been reported that the crossmatch can be
omitted in selected non-sensitized recipients when antibody
specificities were precisely defined against donor HLA
(565,1092). However, omission of the crossmatch reduced
cold ischemia time by only 3–4 hours, making it questionable
whether the overall benefit would warrant any increase in
risk. Results of another study suggested that methods more
sensitive than AHG-CDC should be used to determine
whether or not anti-HLA antibodies are present in the recipi-
ent, if the final crossmatch is omitted (1093).
It is clear that using an AHG or flow cytometry crossmatching
should protect against the occurrence of a hyperacute and/
or accelerated rejection. However, these two crossmatch as-
says are membrane-dependent, and do not necessarily
identify anti-HLA reactivity. Newer assays, utilizing more sen-
sitive methods, e.g. enzyme-linked immunosorbent assay
(ELISA) and Flow Bead, and using specific HLA antigens as
targets have been introduced to identify antibodies specific
to HLA antigens (1094–1099). Knowing whether there are
antibodies specific to HLA antigens helps in correctly inter-
preting the crossmatch results.
Methods used to detect the presence of anti-HLA antibodies
include the NIH-CDC, Amos-modified NIH-CDC, AHG-CDC
and flow cytometry (Table 81) (1068,1070,1080,1081). These
assays report a percentage of PRA against HLA antigens.
Because the PRA may fluctuate, serial measurement of the
PRA status is important to identify which reactive sera (anti-
HLA reactivity) to test against specific donors in a cross-
match. The standard of practice is to use the historically
highest PRA, a current and the pretransplant sera in a donor-
specific crossmatch. Some centers limit their historical PRA
sera to 3–6 months; however, this may not adequately re-
flect immune memory of a high PRA sera from 12–18
months past, and could result in an apparently negative
crossmatch in a sensitized patient. The NIH, AMOS-modi-
fied, AHG and flow cytometry assays are membrane-de-
pendent assays, and unless antibody specificity studies are
performed, it is unclear whether the cytotoxic or antibody
binding read-out reflects anti-HLA or non-HLA reactivity
(1075).
Recently, newer assays have been introduced that use more
sensitive methods (ELISA and Flow Bead), and use specific
soluble HLA target antigens immobilized in tray wells or on
microbeads, to identify sera with IgG antibodies to HLA anti-
gens (1094–1099). Results from the ELISA-PRA have been
shown to be more predictive of a posttransplant acute rejec-
tion and graft loss than the membrane dependent AHG-PRA
assay (1094–1098). The Flow Bead PRA (Flow PRA) pro-
cedure can detect IgG antibody to HLA antigens in sera that
are reported to be non-reactive (0% PRA) by ELISA (1093). In
a recent study of CsA and prednisone treated renal allograft
recipients pretransplant HLA antibodies only detected by
Flow PRA were shown to be a significant risk factor for post-
transplant rejection (1100). These data suggest that Flow PRA
can detect the presence of clinically relevant IgG antibodies
to HLA antigens. Sera to be tested in crossmatches should
therefore first be tested for the presence of IgG antibodies to
HLA antigens. Then the crossmatch evaluation will allow for
the interpretation of whether positive crossmatch sera are di-
rected against HLA or non-HLA antigens (as discussed
above).
In the past few years the percent of transplant candidates
who have high PRA’s has fallen (1101). This is likely due to
the reduction in the use of blood transfusions. It also sug-
gests that avoiding blood transfusions may help to reduce
the number of patients who have difficulty obtaining a cada-
veric kidney because of preformed antibodies, and may the-
oretically improve outcomes. The highly sensitized recipient
whose serum demonstrates alloreactivity with a high PRA re-
mains a major clinical challenge (1083). The presence of high
titers of alloreactive antibodies may reflect prior transplant,
pregnancies and/or blood transfusions (1057,1102,1103). The
ability to transplant highly sensitized patients may be en-
hanced by avoiding blood transfusions, which has become
more feasible today with the use of human recombinant
erythropoietin (1104,1105). Over the past decade, several clin-
ical trials of procedures designed to reduce titers of alloanti-
bodies, e.g. plasmapheresis, immunoadsorption, intravenous
immunoglobulin and intensified immunosuppression, have
yielded promising, albeit preliminary results (1096,1106–
1111).

66 2001; Suppl. 1: Vol. 2: 5–95

 The Evaluation of Renal Transplant Candidates: Clinical Practice Guidelines
Acknowledgments
We thank the following reviewers for their helpful suggestions
and comments: Margaret J. Bia, MD, Daniel C. Brennan, MD,
Ginny L. Bumgardner, MD, Blanche M. Chavers, MD, David J.
Cohen, MD, Fernando G. Cosio, MD, Gabriel M. Danovitch,
MD, Connie Davis, MD, Francis L. Delmonico, MD, Richard N.
Fine, MD, M. Roy First, MD, Jay A. Fishman, MD, John J. Fung,
MD, Robert S. Gaston, MD, Thomas A. Gonwa, MD, Mitchel L.
Henry, MD, Charles A. Herzog, MD, Marshall I. Hertz, MD, Clif-
ton E. Kashtan, MD, Andrew S. Levey, MD, James A. Light,
MD, Arthur J. Matas, MD, Susan R. Mendley, MD, John F. Ney-
lan, MD, Mary Ellen Olbrisch, PhD, Todd E. Pesavento, MD,
Mark D. Pescovitz, MD, Robert H. Rubin, MD, John D.
Scandling, MD, Shirley D. Schlessinger, MD, Ronald Shapiro,
MD, David R. Snydman, MD, Lawrence A. Turka, MD, Alan H.
Wilkinson, MD, and James B. Young, MD.
References
1. Kasiske BL, Ramos EL, Gaston RS, Bia MJ, Danovitch GM, Bowen PA
et al. The evaluation of renal transplant candidates: clinical practice
guidelines. Patient Care and Education Committee of the American
Society of Transplantation Physicians. J Am Soc Nephrol 1995; 6: 1–
34.
2. Canadian Task Force on the Periodic Health Examination. Task Force
Report on the Periodic Health Examination. Can Med Assoc J 1979;
121: 1193–1254.
3. US Preventative Services Task Force. Guide to Clinical Preventative Ser-
vices: An Assessment of the Effectiveness of 169 Interventions. Balti-
more: Williams & Wilkins; 1989.
4. Holley JL, Monaghan J, Byer B, Bronsther O. An evaluation of the
renal transplant evaluation process focusing on cost and the reasons
for patient exclusion. Am J Kidney Dis 1998; 32: 567–574.
5. Migliori RJ, Simmons RL, Payne WD, Ascher NL, Sutherland DE, Naj-
arian JS et al. Renal transplantation done safely without prior chronic
dialysis therapy. Transplantation 1987; 43: 51–55.
6. Katz SM, Kerman RH, Golden D, Grevel J, Camel S, Lewis RM et al.
Preemptive transplantation–an analysis of benefits and hazards in 85
cases. Transplantation 1991; 51: 351–355.
7. Ekstrand A. Kidney transplantation with and without prior dialysis ther-
apy in diabetic patients with end-stage renal failure. Scand J Urol
Nephrol 1993; 27: 83–87.
8. Roake JA, Cahill AP, Gray CM, Gray DW, Morris PJ. Preemptive cada-
veric renal transplantation –clinical outcome. Transplantation 1996;
62: 1411–1416.
9. Asderakis A, Augustine T, Dyer P, Short C, Campbell B, Parrott NR et
al. Pre-emptive kidney transplantation: the attractive alternative.
Nephrol Dial Transplant 1998; 13: 1799–1803.
10. Hakim NS, Benedetti E, Payne WD, Gruessner R, Gores P, Sutherland
DE et al. Pre-emptive renal transplantation. Int Surg 1998; 83: 330–
332.
11. Flom LS, Reisman EM, Donovan JM, Zaontz MR, Stein J, Firlit CF
et al. Favorable experience with pre-emptive renal transplantation in
children. Pediatr Nephrol 1992; 6: 258–261.
12. Offner G, Hoyer PF, Meyer B, Pichlmayr R, Brodehl J. Pre-emptive
renal transplantation in children and adolescents. Transplant Int 1993;
6: 125–128.
13. Fine RN, Tejani A, Sullivan EK. Pre-emptive renal transplantation in
children: report of the North American Pediatric Renal Transplant Co-
operative Study NAPRTCS. Clin Transplant 1994; 8: 474–478.
2001; Suppl. 1: Vol. 2: 5–95
14. Vats AN, Donaldson L, Fine RN, Chavers BM. Pretransplant dialysis
status and outcome of renal transplantation in North American
children: a NAPRTCS study. Transplantation 2001; 69: 1414–1419.
15. United Network for Organ Sharing 1999 Scientific Registry and Organ
Procurment Transplantation Network Annual Report. www.unos.org/
data/anrpt99/ar99–table59–05–ki htm. 1999.
16. Cecka JM. The UNOS scientific renal transplant registry. In: Cecka
JM, Terasaki PI, eds. Clinical transplants 1998. Los Angeles: UCLA
Tissue Typing Laboratory; 1999. p. 1–16.
17. Kaufman DB. Transplantation of kidneys from zero haplotype-matched
living donors and from distantly related and unrelated donors in the
cyclosporine era. Transplant Proc 1993; 25: 1530–1531.
18. Sesso R. Kidney Transplantation from living unrelated donors. Ann In-
tern Med 1992; 117: 983–989.
19. Humar A, Durand B, Gillingham K, Payne WD, Sutherland DE, Matas
AJ. Living unrelated donors in kidney transplants: better long-term
results than with non-HLA-identical living related donors? Transplan-
tation 2000; 69: 1942–1945.
20. Terasaki PI, Cecka JM, Gjertson DW, Takemoto S. High survival rates
of kidney transplants from spousal and living unrelated donors. N Engl
J Med 1995; 333: 333–336.
21. D’Alessandro AM, Pirsch JD, Knechtle SJ, Odorico JS, van der Werf
WJ, Collins BH et al. Living unrelated renal donation: the University of
Wisconsin experience. Surgery 1998; 124: 604–610.
22. Flowers JL, Jacobs S, Cho E, Morton A, Rosenberger WF, Evans D et
al. Comparison of open and laparoscopic live donor nephrectomy. Ann
Surg 1997; 226: 483–489.
23. Ratner LE, Hiller J, Sroka M, Weber R, Sikorsky I, Montgomery RA et
al. Laparoscopic live donor nephrectomy removes disincentives to live
donation. Transplant Proc 1997; 29: 3402–3403.
24. Kuo PC, Johnson LB, Sitzmann JVS. Laparoscopic donor nephrectomy
with a 23-hour stay: a new standard for transplantation surgery. Ann
Surg 2000; 231: 772–779.
25. Kuo PC, Johnson LB. Laparoscopic donor nephrectomy increases the
supply of living donor kidneys: a center-specific microeconomic
analysis. Transplantation 2000; 69: 2211–2213.
26. Wolf JS, Jr, Marcovich R, Merion JW, Konnak RM. Prospective, case
matched comparison of hand assisted laparoscopic and open surgical
live donor nephrectomy. J Urol 2000; 163: 1650–1653.
27. Jacobbi LM, McBride VA, Etheredge EE, McDonald JC, Cooper ES,
Frey D et al. The risks, benefits, and costs of expanding donor criteria.
A collaborative prospective three-year study. Transplantation 1995;
60: 1491–1496.
28. First MR. Expanding the donor pool. Semin Nephrol 1997; 17: 373–
380.
29. Cho YW, Terasaki PI, Cecka JM, Gjertson DW. Transplantation of kid-
neys from donors whose hearts have stopped beating. N Engl J Med
1998; 338: 221–225.
30. Burrows L, Knight R, Polokoff E, Schanzer H, Panico M, Solomon M.
Expanding the donor pool with the use of en bloc pediatric kidneys
in adult recipients. Transplant Proc 1996; 28: 173–174.
31. Nahas WC, Lucon AM, Mazzucchi E, Scafuri AG, Neto ED, Ianhez LE
et al. Kidney transplantation: the use of living donors with renal artery
lesions. J Urol 1998; 160: 1244–1247.
32. Johnson LB, Kuo PC, Dafoe DC, Drachenberg CB, Schweitzer EJ, Alf-
rey EJ et al. The use of bilateral adult renal allografts – a method to
optimize function from donor kidneys with suboptimal nephron mass.
Transplantation 1996; 61: 1261–1263.
33. Johnson LB, Kuo PC, Schweitzer EJ, Ratner LE, Klassen DK, Hoehn-
Saric EW et al. Double renal allografts successfully increase utilization
of kidneys from older donors within a single organ procurement or-
ganization. Transplantation 1996; 62: 1581–83.
34. Alfrey EJ, Lee CM, Scandling JD, Pavlakis M, Markezich AJ, Dafoe
DC. When should expanded criteria donor kidneys be used for single
67
Kasiske et al.
versus dual kidney transplants? Transplantation 1997; 64: 1142–
1146.
35. Remuzzi G, Grinyo J, Ruggenenti P, Beatini M, Cole EH, Milford EL et
al. Early experience with dual kidney transplantation in adults using
expanded donor criteria. Double Kidney Transplant Group DKG. J Am
Soc Nephrol 1999; 10: 2591–2598.
36. Lee CM, Carter JT, Weinstein RJ, Pease HM, Scandling JD, Pavalakis
M et al. Dual kidney transplantation: older donors for older recipients.
J Am Coll Surg 1999; 189: 82–91.
37. Lu AD, Carter JT, Weinstein RJ, Stratta RJ, Taylor RJ, Bowers VD et
al. Outcome in recipients of dual kidney transplants: an analysis of the
dual registry patients. Transplantation 2000; 69: 281–285.
38. Jerius JT, Taylor RJ, Murillo D, Leone JP. Double renal transplants from
marginal donors: 2-year results. J Urol 2000; 163: 423–425.
39. Dietl KH WH. Cadaveric ‘‘two-in-one’’ kidney transplantation from
marginal donors: experience of 26 cases after 3 years. Transplantation
2000; 70: 790–794.
40. Hobart MG, Modlin CS, Kapoor A, Boparai N, Mastroianni B, Papajcik
D et al. Transplantation of pediatric en bloc cadaver kidneys into adult
recipients. Transplantation 1998; 66: 1689–1694.
41. Kauffman HM, Bennett LE, McBride MA, Ellison MD. The expanded
donor. Transplant Revs 1997; 11: 165–190.
42. Mandal AK, Kalligonis AN, Ratner LE. Expanded criteria donors:
attempts to increase the renal transplant donor pool. Adv Ren Replace
Ther 2000; 7: 117–130.
43. U.S. Renal Data System. Causes of death. USRDS 1999 Annual Data
Report. Bethesda, MD: National Institutes of Health, National Institute
of Diabetes, Digestive and Kidney Diseases; 1999. p. 89–100.
44. Maisonneuve P, Agodoa L, Gellert R, Stewart J, Buccianti G, Lowenfels
AB et al. Cancer in patients on dialysis for end-stage renal disease:
an international collaborative study. Lancet 1999; 354: 93–99.
45. Chertow G, Paltiel A, Owen Jr W, Lazarus JM. Cost-effectiveness of
cancer screening in end-stage renal disease. Arch Intern Med 1996;
156: 1345–1350.
46. LeBrun CJ, Diehl LF, Abbott KC, Welch PG, Yuan CM. Life expectancy
benefits of cancer screening in the end-stage renal disease popula-
tion. Am J Kidney Dis 2000; 35: 237–243.
47. Penn I. Evaluation of transplant candidates with pre-existing malig-
nancies. Ann Transplant 1997; 2: 14–17.
48. Sheil AGR. Patterns of malignancies following renal transplantation.
Transplant Proc 1999; 31: 1263–1265.
49. Lornoy W, Becaus S, de Vleeschouwer M, Morelle V, Fonteyne E,
Thienpoint L et al. Renal cell carcinoma, a new complication of
analgesic nephropathy. Lancet 1986; i: 1271–1272.
50. Cuckovic C, Djukanovic L, Jankovic S, Stanojcic A, Dragicevic P, Rad-
milovic A et al. Malignant tumors in hemodialysis patients. Nephron
1996; 73: 710–712.
51. Cosyns J-P, Jadoul M, Squifflet J, Wese F, van Ypersele de Strihou C.
Urothelial lesions in Chinese-herb nephropathy. Am J Kidney Dis
1999; 33: 1011–1017.
52. Heinz-Peer G, Schoder M, Rand T, Mayer G, Mostbeck G. Prevalence
of acquired cystic kidney disease and tumors in native kidneys of renal
transplant recipients: a prospective US study. Radiology 1995; 195:
667–671.
53. Gulanikar A, Daily PP, Kilambi N, Hamrick-Turner J, Butkus DE. Pros-
pective pretransplant ultrasound screening in 206 patients for ac-
quired renal cysts and renal cell carcinoma. Transplantation 1998; 66:
1669–1672.
54. Lien Y-HH, Hunt KR, Siskind MS, Zukoski C. Association of cyclosporin
A with acquired cystic kidney disease of the native kidneys in renal
transplant recipients. Kidney Int 1993; 44: 613–616.
55. Penn I. Primary kidney tumors before and after renal transplantation.
Transplantation 1995; 59: 480–485.
56. Doublet JD, Peraldi MN, Gattegno B, Thibault P, Sraer JD. Renal cell
68
carcinoma of native kidneys: prospective study of 129 renal transplant
patients. J Urol 1997; 158: 42–44.
57. Ishikawa I, Saito Y, Shikura N, Kitada H, Shinoda A, Suzuki S. Ten-year
prospective study on the development of renal cell carcinoma in dialy-
sis patients. Am J Kidney Dis 1990; 16: 452–458.
58. Pais E, Pirson Y, Squifflet J-P, Ninane J, Cornu G, Alexandre GPJ et al.
Kidney transplantation in patients with Wilm’s tumor. Transplantation
1992; 53: 782–785.
59. Hamida MB, Bedrossian J, Pruna A, Fouqueray B, Metivier F, Idatte
JM. Wilm’s tumor and renal transplantation: a case report and litera-
ture review. Transplant Proc 1993; 25: 2346–2347.
60. Penn I. The effect of immunosuppression on pre-existing cancers.
Transplantation 1993; 55: 742–747.
61. Schumacher V, Scharer K, Wuhl E, Altrogge H, Bonzel KE, Guschmann
M et al. Spectrum of early onset nephrotic syndrome associated with
WT1 missense mutations. Kidney Int 1998; 53: 1594–1600.
62. Jeanpierre C, Denamur E, Henry I, Cabanis MO, Luce S, Cecille A et
al. Identification of constitutional WT1 mutations, in patients with iso-
lated diffuse mesangial sclerosis, and analysis of genotype/phenotype
correlations by use of a computerized mutation database. Am J Hum
Genet 1998; 62: 824–833.
63. The United States Renal Data System. Atlas of End-Stage Renal Dis-
ease in the United States 2000. Washington, D.C.: The National Insti-
tutes of Health; 2000.
64. Kohler B, Schumacher V, Schulte-Overberg U, Biewald W, Lennert T,
l’Allemand D et al. Bilateral Wilms tumor in a boy with severe hy-
pospadias and cryptochidism due to a heterozygous mutation in the
WT1 gene. Pediatr Res 1999; 45: 187–190.
65. Barbosa AS, Hadjiathanasiou CG, Theodoridis C, Papathanasiou A, Tar
A, Merksz M et al. The same mutation affecting the splicing of WT1
gene is present on Frasier syndrome patients with or without Wilms’
tumor. Hum Mutat 1999; 13: 146–153.
66. Bjorge T. Prospective seroepidemiological study of role of human pap-
illomavirus in non-cervical anogenital cancers. Br Med J 1997; 315:
646–649.
67. Xi LF, Critchlow CW, Wheeler CM, Koutsky LA, Galloway DA, Kuypers
J et al. Risk of anal carcinoma in situ in relation to human papillomavi-
rus type 16 variants. Cancer Res 1998; 58: 3839–3844.
68. Strickler HD, Schiffman MH, Shah KV, Schiller JT, Wacholder S, Clay-
man B et al. A survey of human papillomavirus 16 antibodies in pa-
tients with epithelial cancers. Eur J Cancer Prev 1998; 7: 305–313.
69. Caruso ML, Valentini AM. Different human papillomavirus genotypes
in ano-genital lesions. Anticancer Res 1999; 19: 3049–53.
70. Euvrard S, Kanitakis J, Chardonnet Y, Noble C, Touraine JL, Faure M
et al. External anogenital lesions in organ transplant recipients. Arch
Dermatol 1997; 133: 175–178.
71. Birkeland SA, Storm HH, Lamm L, Barlow L, Blohme I, Forsberg B et
al. Cancer risk after renal transplantation in the Nordic countries,
1964–1986. Int J Cancer 1995; 60: 183–189.
72. Ylitalo N, Josefsson A, Melbye M, Sorensen P, Frisch M, Andersen PK
et al. A prospective study showing long-term infection with human
papillomavirus 16 before the development of cervical carcinoma in
situ. Cancer Res 2000; 60: 6027–6032.
73. Ylitalo N, Sorensen P, Josefsson AM, Magnusson PK, Andersen PK,
Ponten J et al. Consistent high viral load of human papillomavirus 16
and risk of cervical carcinoma in situ: a nested case-control study.
Lancet 2000; 355: 2194–2198.
74. Josefsson AM, Magnusson PK, Ylitalo N, Sorensen P, Qwarforth-Tub-
bin P, Andersen PK et al. Viral load of human papilloma virus 16 as a
determinant for development of cervical carcinoma in situ: a nested
case-control study. Lancet 2000; 355: 2189–2193.
75. US Preventative Services Task Force. Screening for cervical cancer. In:
Di Giuseppi C, Atkins D, Woolf S, eds. Guide to clinical preventive
services, 2nd edn. Baltimore: Williams & Wilkins; 1996. p. 105–117.
2001; Suppl. 1: Vol. 2: 5–95
 The Evaluation of Renal Transplant Candidates: Clinical Practice Guidelines
76. Sox HC, Jr. Preventive health services in adults. N Engl J Med 1994;
330: 1589–1595.
77. ACOG Committee. Recommendations on frequency of Pap test
screening 152. The American College of Obstetricians and Gynecolog-
ists; 1995.
78. US Preventative Services Task Force. Screening for testicular cancer.
In: Di Giuseppi C, Atkins D, Woolf S, eds. Guide to clinical preventive
services, 2nd edn. Baltimore: Williams & Wilkins; 1996. p. 153–157.
79. Buccianti G, Maisonneuve P, Ravasi B, Cresseri D, Locatelli F, Boyle P.
Cancer among patients on renal replacement therapy: a population-
based survey in Lombardy, Italy. Int J Cancer 1996; 66: 591–593.
80. Brunner FP, Landais P, Selwood N. Malignancies after renal transplan-
tation: the EDTA-ERA registry experience. Nephrol Dial Transplant
1995; 10: 74–80.
81. Farge D. Kaposi’s sarcoma in organ transplant recipients. The Colla-
borative Transplantation Research Group of Ile de France. Eur J Med
1993; 2: 339–343.
82. Penn I. Sarcomas in organ allograft recipients. Transplantation 1995;
60: 1485–1491.
83. Penn I. Posttransplant malignancies. Transplant Proc 1999; 31: 1260–
1262.
84. Penn I. Kaposi’s sarcoma in transplant recipients. Transplantation
1997; 64: 669–673.
85. Doutrelepont J-M, de Pauw L, Gruber S, Dunn D, Qunibi W, Kinnaert
P et al. Renal transplantation exposes patients with previous Kaposi’s
sarcoma to a high risk of recurrence. Transplantation 1996; 62: 463–
466.
86. Lebbe C, Agbalika F, de Cremoux P, Deplanche M, Rybojad M, Mas-
grau E et al. Detection of human herpesvirus 8 and human T-cell
lymphotropic virus type 1 sequences in Kaposi sarcoma. Arch Derma-
tol 1997; 133: 25–30.
87. Angeloni A, Heston L, Uccini S, Sirianni MC, Cottoni F, Masala MV et
al. High prevalence of antibodies to human herpesvirus 8 in relatives
of patients with classic Kaposi’s sarcoma from Sardinia. J Infect Dis
1998; 177: 1715–1718.
88. Melbye M, Cook PM, Hjalgrim H, Begtrup K, Simpson GR, Biggar RJ
et al. Risk factors for Kaposi’s-sarcoma-associated herpesvirus KSHV/
HHV-8. seropositivity in a cohort of homosexual men, 1981–1996. Int
J Cancer 1998; 77: 543–548.
89. Moosa MR, Treurnicht FK, van Rensburg EJ, Schneider JW, Jordaan
HF, Engelbrecht S. Detection and subtyping of human herpesvirus-8
in renal transplant patients before and after remission of Kaposi’s sar-
coma. Transplantation 1998; 66: 214–218.
90. Kempf W, Perniciaro C, Adams V, Mueller B, Burg G. Human herpesvi-
rus 8 HHV-8. in familial Kaposi’s sarcoma. Exp Dermatol 1999; 8: 68–
70.
91. Sitas F, Carrara H, Beral V, Newton R, Reeves G, Bull D et al. Anti-
bodies against human herpesvirus 8 in black South African patients
with cancer. N Engl J Med 1999; 340: 1863–1871.
92. Farge D, Lebbe C, Marjanovic Z, Tuppin P, Mouquet C, Peraldi MN et
al. Human herpes virus-8 and other risk factors for Kaposi’s sarcoma
in kidney transplant recipients. Groupe Cooperatif de Transplantation
d’ Ile de France GCIF. Transplantation 1999; 67: 1236–1242.
93. Frances C, Mouquet C, Marcelin AG, Barete S, Agher R, Charron D
et al. Outcome of kidney transplant recipients with previous human
herpesvirus-8 infection. Transplantation 2000; 69: 1776–1779.
94. Stewart T, Tsai S-C, Grayson H, Henderson R, Opelz G. Incidence of
de-novo breast cancer in women chronically immunosuppressed after
organ transplantation. Lancet 1995; 346: 796–798.
95. US Preventative Services Task Force. Screening for breast cancer. In:
Di Giuseppi C, Atkins D, Woolf S, eds. Guide to clinical preventive
services, 2nd edn. Baltimore: Williams & Wilkins; 1996. p. 73–87.
96. Leitch A, Dodd G, Costanza M, Linver M, Pressman P, McGinnis L et
al. American Cancer Society guidelines for the early detection of
breast cancer: Update 1997. CA: Cancer J Clin 1997; 47: 150–153.
2001; Suppl. 1: Vol. 2: 5–95
97. Chlebowski RT, Collyar DE, Somerfield MR, Pfister DG. American
Society of Clinical Oncology technology assessment on breast can-
cer risk reduction strategies: tamoxifen and raloxifene. J Clin Oncol
1999; 17: 1939–1955.
98. Gail MH, Costantino JP, Bryant J, Croyle R, Freedman L, Helzlsouer
K et al. Weighing the risks and benefits of tamoxifen treatment for
preventing breast cancer. J Natl Cancer Inst 1999; 91: 1829–1846.
99. Suggested technique for fecal occult blood testing and interpretation
in colorectal cancer screening. American College of Physicians. Ann
Intern Med 1997; 126: 808–810.
100. Byers T, Levin B, Rothenberger D, Dodd G, Smith R. American Can-
cer Society guidelines for screening and surveillance for early detec-
tion of colorectal polyps and cancer: update 1997. Cancer J Clin
1997; 47: 154–160.
101. Ransohoff DF, Lang CA. Screening for colorectal cancer with the
fecal occult blood test: a background paper. American College of
Physicians. Ann Intern Med 1997; 126: 811–822.
102. Winawer SJ, Fletcher R, Miller L, Godlee F, Stolar MH, Mulrow C
et al. Colorectal cancer screening: clinical guidelines and rationale.
Gastroenterology 1997; 112: 594–642.
103. Rex DK, Johnson DA, Lieberman DA, Burt RW, Sonnenberg A. Col-
orectal cancer prevention 2000: screening recommendations of the
American College of Gastroenterology. American College of Gastro-
enterology. Am J Gastroenterol 2000; 95: 868–877.
104. Sonnenberg A, Delco F, Inadomi JM. Cost-Effectiveness of Colonos-
copy in Screening for Colorectal Cancer. Ann Intern Med 2000; 133:
573–584.
105. Mandel JS, Church TR, Bond JH, Ederer F, Geisser MS, Mongin SJ
et al. The effect of fecal occult-blood screening on the incidence of
colorectal cancer. N Engl J Med 2000; 343: 1603–1607.
106. Patz EF, Goodman PC, Bepler G. Screening for Lung Cancer. N Engl
J Med 2000; 343: 1627–1633.
107. Woolfe SH. The best screening test for colorectal cancer – a per-
sonal choice. N Engl J Med 2000; 343: 1641–1643.
108. US Preventative Services Task Force. Screening for prostate cancer.
In: Di Giuseppi C, Atkins D, Woolf S, eds. Guide to clinical preventive
services, 2nd edn. Baltimore: Williams & Wilkins; 1996. p. 119–134.
109. Konety B, Tewari A, Howard R, Barry J, Hodge E, Taylor R et al.
Prostate cancer in the post-transplant population. Urology 1998; 52:
428–432.
110. Coley CM, Barry MJ, Fleming C, Mulley AG. Early detection of pros-
tate cancer. Part I: Prior probability and effectiveness of tests. The
American College of Physicians. Ann Intern Med 1997; 126: 394–
406.
111. Coley CM, Barry MJ, Fleming C, Fahs MC, Mulley AG. Early detection
of prostate cancer. Part II: Estimating the risks, benefits, and costs.
American College of Physicians. Ann Intern Med 1997; 126: 468–
479.
112. von Eschenbach A, Ho R, Murphy G, Cunningham M, Lins N. Ameri-
can Cancer Society guideline for the early detection of prostate can-
cer: update 1997. Cancer J Clin 1997; 47: 261–264.
113. Djavan B, Shariat S, Ghawidel K, Guven-Marberger K, Remzi M, Kov-
arik J et al. Impact of chronic dialysis on serum PSA, free PSA, and
free/total PSA ratio: is prostate cancer detection compromised in
patients receiving long-term dialysis? Urology 1999; 53: 1169–1174.
114. Pereira BJG, Levey AS. Hepatitis C virus infection in dialysis and renal
transplantation. Kidney Int 1997; 51: 981–999.
115. Hiesse C, Cantarovich M, Charpentier B, Francais P, Benoit G, Fries
D. Need for hepatocellular carcinoma screening before renal trans-
plantation in HBs π, HBe π, western African. Clin Nephrol 1985;
24: 209–211.
116. Penn I. Hepatic transplantation for primary and metastatic cancers
of the liver. Surgery 1991; 110: 726–34.
117. Ranjan D, Johnston T. Liver transplantation for hepatocellular carci-
noma. Hepato-Gastroenterology 1998; 45: 1369–1374.
69
Kasiske et al.
118. Rostaing L, Modesto A, Abbal M, Durand D. Long-term follow-up of
monoclonal gammopathy of undetermined significance in transplant
patients. Am J Nephrol 1994; 14: 187–191.
119. de Lima JJ, Kourilsky O, Meyrier A, Morel-Maroger L, Sraer JD. Kid-
ney transplant in multiple myeloma. Early recurrence in the graft with
sustained normal renal function. Transplantation 1981; 31: 223–224.
120. Bumgardner GL, Matas AJ, Payne WD, Dunn DL, Sutherland DER,
Najarian JS. Renal transplantation in patients with paraproteinemias.
Clin Sci 1990; 4: 399–405.
121. Dagher F, Sammett D, Tomasula J, Delaney, Butt K. Renal transplan-
tation in multiple myeloma. Case report and review of the literature.
Transplantation 1996; 62: 1577–1580.
122. Spitzer TR, Delmonico F, Tolkoff-Rubin N, McAfee S, Sackstein R,
Saidman S et al. Combined histocompatibility leukocyte antigen-
matched donor bone marrow and renal transplantation for multiple
myeloma with end stage renal disease: the induction of allograft
tolerance through mixed lymphohematopoietic chimerism. Trans-
plantation 1999; 68: 480–484.
123. Opelz G, Henderson R. Incidence of non-Hodgkin lymphoma in kid-
ney and heart transplant recipients. Lancet 1993; 342: 1514–1516.
124. Nelson BP, Nalesnik MA, Bahler DW, Locker J, Fung JJ, Swerdlow
SH. Epstein-Barr virus-negative post-transplant lymphoproliferative
disorders: a distinct entity? Am J Surg Pathol 2000; 24: 375–385.
125. Birkeland SA, Andersen HK, Hamilton-Dutoit SJ. Preventing acute
rejection, Epstein-Barr virus infection, and posttransplant lympho-
proliferative disorders after kidney transplantation: use of aciclovir
and mycophenolate mofetil in a steroid-free immunosuppressive
protocol. Transplantation 1999; 67: 1209–1214.
126. Darenkov IA, Marcarelli MA, Basadonna GP, Friedman AL, Lorber
KM, Howe JG et al. Reduced incidence of Epstein-Barr virus-associ-
ated posttransplant lymphoproliferative disorder using preemptive
antiviral therapy. Transplantation 1997; 64: 848–852.
127. Torre D, Tambini R. Acyclovir for treatment of infectious mononu-
cleosis: a meta-analysis. Scand J Infect Dis 1999; 31: 543–547.
128. Kaden J, Petersen S, Kaden K, May G. Epstein-Barr virus infection
after kidney transplantation. Transplant Int 1998; 11 Suppl 1: S119-
S124.
129. Schwab M, Boswald M, Korn K, Ruder H. Epstein-Barr virus in pedi-
atric patients after renal transplantation. Clin Nephrol 2000; 53:
132–139.
130. Ellis D, Jaffe R, Green M, Janosky JJ, Lombardozzi-Lane S, Shapiro
R et al. Epstein-Barr virus-related disorders in children undergoing
renal transplantation with tacrolimus-based immunosuppression.
Transplantation 1999; 68: 997–1003.
131. Gu SY, Huang TM, Ruan L, Miao YH, Lu H, Chu CM et al. First EBV
vaccine trial in humans using recombinant vaccinia virus expressing
the major membrane antigen. Dev Biol Stand 1995; 84: 171–177.
132. Moss DJ, Suhrbier A, Elliott SL. Candidate vaccines for Epstein-Barr
virus. Br Med J 1998; 317: 423–424.
133. Jackman WT, Mann KA, Hoffmann HJ, Spaete RR. Expression of
Epstein-Barr virus gp350 as a single chain glycoprotein for an EBV
subunit vaccine. Vaccine 1999; 17: 660–668.
134. Hickey DP, Nalesnik MA, Vivas CA, Lopatin WB, Jordan ML, Starzl
TE et al. Renal transplantation in patients who lost their allografts
during management of previous posttransplant lymphoproliferative
disease. Clin Sci 1990; 4: 187–190.
135. Sayegh M, Fine N, Smith J, Rennke H, Milford E, Tilney NL. Immuno-
logic tolerance to renal allografts after bone marrow transplants from
the same donors. Ann Intern Med 1991; 114: 954–955.
136. Helg C, Chapius B, Bolle J-F, Morel P, Salomon D, Roux E et al. Renal
transplantation without immunosuppression in a host with tolerance
induced by allogeneic bone marrow transplantation. Transplantation
1994; 58: 1420–1422.
137. Penn I. Malignant melanoma in organ allograft recipients. Transplan-
tation 1996; 61: 274–278.
70
138. Forslund O. Mucosal human papillomavirus types in squamous cell
carcinomas of the uterine cervix and subsequently on fingers. Br J
Dermatol 2000; 142: 1148–1153.
139. Harwood CA, Surentheran T, McGregor JM, Spink PJ, Leigh IM,
Breuer J et al. Human papillomavirus infection and non-melanoma
skin cancer in immunosuppressed and immunocompetent individ-
uals. J Med Virol 2000; 61: 289–297.
140. US Preventative Services Task Force. Screening for lung cancer. In:
Di Giuseppi C, Atkins D, Woolf S, eds. Guide to clinical preventive
services, 2nd edn. Baltimore: Williams & Wilkins; 1996. p. 135–139.
141. Danpanich E, Kasiske BL. Risk factors for cancer in renal transplant
recipients. Transplantation 1999; 68: 1859–1864.
142. Johnson PC, Norris SJ, Miller GP, Scott LD, Sell S, Kahan BD et al.
Early syphilitic hepatitis after renal transplantation. J Infect Dis 1988;
158: 236–238.
143. Morgan JS, Schaffner W, Stone WJ. Opportunistic strongyloidiasis
in renal transplant recipients. Transplantation 1986; 42: 518–524.
144. Stone WJ, Schaffner W. Strongyloides infections in transplant recipi-
ents. Semin Respir Infect 1990; 5: 58–64.
145. DeVault GA, Jr, King JW, Rohr MS, Landreneau MD, Brown ST, III,
McDonald JC. Opportunistic infections with Strongyloides ster-
coralis in renal transplantation. Rev Infect Dis 1990; 12: 653–671.
146. Renoult E, Georges E, Biava MF, Hulin C, Frimat L, Hestin D et al.
Toxoplasmosis in kidney transplant recipients: report of six cases and
review. Clin Infect Dis 1997; 24: 625–34.
147. Burkhart CG. Persistent cutaneous herpes simplex infection. Int J
Dermatol 1981; 20: 552–54.
148. Schneider V, Behm FG, Mumaw VR. Ascending herpetic endo-
metritis. Obstet Gynecol 1982; 59: 259–262.
149. Gomez E, Melon S, de Ona M, Alvarez R, Laures A, Alvarez-Grande
J. Disseminated herpes simplex virus infection in a renal transplant
patient as possible cause of repeated urinary extravasations. Neph-
ron 1999; 82: 59–64.
150. Boubenider S, Hiesse C, Marchand S, Hafi A, Kriaa F, Charpentier B.
Post-transplantation polyomavirus infections. J Nephrol 1999; 12:
24–29.
151. Drachenberg CB, Beskow CO, Cangro CB, Bourquin PM, Simsir A,
Fink J et al. Human polyoma virus in renal allograft biopsies:
morphological findings and correlation with urine cytology. Hum
Pathol 1999; 30: 970–977.
152. Nickeleit V, Hirsch HH, Binet IF, Gudat F, Prince O, Dalquen P et al.
Polyomavirus infection of renal allograft recipients: from latent infec-
tion to manifest disease. J Am Soc Nephrol 1999; 10: 1080–1089.
153. Randhawa PS, Finkelstein S, Scantlebury V, Shapiro R, Vivas C, Jord-
an M et al. Human polyoma virus-associated interstitial nephritis in
the allograft kidney. Transplantation 1999; 67: 103–109.
154. Nickeleit V, Hirsch HH, Zeiler M, Gudat F, Prince O, Thiel G et al. BK-
virus nephropathy in renal transplants – tubular necrosis, MHC-class
II expression and rejection in a puzzling game. Nephrol Dial Trans-
plant 2000; 15: 324–332.
155. Nickeleit V, Klimkait T, Binet IF, Dalquen P, del Zenero V, Thiel G et
al. Testing for polyomavirus type BK DNA in plasma to identify renal-
allograft recipients with viral nephropathy. N Engl J Med 2000; 342:
1309–1315.
156. Marcus R, Favero MS, Banerjee S, Solomon SL, Bell DM, Jarvis WR
et al. Prevalence and incidence of human immunodeficiency virus
among patients undergoing long-term hemodialysis. The Coopera-
tive Dialysis Study Group. Am J Med 1991; 90: 614–619.
157. Lago M, Perez-Garcia R, Garcia d, V, Anaya F, Valderrabano F. Human
immunodeficiency virus infection in patients on maintenance dialy-
sis. Nephron 1996; 72: 727.
158. Spital A. Should all human immunodeficiency virus-infected patients
with end- stage renal disease be excluded from transplantation? The
views of U.S. transplant centers. Transplantation 1998; 65: 1187–
1191.
2001; Suppl. 1: Vol. 2: 5–95
 The Evaluation of Renal Transplant Candidates: Clinical Practice Guidelines
159. Ethical considerations in the allocation of organs and other scarce
medical resources among patients. Council on Ethical and Judicial
Affairs, American Medical Association. Arch Intern Med 1995; 155:
29–40.
160. Oliveira DB, Winearls CG, Cohen J, Ind PW, Williams G. Severe im-
munosuppression in a renal transplant recipient with HTLV-III anti-
bodies. Transplantation 1986; 41: 260–262.
161. Rubin RH, Jenkins RL, Shaw BW, Jr, Shaffer D, Pearl RH, Erb S et
al. The acquired immunodeficiency syndrome and transplantation.
Transplantation 1987; 44: 1–4.
162. Feduska NJ, Perkins HA, Melzer J, Amend WJ, Vincenti F, Tomlanov-
ich S et al. Observations relating to the incidence of the acquired
immune deficiency syndrome and other possibly associated con-
ditions in a large population of renal transplant recipients. Transplant
Proc 1987; 19: 2161–2166.
163. Shaffer D, Hammer SM, Monaco AP. Infectious complications with
the use of cyclosporine versus azathioprine after cadaveric kidney
transplantation. Am J Surg 1987; 153: 381–386.
164. Hogg RS, Heath KV, Yip B, Craib KJ, O’Shaughnessy MV, Schechter
MT et al. Improved survival among HIV-infected individuals following
initiation of antiretroviral therapy. JAMA 1998; 279: 450–454.
165. Glassock RJ, Cohen AH, Danovitch G, Parsa KP. Human immuno-
deficiency virus infection and the kidney. Ann Intern Med 1990; 112:
35–49.
166. Schoenfeld P, Feduska NJ. Acquired immunodeficiency syndrome
and renal disease: report of the National Kidney Foundation-National
Institutes of Health Task Force on AIDS and Kidney Disease. Am J
Kidney Dis 1990; 16: 14–25.
167. Tzakis AG, Cooper MH, Dummer JS, Ragni M, Ward JW, Starzl TE.
transplantation in HIVπ patients. Transplantation 1990; 49: 354–
358.
168. Ahuja TS, Zingman B, Glicklich D. Long-term survival in an HIV-in-
fected renal transplant recipient. Am J Nephrol 1997; 17: 480–482.
169. Purgus R, Tamalet C, Poignard P, Spire B, George F, Robert A et al.
Long-term nonprogressive human immunodeficiency virus-1 infec-
tion in a kidney allograft recipient. Transplantation 1998; 66: 1384–
1386.
170. Woeltje KF, Mathew A, Rothstein M, Seiler S, Fraser VJ. Tuberculosis
infection and anergy in hemodialysis patients. Am J Kidney Dis
1998; 31: 848–852.
171. Lloveras J, Peterson PK, Simmons RL, Najarian JS. Mycobacterial
infections in renal transplant recipients. Seven cases and a review of
the literature. Arch Intern Med 1982; 142: 888–892.
172. Higgins RM, Cahn AP, Porter D, Richardson AJ, Mitchell RG, Hopkin
JM et al. Mycobacterial infections after renal transplantation. Q J
Med 1991; 78: 145–153.
173. Sakhuja V, Jha V, Varma PP, Joshi K, Chugh KS. The high incidence
of tuberculosis among renal transplant recipients in India. Transplan-
tation 1996; 61: 211–215.
174. Yildiz A, Sever MS, Turkmen A, Ecder T, Besisik F, Tabak L et al.
Tuberculosis after renal transplantation: experience of one Turkish
centre. Nephrol Dial Transplant 1998; 13: 1872–1875.
175. Apaydin S, Altiparmak MR, Serdengecti K, Ataman R, Ozturk R, Erek
E. Mycobacterium tuberculosis infections after renal transplantation.
Scand J Infect Dis 2000; 32: 501–505.
176. Biz E, Pereira CA, Moura LA, Sesso R, Vaz ML, Silva Filho AP et al.
The use of cyclosporine modifies the clinical and histopathological
presentation of tuberculosis after renal transplantation. Rev Inst Med
Trop Sao Paulo 2000; 42: 225–230.
177. Qunibi WY, al-Sibai MB, Taher S, Harder EJ, de Vol E, al-Furayh O
et al. Mycobacterial infection after renal transplantation–report of 14
cases and review of the literature. Q J Med 1990; 77: 1039–1060.
178. Koselj M, Buturovic J, Malovrh M. Tuberculosis in renal allograft re-
cipients. Transplant Proc 1992; 24: 1909–1910.
2001; Suppl. 1: Vol. 2: 5–95
179. Waiser J, Schotschel R, Budde K, Neumayer HH. Reactivation of
tuberculosis after conversion from azathioprine to mycophenolate
mofetil 16 years after renal transplantation. Am J Kidney Dis 2000;
35: E12.
180. Rubin RH. Infectious disease complications of renal transplantation.
Kidney Int 1993; 44: 221–236.
181. Ramos EL, Kasiske BL, Alexander SR, Danovitch GM, Harmon WE,
Kahana L et al. The evaluation of candidates for renal transplantation:
The current practice of U.S. transplant centers. Transplantation
1994; 57: 490–497.
182. Singh N, Paterson DL. Mycobacterium tuberculosis infection in solid-
organ transplant recipients: impact and implications for manage-
ment. Clin Infect Dis 1998; 27: 1266–1277.
183. Essentials of tuberculosis control for the practising physician. Tu-
berculosis Committee, Canadian Thoracic Society. Can Med Assoc J
1994; 150: 1561–1571.
184. Control and prevention of tuberculosis in the United Kingdom: Code
of Practice 1994. Joint Tuberculosis Committee of the British Tho-
racic Society. Thorax 1994; 49: 1193–1200.
185. The role of BCG vaccine in the prevention and control of tuberculosis
in the United States. A joint statement by the Advisory Council for
the Elimination of Tuberculosis and the Advisory Committee on Im-
munization Practices. MMWR Morb Mortal Wkly Rep 1996; 45: 1–
18.
186. Jassal SV, Roscoe JM, Zaltzman JS, Mazzulli T, Krajden M, Gadawski
M et al. Clinical practice guidelines: prevention of cytomegalovirus
disease after renal transplantation. J Am Soc Nephrol 1998; 9:
1697–1708.
187. Sagedal S, Nordal KP, Hartmann A, Degre M, Holter E, Foss A et al.
A prospective study of the natural course of cytomegalovirus infec-
tion and disease in renal allograft recipients. Transplantation 2000;
70: 1166–1174.
188. Bergan S, Rugstad HE, Bentdal Ø, Sodal G, Hartmann A, Leivestad
T et al. Monitored high-dose azathioprine treatment reduces acute
rejection episodes after renal transplantation. Transplantation 1998;
66: 334–339.
189. Moreso F, Seron D, Morales JM, Cruzado JM, Gil-Vernet S, Perez JL
et al. Incidence of leukopenia and cytomegalovirus disease in kidney
transplants treated with mycophenolate mofetil combined with low
cyclosporine and steroid doses. Clin Sci 1998; 12: 198–205.
190. ter Meulen CG, Wetzels JF, Hilbrands LB. The influence of myco-
phenolate mofetil on the incidence and severity of primary cytomeg-
alovirus infections and disease after renal transplantation. Nephrol
Dial Transplant 2000; 15: 711–714.
191. Sarmiento JM, Dockrell DH, Schwab TR, Munn SR, Paya CVS. My-
cophenolate mofetil increases cytomegalovirus invasive organ dis-
ease in renal transplant patients. Clin Transplant 2000; 14: 136–
138.
192. Snydman DR, Werner BG, Heinze-Lacey B, Berardi VP, Tilney NL,
Kirkman RL et al. Use of cytomegalovirus immune globulin to pre-
vent cytomegalovirus disease in renal-transplant recipients. N Engl J
Med 1987; 317: 1049–1054.
193. Balfour HH, Jr, Chace BA, Stapleton JT, Simmons RL, Fryd DS. A
randomized, placebo-controlled trial of oral acyclovir for the preven-
tion of cytomegalovirus disease in recipients of renal allografts. N
Engl J Med 1989; 320: 1381–1387.
194. Steinmuller DR, Novick AC, Streem SB, Graneto D, Swift C. Intra-
venous immunoglobulin infusions for the prophylaxis of secondary
cytomegalovirus infection. Transplantation 1990; 49: 68–70.
195. Rondeau E, Bourgeon B, Peraldi MN, Lang P, Buisson C, Schulte KM
et al. Effect of prophylactic ganciclovir on cytomegalovirus infection
in renal transplant recipients. Nephrol Dial Transplant 1993; 8: 858–
862.
196. Hibberd PL, Tolkoff-Rubin NE, Conti D, Stuart F, Thistlethwaite JR,
71
Kasiske et al.
Neylan JF et al. Preemptive ganciclovir therapy to prevent cytomeg-
alovirus disease in cytomegalovirus antibody-positive renal trans-
plant recipients. A randomized controlled trial. Ann Intern Med 1995;
123: 18–26.
197. Flechner SM, Avery RK, Fisher R, Mastroianni BA, Papajcik DA, O’M-
alley KJ et al. A randomized prospective controlled trial of oral acyclo-
vir versus oral ganciclovir for cytomegalovirus prophylaxis in high-
risk kidney transplant recipients. Transplantation 1998; 66: 1682–
1688.
198. Lowance D, Neumayer HH, Legendre CM, Squifflet JP, Kovarik J,
Brennan PJ et al. Valacyclovir for the prevention of cytomegalovirus
disease after renal transplantation. International Valacyclovir Cyto-
megalovirus Prophylaxis Transplantation Study Group. N Engl J Med
1999; 340: 1462–1470.
199. Couchoud C. Cytomegalovirus prophylaxis with antiviral agents for
solid organ transplantation. Cochrane Database Syst Revs 2000;
CD001320.
200. Brennan DC, Garlock KA, Lippmann BA, Buller RS, Gaudreault-Keen-
er M, Lowell JA et al. Control of cytomegalovirus-associated mor-
bidity in renal transplant patients using intensive monitoring and
either preemptive or deferred therapy. J Am Soc Nephrol 1997; 8:
118–125.
201. Mauskopf JA, Richter A, Annemans L, Maclaine G. Cost-effective-
ness model of cytomegalovirus management strategies in renal
transplantation. Comparing valaciclovir prophylaxis with current prac-
tice. Pharmacoeconomics 2000; 18: 239–251.
202. Legendre CM, Norman DJ, Keating MR, Maclaine GD, Grant DM.
Valaciclovir prophylaxis of cytomegalovirus infection and disease in
renal transplantation: an economic evaluation. Transplantation 2000;
70: 1463–1468.
203. Limaye AP, Corey L, Koelle DM, Davis CL, Boeckh M. Emergence
of ganciclovir-resistant cytomegalovirus disease among recipients of
solid-organ transplants. Lancet 2000; 356: 645–649.
204. Bakir N, Surachno S, Sluiter WJ, Struijk DG. Peritonitis in peritoneal
dialysis patients after renal transplantation. Nephrol Dial Transplant
1998; 13: 3178–83.
205. Passalacqua JA, Wiland AM, Fink JC, Bartlett ST, Evans DA, Keay
S. Increased incidence of postoperative infections associated with
peritoneal dialysis in renal transplant recipients. Transplantation
1999; 68: 535–540.
206. Leichter HE, Salusky IB, Ettenger RB, Jordan SC, Hall TL, Marik J
et al. Experience with renal transplantation in children undergoing
peritoneal dialysis CAPD/CCPD. Am J Kidney Dis 1986; 8: 181–185.
207. Yamalik N, Avcikurt UF, Caglayan F, Eratalay K. The importance of
oral foci of infection in renal transplantation. Aust Dent J 1993; 38:
108–113.
208. Wilson RL, Martinez-Tirado J, Whelchel J, Lordon RE. Occult dental
infection causing fever in renal transplant patients. Am J Kidney Dis
1982; 2: 354–356.
209. Margiotta V, Pizzo I, Pizzo G, Barbaro A. Cyclosporin- and nifedipine-
induced gingival overgrowth in renal transplant patients: correlations
with periodontal and pharmacological parameters, and HLA-anti-
gens. J Oral Pathol Med 1996; 25: 128–134.
210. Seymour RA, Smith DG. The effect of a plaque control programme
on the incidence and severity of cyclosporin-induced gingival
changes. J Clin Periodontol 1991; 18: 107–110.
211. Varga E, Lennon MA, Mair LH. Pre-transplant gingival hyperplasia
predicts severe cyclosporin-induced gingival overgrowth in renal
transplant patients. J Clin Periodontol 1998; 25: 225–230.
212. Aufricht C, Hogan EL, Ettenger RB. Oral metronidazole does not im-
prove cyclosporine A-induced gingival hyperplasia. Pediatr Nephrol
1997; 11: 552–555.
213. Gomez E. Treatment of cyclosporin-induced gingival hyperplasia
with azithromycin. Nephrol Dial Transplant 1997; 12: 2694–2697.
72
214. Nash MM, Zaltzman JS. Efficacy of azithromycin in the treatment of
cyclosporine-induced gingival hyperplasia in renal transplant recipi-
ents. Transplantation 1998; 65: 1611–1615.
215. Mattila KJ, Nieminen MS, Valtonen VV, Rasi VP, Kesaniemi YA, Syrja-
la SL et al. Association between dental health and acute myocardial
infarction. BMJ 1989; 298: 779–781.
216. DeStefano F, Anda RF, Kahn HS, Williamson DF, Russell CM. Dental
disease and risk of coronary heart disease and mortality. Br Med J
1993; 306: 688–691.
217. Mattila KJ, Valle MS, Nieminen MS, Valtonen VV, Hietaniemi KL.
Dental infections and coronary atherosclerosis. Atherosclerosis
1993; 103: 205–211.
218. Paunio K, Impivaara O, Tiekso J, Maki J. Missing teeth and ischaemic
heart disease in men aged 45–64 years. Eur Heart J 1993; 14 Suppl
K: 54–56.
219. Mattila KJ, Valtonen VV, Nieminen M, Huttunen JK. Dental infection
and the risk of new coronary events: prospective study of patients
with documented coronary artery disease. Clin Infect Dis 1995; 20:
588–592.
220. Joshipura KJ, Rimm EB, Douglass CW, Trichopoulos D, Ascherio A,
Willett WC. Poor oral health and coronary heart disease. J Dent Res
1996; 75: 1631–1636.
221. Beck J, Garcia R, Heiss G, Vokonas PS, Offenbacher S. Periodontal
disease and cardiovascular disease. J Periodontol 1996; 67: 1123–
1137.
222. Wu T, Trevisan M, Genco RJ, Falkner KL, Dorn JP, Sempos CT. Exami-
nation of the relation between periodontal health status and cardio-
vascular risk factors: serum total and high density lipoprotein chol-
esterol, C-reactive protein, and plasma fibrinogen. Am J Epidemiol
2000; 151: 273–282.
223. Wu T, Trevisan M, Genco RJ, Dorn JP, Falkner KL, Sempos CT. Peri-
odontal disease and risk of cerebrovascular disease: the first national
health and nutrition examination survey and its follow-up study. Arch
Intern Med 2000; 160: 2749–2755.
224. Belshe RB. Influenza prevention and treatment: current practices and
new horizons. Ann Intern Med 1999; 131: 621–624.
225. Rangel MC, Coronado VG, Euler GL, Strikas RA. Vaccine recommen-
dations for patients on chronic dialysis. The Advisory Committee on
Immunization Practices and the American Academy of Pediatrics.
Semin Dial 2000; 13: 101–107.
226. Grekas D, Alivanis P, Kotzadamis N, Kiriazopoulou V, Pyrpasopoulos
M, Tourkantonis A. Influenza vaccination in chronic hemodialysis pa-
tients. The effect of zinc supplementation. Ren Fail 1992; 14: 575–
578.
227. Turk S, Bozfakioglu S, Ecder ST, Kahraman T, Gurel N, Erkoc R et al.
Effects of zinc supplementation on the immune system and on anti-
body response to multivalent influenza vaccine in hemodialysis pa-
tients. Int J Artif Organs 1998; 21: 274–278.
228. Antonen JA, Hannula PM, Pyhala R, Saha HH, Ala-Houhala IO, Pas-
ternack AI. Adequate seroresponse to influenza vaccination in dialy-
sis patients. Nephron 2000; 86: 56–61.
229. MacKenzie JS. Influenza subunit vaccine: antibody responses to one
and two doses of vaccine and length of response, with particular
reference to the elderly. Br Med J 1977; 1: 200–202.
230. Gross PA, Weksler ME, Quinnan GV, Jr, Douglas RG, Jr, Gaerlan PF,
Denning CR. Immunization of elderly people with two doses of in-
fluenza vaccine. J Clin Microbiol 1987; 25: 1763–1765.
231. Linnemann CC, Jr, First MR. Risk of pneumococcal infections in renal
transplant patients. JAMA 1979; 241: 2619–2621.
232. Prevention of pneumococcal disease: recommendations of the Ad-
visory Committee on Immunization Practices ACIP. MMWR Morb
Mortal Wkly Rep 1997; 46: 1–24.
233. Furth SL, Neu AM, Case B, Lederman HM, Steinhoff M, Fivush B.
Pneumococcal polysaccharide vaccine in children with chronic renal
2001; Suppl. 1: Vol. 2: 5–95
 The Evaluation of Renal Transplant Candidates: Clinical Practice Guidelines
disease: a prospective study of antibody response and duration. J
Pediatr 1996; 128: 99–101.
234. Fuchshuber A, Kuhnemund O, Keuth B, Lutticken R, Michalk D, Quer-
feld U. Pneumococcal vaccine in children and young adults with
chronic renal disease. Nephrol Dial Transplant 1996; 11: 468–473.
235. Miller JL. Pneumococcal vaccine for infants, toddlers licensed. Am
J Health Syst Pharm 2000; 57: 625.
236. Agamanolis DP, Tan JS, Parker DL. Immunosuppressive measles en-
cephalitis in a patient with a renal transplant . Arch Neurol 1979; 36:
686–690.
237. Nakano T, Shimono Y, Sugiyama K, Nishihara H, Higashigawa M,
Komada Y et al. Clinical features of measles in immunocompromised
children. Acta Paediatr Jpn 1996; 38: 212–217.
238. Mazariegos GV, Green M, Reyes J, Nour B, Tzakis A, Starzl TE. Ru-
bella infection after orthotopic liver transplantation. Pediatr Infect Dis
J 1994; 13: 161–162.
239. Watson JC, Hadler SC, Dykewicz CA, Reef S, Phillips L. Measles,
mumps, and rubella–vaccine use and strategies for elimination of
measles, rubella, and congenital rubella syndrome and control of
mumps: recommendations of the Advisory Committee on Immuniz-
ation Practices ACIP. MMWR Morb Mortal Wkly Rep 1998; 47: 1–
57.
240. Schulman SL, Deforest A, Kaiser BA, Polinsky MS, Baluarte HJ. Re-
sponse to measles-mumps-rubella vaccine in children on dialysis.
Pediatr Nephrol 1992; 6: 187–189.
241. Pertussis vaccination: use of acellular pertussis vaccines among in-
fants and young children. Recommendations of the Advisory Com-
mittee on Immunization Practices ACIP. MMWR Morb Mortal Wkly
Rep 1997; 46: 1–25.
242. Kruger S, Seyfarth M, Sack K, Kreft B. Defective immune response
to tetanus toxoid in hemodialysis patients and its association with
diphtheria vaccination. Vaccine 1999; 17: 1145–1150.
243. Guerin A, Buisson Y, Nutini MT, Saliou P, London G, Marchais S.
Response to vaccination against tetanus in chronic haemodialysed
patients. Nephrol Dial Transplant 1992; 7: 323–326.
244. Kreft B, Klouche M, Kreft R, Kirchner H, Sack K. Low efficiency of
active immunization against diphtheria in chronic hemodialysis pa-
tients. Kidney Int 1997; 52: 212–216.
245. Prevots DR, Sutter RW, Strebel PM, Wharton M, Hadler SC. Poliomy-
elitis prevention in the United States: introduction of a sequential
vaccination schedule of inactivated poliovirus vaccine followed by
oral poliovirus vaccine. Recommendations of the Advisory Commit-
tee on Immunization Practices ACIP. MMWR Morb Mortal Wkly Rep
1997; 46: 1–25.
246. Neu AM, Lederman HM, Warady BA, Fivush BA. Haemophilus in-
fluenzae type b immunization in infants on peritoneal dialysis. Pedi-
atric Peritoneal Dialysis Study Consortium. Pediatr Nephrol 1996; 10:
84–85.
247. Fivush BA, Case B, Warady BA, Lederman H. Defective antibody
response to Hemophilus influenzae type b immunization in children
receiving peritoneal dialysis. Pediatr Nephrol 1993; 7: 548–550.
248. Broyer M, Tete MJ, Guest G, Gagnadoux MF, Rouzioux C. Varicella
and zoster in children after kidney transplantation: long- term results
of vaccination. Pediatrics 1997; 99: 35–39.
249. Webb NJ, Fitzpatrick MM, Hughes DA, Brocklebank TJ, Judd BA,
Lewis MA et al. Immunisation against varicella in end stage and pre-
end stage renal failure. Trans-Pennine Paediatric Nephrology Study
Group. Arch Dis Child 2000; 82: 141–143.
250. Gershon AA. Immunizations for pediatric transplant patients. Kidney
Int Suppl 1993; 43: S87-S90.
251. From the Centers for Disease Control and Prevention. Recommended
childhood immunization schedule–United States, July-December
1996. JAMA 1996; 276: 775–776.
252. Update: vaccine side effects, adverse reactions, contraindications,
2001; Suppl. 1: Vol. 2: 5–95
and precautions. Recommendations of the Advisory Committee on
Immunization Practices ACIP. [published erratum appears in MMWR
Morb Mortal Wkly Rep 1997 Mar 14; 4610.: 227]. MMWR Morb
Mortal Wkly Rep 1996; 45: 1–35.
253. Fivush BA, Neu AM. Immunization guidelines for pediatric renal dis-
ease. Semin Nephrol 1998; 18: 256–263.
254. Fivush BA, Furth SL, Neu AM. Immunizations in children on PD: cur-
rent guidelines and recommendations. Adv Perit Dial 1995; 11: 270–
273.
255. Recommended childhood immunization schedule. United States,
January–December 1999. American Academy of Pediatrics Commit-
tee on Infectious Diseases. Pediatrics 1999; 103: 182–185.
256. Neumayer HH, Wagner K, Kresse S. HTLV-III antibodies in patients
with kidney transplants or on haemodialysis [letter]. Lancet 1986; i:
497.
257. Mathew TH. Recurrence of disease following renal transplantation.
Am J Kidney Dis 1988; 12: 85–96.
258. Mathew TH. Recurrent disease after renal transplantation. Transplant
Revs 1991; 5: 31–45.
259. Cameron JS. Recurrent primary disease and de novo nephritis fol-
lowing renal transplantation. Pediatr Nephrol 1991; 5: 412–421.
260. Cameron JS. Recurrent disease in renal allografts. Kidney Int Suppl
1993; 43: S91-S94.
261. Ramos EL. Recurrent diseases in the renal allograft. J Am Soc
Nephrol 1991; 2: 109–121.
262. Ramos EL, Tisher CC. Recurrent diseases in the kidney transplant.
Am J Kidney Dis 1994; 24: 142–154.
263. Cameron JS. Recurrent renal disease after renal transplantation. Curr
Opin Nephrol Hypertens 1994; 3: 602–607.
264. Davison AM. Renal transplantation: recurrence of original disease
with particular reference to primary glomerulonephritis. Nephrol Dial
Transplant 1995; 10 Suppl 1: 81–84.
265. Michielsen P. Recurrence of the original disease. Does this influence
renal graft failure? Kidney Int Suppl 1995; 52: S79-S84.
266. Dantal J, Giral M, Hoormant M, Soulillou JP. Glomerulonephritis re-
currences after kidney transplantation. Curr Opin Nephrol Hypertens
1995; 4: 146–154.
267. Kotanko P, Pusey CD, Levy JB. Recurrent glomerulonephritis follow-
ing renal transplantation. Transplantation 1997; 63: 1045–1052.
268. Baqi N, Tejani A. Recurrence of the original disease in pediatric renal
transplantation. J Nephrol 1997; 10: 85–92.
269. Denton MD, Singh AK. Recurrent and de novo glomerulonephritis in
the renal allograft. Semin Nephrol 2000; 20: 164–175.
270. Briggs JD, Jones E. Recurrence of glomerulonephritis following renal
transplantation. Scientific Advisory Board of the ERA-EDTA Registry.
European Renal Association-European Dialysis and Transplant As-
sociation. Nephrol Dial Transplant 1999; 14: 564–565.
271. Hariharan S, Adams MB, Brennan DC, Davis CL, First MR, Johnson
CP et al. Recurrent and de novo glomerular disease after renal trans-
plantation: a report from Renal Allograft Disease Registry RADR.
Transplantation 1999; 68: 635–641.
272. Pinto J, Lacerda G, Cameron JS, Turner DR, Bewick M, Ogg CS.
Recurrence of focal segmental glomerulosclerosis in renal allografts.
Transplantation 1981; 32: 83–89.
273. Morzycka M, Croker BP, Jr, Seigler HF, Tisher CC. Evaluation of recur-
rent glomerulonephritis in kidney allografts. Am J Med 1982; 72:
588–598.
274. Cheigh JS, Mouradian J, Soliman M, Tapia L, Riggio RR, Stenzel KH
et al. Focal segmental glomerulosclerosis in renal transplants. Am J
Kidney Dis 1983; 2: 449–455.
275. O’Meara Y, Green A, Carmody M, Donohoe J, Campbell E, Browne
O et al. Recurrent glomerulonephritis in renal transplants: fourteen
years’ experience. Nephrol Dial Transplant 1989; 4: 730–734.
276. Cameron JS, Senguttuvan P, Hartley B, Rigden SP, Chantler C, Koff-
73
Kasiske et al.
man G et al. Focal segmental glomerulosclerosis in fifty-nine renal
allografts from a single centre, analysis of risk factors for recurrence.
Transplant Proc 1989; 21: 2117–2118.
277. Vincenti F, Biava C, Tomlanovich S, Amend WJ, Jr, Garovoy M, Melz-
er J et al. Inability of cyclosporine to completely prevent the recur-
rence of focal glomerulosclerosis after kidney transplantation. Trans-
plantation 1989; 47: 595–598.
278. Vangelista A, Frasca GM, Martella D, Bonomini VS. Glomeru-
lonephritis in renal transplantation. Nephrol Dial Transplant 1990; 5
Suppl 1: 42–46.
279. Banfi G, Colturi C, Montagnino G, Ponticelli C. The recurrence of focal
segmental glomerulosclerosis in kidney transplant patients treated
with cyclosporine. Transplantation 1990; 50: 594–596.
280. Senggutuvan P, Cameron JS, Hartley RB, Rigden S, Chantler C, Hay-
cock G et al. Recurrence of focal segmental glomerulosclerosis in
transplanted kidneys: analysis of incidence and risk factors in 59
allografts. Pediatr Nephrol 1990; 4: 21–28.
281. Dantal J, Baatard R, Hourmant M, Cantarovich D, Buzelin F, Soulillou
JP. Recurrent nephrotic syndrome following renal transplantation in
patients with focal glomerulosclerosis. A one-center study of plasma
exchange effects. Transplantation 1991; 52: 827–831.
282. Artero M, Biava C, Amend W, Tomlanovich S, Vincenti F. Recurrent
focal glomerulosclerosis: natural history and response to therapy.
Am J Med 1992; 92: 375–383.
283. Odorico JS, Knechtle SJ, Rayhill SC, Pirsch JD, D’Alessandro AM,
Belzer FO et al. The influence of native nephrectomy on the inci-
dence of recurrent disease following renal transplantation for primary
glomerulonephritis. Transplantation 1996; 61: 228–234.
284. Wuhl E, Fydryk J, Wiesel M, Mehls O, Schaefer F, Scharer K. Impact
of recurrent nephrotic syndrome after renal transplantation in young
patients. Pediatr Nephrol 1998; 12: 529–533.
285. Butani L, Polinsky MS, Kaiser BA, Baluarte HJ. Predictive value of
race in post-transplantation recurrence of focal segmental glomeru-
losclerosis in children. Nephrol Dial Transplant 1999; 14: 166–168.
286. Dall’Amico R, Ghiggeri G, Carraro M, Artero M, Ghio L, Zamorani E
et al. Prediction and treatment of recurrent focal segmental glomeru-
losclerosis after renal transplantation in children. Am J Kidney Dis
1999; 34: 1048–1055.
287. Raafat R, Travis LB, Kalia A, Diven S. Role of transplant induction
therapy on recurrence rate of focal segmental glomerulosclerosis.
Pediatr Nephrol 2000; 14: 189–194.
288. Cheong HI, Han HW, Park HW, Ha IS, Han KS, Lee HS et al. Early
recurrent nephrotic syndrome after renal transplantation in children
with focal segmental glomerulosclerosis. Nephrol Dial Transplant
2000; 15: 78–81.
289. Greenstein SM, Delrio M, Ong E, Feuerstein D, Schechner R, Kim D
et al. Plasmapheresis treatment for recurrent focal sclerosis in pedi-
atric renal allografts. Pediatr Nephrol 2000; 14: 1061–1065.
290. Kim SJ, Kim M, Ha J, Jung IM, Lee TS, Cheong HI et al. Focal seg-
mental glomerulosclerosis progression to end-stage renal disease
within 48 months is a risk factor for recurrence after pediatric renal
transplantation. Transplant Proc 1999; 31: 1393–1394.
291. Stephanian E, Matas AJ, Mauer SM, Chavers B, Nevins T, Kashtan
C et al. Recurrence of disease in patients retransplant ed for focal
segmental glomerulosclerosis. Transplantation 1992; 53: 755–
757.
292. Dantal J, Bigot E, Bogers W, Testa A, Kriaa F, Jacques Y et al. Effect
of plasma protein adsorption on protein excretion in kidney-trans-
plant recipients with recurrent nephrotic syndrome. N Engl J Med
1994; 330: 7–14.
293. Savin VJ, Sharma R, Sharma M, McCarthy ET, Swan SK, Ellis E et al.
Circulating factor associated with increased glomerular permeability
to albumin in recurrent focal segmental glomerulosclerosis. N Engl
J Med 1996; 334: 878–883.
74
294. Conlon PJ, Lynn K, Winn MP, Quarles LD, Bembe ML, Pericak-Vance
M et al. Spectrum of disease in familial focal and segmental glo-
merulosclerosis. Kidney Int 1999; 56: 1863–1871.
295. Felldin M, Norden G, Svalander C, Nyberg G. Focal segmental glo-
merulosclerosis in a kidney transplant population: hereditary and
sporadic forms. Transplant Int 1998; 11: 16–21.
296. Toth CM, Pascual M, Williams WW, Jr, Delmonico FL, Cosimi AB,
Colvin RB et al. Recurrent collapsing glomerulopathy. Transplantation
1998; 65: 1009–1010.
297. Clarkson MR, O’Meara YM, Murphy B, Rennke HG, Brady HR. Col-
lapsing glomerulopathy–recurrence in a renal allograft. Nephrol Dial
Transplant 1998; 13: 503–506.
298. Meehan SM, Pascual M, Williams WW, Tolkoff-Rubin N, Delmonico
FL, Cosimi AB et al. De novo collapsing glomerulopathy in renal allo-
grafts. Transplantation 1998; 65: 1192–1197.
299. Stokes MB, Davis CL, Alpers CE. Collapsing glomerulopathy in renal
allografts: a morphological pattern with diverse clinicopathologic as-
sociations. Am J Kidney Dis 1999; 33: 658–666.
300. Andresdottir MB, Hoitsma AJ, Assmann KJM, Koene RAP, Wetzels
JFM. The impact of recurrent glomerulonephritis on graft survival
in recipients of human histocompatibility leucocyte antigen-identical
living renlated donor grafts. Transplantation 1999; 68: 623–627.
301. Baum MA, Stablein DM, Panzarino VM, Tejani A, Harmon WE, Alex-
ander SR. Loss of living donor renal allograft survival advantage in
children with focal segmental glomerulosclerosis. Kidney Int 2001;
59: 328–333.
302. Mowry J, Marik J, Cohen A, Hogg R, Sahney S, Ettenger R. Treat-
ment of recurrent focal segmental glomerulosclerosis with high-dose
cyclosporine A and plasmapheresis. Transplant Proc 1993; 25:
1345–1346.
303. Montagnino G, Tarantino A, Banfi G, Maccario M, Costamagna L,
Ponticelli C. Double recurrence of FSGS after two renal transplants
with complete regression after plasmapheresis and ACE inhibitors.
Transplant Int 2000; 13: 166–168.
304. Saleem MA, Ramanan AV, Rees L. Recurrent focal segmental glo-
merulosclerosis in grafts treated with plasma exchange and in-
creased immunosuppression. Pediatr Nephrol 2000; 14: 361–364.
305. Iguchi Y, Tanabe K, Yagisawa T, Fuchinoue S, Kawai T, Kawaguchi
H et al. Plasmapheresis for prevention of recurrent focal segmental
glomerulosclerosis of kidney allograft in adult recipients. Ther Apher
1997; 1: 191–194.
306. Sharma R, Sharma M, Ge X, McCarthy ET, Savin. Cyclosporine pro-
tects glomeruli from FSGS factor via an increase in glomerular
cAMP. Transplantation 1996; 62: 1916–1920.
307. Kessler M, Champigneulles J, Hestin D, Frimat L, Renoult E. A renal
allograft recipient with late recurrence of focal and segmental glo-
merulosclerosis after switching from cyclosporine to tacrolimus.
Transplantation 1999; 67: 641–643.
308. Odum J, Peh CA, Clarkson AR, Bannister KM, Seymour AE, Gillis D et
al. Recurrent mesangial IgA nephritis following renal transplantation.
Nephrol Dial Transplant 1994; 9: 309–312.
309. Bachman U, Biava C, Amend W, Feduska N, Melzer J, Salvatierra O
et al. The clinical course of IgA-nephropathy and Henoch-Schonlein
purpura following renal transplantation. Transplantation 1986; 42:
511–515.
310. Schwarz A, Krause PH, Offermann G, Keller F. Recurrent and de novo
renal disease after kidney transplantation with or without cyclospor-
ine A. Am J Kidney Dis 1991; 17: 524–531.
311. Kessler M, Hiesse C, Hestin D, Mayeux D, Boubenider K, Charpentier
B. Recurrence of immunoglobulin A nephropathy after renal trans-
plantation in the cyclosporine era. Am J Kidney Dis 1996; 28: 99–
104.
312. Ohmacht C, Kliem V, Burg M, Nashan B, Schlitt HJ, Brunkhorst R et
al. Recurrent immunoglobulin A nephropathy after renal transplan-
2001; Suppl. 1: Vol. 2: 5–95
 The Evaluation of Renal Transplant Candidates: Clinical Practice Guidelines
tation: a significant contributor to graft loss. Transplantation 1997;
64: 1493–1496.
313. Frohnert PP, Donadio JV, Jr, Velosa JA, Holley KE, Sterioff S. The fate
of renal transplants in patients with IgA nephropathy. Clin Sci 1997;
11: 127–133.
314. Bumgardner GL, Amend WC, Ascher NL, Vincenti FG. Single-center
long-term results of renal transplantation for IgA nephropathy. Trans-
plantation 1998; 65: 1053–1060.
315. Freese P, Svalander C, Norden G, Nyberg. Clinical risk factors for
recurrence of IgA nephropathy. Clin Sci 1999; 13: 313–317.
316. Meulders Q, Pirson Y, Cosyns J-P, Squifflet JP, van Ypersele de Strih-
ou C. Course of Henoch-Schonlein nephritis after renal transplan-
tation. Report on ten patients and review of the literature. Transplan-
tation 1994; 58: 1179–1186.
317. Baliah T, Kim KH, Anthone S, Anthone R, Montes M, Andres GA.
Recurrence of Henoch-Schonlein purpura glomerulonephritis in
transplanted kidneys. Transplantation 1974; 18: 343–346.
318. Nast CC, Ward HJ, Koyle MA, Cohen AH. Recurrent Henoch-Schonl-
ein purpura following renal transplantation. Am J Kidney Dis 1987;
9: 39–43.
319. Andresdottir MB, Assmann KJ, Hoitsma AJ, Koene RA, Wetzels JF.
Recurrence of type I membranoproliferative glomerulonephritis after
renal transplantation: analysis of the incidence, risk factors, and im-
pact on graft survival. Transplantation 1997; 63: 1628–1633.
320. Eddy A, Sibley R, Mauer SM, Kim Y. Renal allograft failure due to
recurrent dense intramembranous deposit disease. Clin Nephrol
1984; 21: 305–313.
321. Andresdottir MB, Assmann KJ, Hoitsma AJ, Koene RA, Wetzels JF.
Renal transplantation in patients with dense deposit disease:
morphological characteristics of recurrent disease and clinical out-
come. Nephrol Dial Transplant 1999; 14: 1723–1731.
322. Morales JM, Martinez MA, Munoz dB, Munoz MA, Gota R, Usera
G. Recurrent type III membranoproliferative glomerulonephritis after
kidney transplantation. Transplantation 1997; 63: 1186–1188.
323. Cruzado JM, Gil-Vernet S, Ercilla G, Seron D, Carrera M, Bas J et al.
Hepatitis C virus-associated membranoproliferative glomeru-
lonephritis in renal allografts. J Am Soc Nephrol 1996; 7: 2469–
2475.
324. Brunkhorst R, Kliem V, Koch KM. Recurrence of membranoprolifer-
ative glomerulonephritis after renal transplantation in a patient with
chronic hepatitis C. Nephron 1996; 72: 465–467.
325. Yamabe H, Johnson RJ, Gretch DR, Fukushi K, Osawa H, Miyata M
et al. Hepatitis C virus infection and membranoproliferative glomeru-
lonephritis in Japan. J Am Soc Nephrol 1995; 6: 220–223.
326. Morales JM, Campistol JM, Andres A, Rodicio JL. Glomerular dis-
eases in patients with hepatitis C virus infection after renal transplan-
tation. Curr Opin Nephrol Hypertens 1997; 6: 511–515.
327. Berger BE, Vincenti F, Biava C, Amend WJ, Feduska N, Salvatierra
O. De novo and recurrent membraneous glomerulopathy following
kidney transplantation. Transplantation 1983; 35: 315–319.
328. Montagnino G, Colturi C, Banfi G, Aroldi A, Tarantino A, Ponticelli C.
Membranous nephropathy in cyclosporine-treated renal transplant
recipients. Transplantation 1989; 47: 725–727.
329. Couchoud C, Pouteil-Noble C, Colon S, Touraine JL. Recurrence of
membranous nephropathy after renal transplantation. Incidence and
risk factors in 1614 patients. Transplantation 1995; 59: 1275–1279.
330. Cosyns J-P, Couchoud C, Pouteil-Noble C, Squifflet JP, Pirson Y. Re-
currence of membranous nephropathy after renal transplantation:
probability, outcome and risk factors. Clin Nephrol 1998; 50: 144–
153.
331. Morales JM, Pascual-Capdevila J, Campistol JM, Fernandez-Zata-
rain G, Munoz MA, Andres A et al. Membranous glomerulonephritis
associated with hepatitis C virus infection in renal transplant patients.
Transplantation 1997; 63: 1634–1639.
2001; Suppl. 1: Vol. 2: 5–95
332. Cerilli GJ, Nelsen C, Dorfmann L. Renal homotransplantation in in-
fants and children with the hemolytic- uremic syndrome. Surgery
1972; 71: 66–71.
333. Arias-Rodriguez M, Sraer JD, Kourilsky O, Smith MD, Verroust PJ,
Meyrier A et al. Renal transplantation and immunological abnormali-
ties in thrombotic microangiopathy of adults: report of 5 cases.
Transplantation 1977; 23: 360–365.
334. Grino JM, Caralps A, Carreras L, Nogues R, Castelao AM, Romero R
et al. Apparent recurrence of hemolytic uremic syndrome in azathio-
prine-treated allograft recipients. Nephron 1988; 49: 301–304.
335. van den Berg-Wolf MG, Kootte AM, Weening JJ, Paul LC. Recurrent
hemolytic uremic syndrome in a renal transplant recipient and review
of the Leiden experience. Transplantation 1988; 45: 248–251.
336. Scantlebury VP, Shapiro R, McCauley J, Jordan M, Vivas C, Irish W
et al. Renal transplantation under cyclosporine and FK 506 for hemo-
lytic uremic syndrome. Transplant Proc 1995; 27: 842–843.
337. Hebert D, Kim EM, Sibley RK, Mauer SM. Post-transplantation out-
come of patients with hemolytic-uremic syndrome: update. Pediatr
Nephrol 1991; 5: 162–167.
338. Eijgenraam FJ, Donckerwolcke RA, Monnens LA, Proesmans W,
Wolff ED, van Damme B. Renal transplantation in 20 children with
hemolytic-uremic syndrome. Clin Nephrol 1990; 33: 87–93.
339. Bassani CE, Ferraris J, Gianantonio CA, Ruiz S, Ramierz J. Renal
transplantation in patients with classical haemolytic-uraemic syn-
drome. Pediatr Nephrol 1991; 5: 607–611.
340. Miller RB, Burke BA, Schmidt WJ, Gillingham KJ, Matas AJ, Mauer
M et al. Recurrence of haemolytic-uraemic syndrome in renal trans-
plants: a single-centre report. Nephrol Dial Transplant 1997; 12:
1425–1430.
341. Conlon PJ, Brennan DC, Pfaf WW, Finn WF, Gehr T, Bollinger RR et
al. Renal transplantation in adults with thrombotic thrombocytopenic
purpura/haemolytic-uraemic syndrome. Nephrol Dial Transplant
1996; 11: 1810–1814.
342. Ducloux D, Rebibou JM, Semhoun-Ducloux S, Jamali M, Fournier V,
Bresson-Vautrin C et al. Recurrence of hemolytic-uremic syndrome
in renal transplant recipients: a meta-analysis. Transplantation 1998;
65: 1405–1407.
343. Franz M, Regele H, Schmaldienst S, Stummvoll HK, Horl WH, Pohan-
ka E. Posttransplant hemolytic uremic syndrome in adult retransplant
ed kidney graft recipients: advantage of FK506 therapy? Transplan-
tation 1998; 66: 1258–1262.
344. Hebert D, Sibley RK, Mauer SM. Recurrence of hemolytic uremic
syndrome in renal transplant recipients. Kidney Int Suppl 1986; 19:
S51-S58.
345. Doutrelepont JM, Abramowicz D, Florquin S, de Pauw L, Goldman
M, Kinnaert P et al. Early recurrence of hemolytic uremic syndrome
in a renal transplant recipient during prophylactic OKT3 therapy.
Transplantation 1992; 53: 1378–1379.
346. Lahlou A, Lang P, Charpentier B, Barrou B, Glotz D, Baron C et al.
Hemolytic uremic syndrome. Recurrence after renal transplantation.
Groupe Cooperatif de l’Ile-de-France GCIF. Medicine Baltimore.
2000; 79: 90–102.
347. Hariharan S, Munda R, Cavallo T, Demmy AM, Schroeder TJ, Alex-
ander JW et al. Rescue therapy with tacrolimus after combined kid-
ney/pancreas and isolated pancreas transplantation in patients with
severe cyclosporine nephrotoxicity. Transplantation 1996; 61: 1161–
1165.
348. Morris-Stiff G, Talbot D, Balaji V, Baboolal K, Callanan K, Hails J et
al. Conversion of renal transplant recipients from cyclosporin neoral.
to tacrolimus prograf. for haemolytic uraemic syndrome. Transplant
Int 1998; 11 Suppl 1: S98-S99.
349. Pham PT, Peng A, Wilkinson AH, Gritsch HA, Lassman C, Pham PC
et al. Cyclosporine and tacrolimus-associated thrombotic microangi-
opathy. Am J Kidney Dis 2000; 36: 844–850.
75
Kasiske et al.
350. Walder B, Ricou B, Suter PM. Tacrolimus FK 506.-induced hemolytic
uremic syndrome after heart transplantation. J Heart Lung Transplant
1998; 17: 1004–1006.
351. Burke GW, Ciancio G, Cirocco R, Markou M, Olson L, Contreras N
et al. Microangiopathy in kidney and simultaneous pancreas/kidney
recipients treated with tacrolimus: evidence of endothelin and cyto-
kine involvement. Transplantation 1999; 68: 1336–1342.
352. Randhawa PS, Tsamandas AC, Magnone M, Jordan M, Shapiro R,
Starzl TE et al. Microvascular changes in renal allografts associated
with FK506 Tacrolimus. therapy. Am J Surg Pathol 1996; 20: 306–
312.
353. Kaplan BS, Papadimitriou M, Brezin JH, Tomlanovich SJ, Zulkharnain.
Renal transplantation in adults with autosomal recessive inheritance
of hemolytic uremic syndrome. Am J Kidney Dis 1997; 30: 760–
765.
354. Kaplan BS, Leonard MB. Autosomal dominant hemolytic uremic syn-
drome: variable phenotypes and transplant results. Pediatr Nephrol
2000; 14: 464–468.
355. Remuzzi G, Marchesi D, Misiani R, Mecca G, de Gaetano G, Donati
MB. Familial deficiency of a plasma factor stimulating vascular
prostacyclin activity. Thromb Res 1979; 16: 517–525.
356. Bobbio-Pallavicini E, Gugliotta L, Centurioni R, Porta C, Vianelli N,
Billio A et al. Antiplatelet agents in thrombotic thrombocytopenic
purpura TTP. Results of a randomized multicenter trial by the Italian
Cooperative Group for TTP. Haematologica 1997; 82: 429–435.
357. Bennett CL, Connors JM, Carwile JM, Moake JL, Bell WR, Tarantolo
SR et al. Thrombotic thrombocytopenic purpura associated with clo-
pidogrel. N Engl J Med 2000; 342: 1773–1777.
358. Couser WG, Wallace A, Monaco AP, Lewis EJ. Successful renal
transplantation in patients with circulating antibody to glomerular
basement membrane: Report of two cases. Clin Nephrol 1973; 1:
381–388.
359. Nachman PH, Segelmark M, Westman K, Hogan SL, Satterly KK,
Jennette JC et al. Recurrent ANCA-associated small vessel vasculitis
after transplantation: A pooled analysis. Kidney Int 1999; 56: 1544–
1550.
360. Toussaint C, Thoua Y, Goldman M, de Pauw L, Catalano C, Vereer-
straeten P. Early renal graft failure due to recurrence of Wegener’s
granulomatosis under cyclosporine therapy. Clin Sci 1989; 3: 27–
30.
361. Aunsholt NAa, Ahlbom G. Recurrence of Wegener’s granulomatosis
after kidney transplantation involving the kidney graft. Clin Sci 1989;
3: 159–161.
362. Nyberg G, Akesson P, Norden G, Wieslander J. Systemic vasculitis
in a kidney transplant population. Transplantation 1997; 63: 1273–
1277.
363. Schmitt WH, Haubitz M, Mistry N, Brunkhorst R, Erbslöh-Möller B,
Gross WL. Renal transplantation in Wegener’s granulomatosis [let-
ter]. Lancet 1993; 342: 860.
364. Stegeman CA, Cohen Tervaert JW, de Jong PE, Kallenberg CG. Tri-
methoprim-sulfamethoxazole co-trimoxazole. for the prevention of
relapses of Wegener’s granulomatosis. Dutch Co-Trimoxazole Weg-
ener Study Group. N Engl J Med 1996; 335: 16–20.
365. de Groot K, Reinhold-Keller E, Tatsis E, Paulsen J, Heller M, Nolle B
et al. Therapy for the maintenance of remission in sixty-five patients
with generalized Wegener’s granulomatosis. Methotrexate versus tri-
methoprim/sulfamethoxazole. Arthritis Rheum 1996; 39: 2052–
2061.
366. Mejia G, Zimmerman SW, Glass NR, Miller DT, Sollinger HW, Belzer
FO. Renal transplantation in patients with systemic lupus ery-
thematosus. Arch Intern Med 1983; 143: 2089–2092.
367. Roth D, Milgrom M, Esquenazi V, Strauss J, Zilleruelo G, Miller J.
Renal transplantation in systemic lupus erythematosus: One center’s
experience. Am J Nephrol 1987; 7: 367–74.
76
368. Bumgardner GL, Mauer SM, Payne W, Dunn DL, Sutherland DE, Fryd
DS et al. Single-center 1–15-year results of renal transplantation in
patients with systemic lupus erythematosus. Transplantation 1988;
46: 703–9.
369. Cheigh JS, Kim H, Stenzel KH, Tapia L, Sullivan JF, Stubenbord W
et al. Systemic lupus erythematosus in patients with end-stage renal
disease: long-term follow-up on the prognosis of patients and the
evolution of lupus activity. Am J Kidney Dis 1990; 16: 189–195.
370. Rivera M, Marcen R, Pascual J, Naya MT, Orofino L, Ortuno J. Kidney
transplantation in systemic lupus erythematosus nephritis: a one-
center experience. Nephron 1990; 56: 148–151.
371. Goss JA, Cole BR, Jendrisak MD, McCullough CS, So SKS, Windus
DW et al. Renal transplantation for systemic lupus erythematosus
and recurrent lupus nephritis. Transplantation 1991; 52: 805–810.
372. Nossent HC, Swaak TJG, Berden JHM. Systemic lupus ery-
thematosus after renal transplantation: Patient and graft survival and
disease activity. Ann Intern Med 1991; 114: 183–188.
373. Lochhead KM, Pirsch JD, D’Alessandro AM, Knechtle SJ, Kalayoglu
M, Sollinger HW et al. Risk factors for renal allograft loss in patients
with systemic lupus erythematosus. Kidney Int 1996; 49: 512–
517.
374. Azevedo LS, Romao JE, Jr, Malheiros D, Saldanha LB, Ianhez LE,
Sabbaga E. Renal transplantation in systemic lupus erythematosus.
A case control study of 45 patients. Nephrol Dial Transplant 1998;
13: 2894–2898.
375. Grimbert P, Frappier J, Bedrossian J, Legendre C, Antoine C, Hiesse
C et al. Long-term outcome of kidney transplantation in patients with
systemic lupus erythematosus: a multicenter study. Groupe
Cooperatif de Transplantation d’ile de France. Transplantation 1998;
66: 1000–1003.
376. Magee JC, Leichtman AB, Merion RM. Renal transplantation for sys-
temic lupus erythematosis: excellent long- term results with both
living and cadaveric donors. Transplant Proc 1998; 30: 1798–1799.
377. Stone JH, Millward CL, Olson JL, Amend WJ, Criswell LA. Frequency
of recurrent lupus nephritis among ninety-seven renal transplant pa-
tients during the cyclosporine era. Arthritis Rheum 1998; 41: 678–
686.
378. Nyberg G, Blohme I, Persson H, Olausson M, Svalander C. Recur-
rence of SLE in transplanted kidneys: a follow-up transplant biopsy
study. Nephrol Dial Transplant 1992; 7: 1116–1123.
379. Nyberg G, Karlberg I, Svalander C, Hedman L, Blohme I. Renal trans-
plantation in patients with systemic lupus erythematosus: increased
risk of early graft loss. Scand J Urol Nephrol 1990; 24: 307–313.
380. Ward MM. Outcomes of renal transplantation among patients with
end-stage renal disease caused by lupus nephritis. Kidney Int 2000;
57: 2136–2143.
381. Ward. Access to renal transplantation among patients with end-
stage renal disease due to lupus nephritis. Am J Kidney Dis 2000;
35: 915–922.
382. Milliner DS, Eickholt JT, Bergstralh EJ, Wilson DM, Smith LH. Results
of long-term treatment with orthophosphate and pyridoxine in pa-
tients with primary hyperoxaluria. N Engl J Med 1994; 331: 1553–
1558.
383. Cochat P, Gaulier JM, Koch Nogueira PC, Feber J, Jamieson NV,
Rolland MO et al. Combined liver-kidney transplantation in primary
hyperoxaluria type 1. Eur J Pediatr 1999; 158 Suppl 2: S75-S80.
384. Latta K, Jamieson NV, Scheinman JI, Scharer K, Bensman A, Cochat
P et al. Selection of transplantation procedures and perioperative
management in primary hyperoxaluria type 1. Nephrol Dial Trans-
plant 1995; 10 Suppl 8: 53–57.
385. Kemper MJ, Nolkemper D, Rogiers X, Timmermann K, Sturm E, Mal-
ago M et al. Preemptive liver transplantation in primary hyperoxaluria
type 1: timing and preliminary results. J Nephrol 1998; 11 Suppl 1:
46–48.
2001; Suppl. 1: Vol. 2: 5–95
 The Evaluation of Renal Transplant Candidates: Clinical Practice Guidelines
386. Hoppe B, Kemper MJ, Bokenkamp A, Portale AA, Cohn RA, Lang-
man CB. Plasma calcium oxalate supersaturation in children with
primary hyperoxaluria and end-stage renal failure. Kidney Int 1999;
56: 268–274.
387. Thervet E, Legendre C, Daudon M, Chretien Y, Mejean A, Jungers P
et al. Is there a place for isolated renal transplantation in the treat-
ment of primary hyperoxaluria type 1? Experience from Paris.
Nephrol Dial Transplant 1995; 10 Suppl 8: 38–41.
388. Allen AR, Thompson EM, Williams G, Watts RW, Pusey CD. Selective
renal transplantation in primary hyperoxaluria type 1. Am J Kidney
Dis 1996; 27: 891–895.
389. Saborio P, Scheinman JI. Transplantation for primary hyperoxaluria
in the United States. Kidney Int 1999; 56: 1094–1100.
390. Drachman R, Dollberg L, Drukker A. Recurrence of oxalate depo-
sition in a renal transplant during ciclosporin A therapy. Child Nephrol
Urol 1988; 9: 90–92.
391. Knols G, Leunissen KM, Spaapen LJ, Bosman FT, vs.d.Wiel TW, Koot-
stra G et al. Recurrence of nephrocalcinosis after renal transplan-
tation in an adult patient with primary hyperoxaluria type I. Nephrol
Dial Transplant 1989; 4: 137–139.
392. Jamieson NVS. The results of combined liver/kidney transplantation
for primary hyperoxaluria PH1. 1984–1997. The European PH1 Trans-
plant registry report. European PH1 Transplantation Study Group. J
Nephrol 1998; 11 Suppl 1: 36–41.
393. Toussaint C, Vienne A, de Pauw L, Gelin M, Janssen F, Hall M et al.
Combined liver-kidney transplantation in primary hyperoxaluria type
1. Bone histopathology and oxalate body content. Transplantation
1995; 59: 1700–1704.
394. Walden U, Boswald M, Dorr HG, Ruder H. Primary hyperoxaluria 1:
catch up growth and normalization of oxaluria 6 years after hepator-
enal transplantation in a prepubertal boy. Eur J Pediatr 1999; 158:
727–729.
395. Broyer M, Jouvet P, Niaudet P, Daudon M, Revillon Y. Management
of oxalosis. Kidney Int Suppl 1996; 53: S93-S98.
396. Scheinman JI, Najarian JS, Mauer SM. Successful strategies for re-
nal transplantation in primary oxalosis. Kidney Int 1984; 25: 804–
811.
397. Mansell MA. Primary hyperoxaluria type 2. Nephrol Dial Transplant
1995; 10 Suppl 8: 58–60.
398. Milliner DS, Wilson DM, Smith LH. Clinical expression and long-term
outcomes of primary hyperoxaluria types 1 and 2. J Nephrol 1998;
11 Suppl 1: 56–59.
399. Markello TC, Bernardini IM, Gahl WA. Improved renal function in
children with cystinosis treated with cysteamine. N Engl J Med
1993; 328: 1157–1162.
400. Gahl WA. Nephropathic cystinosis. Pediatr Revs 1997; 18: 302–304.
401. Lawson RK, Talwalkar YB, Hodges CVS. Renal transplantation in cys-
tinosis. J Urol 1975; 113: 552–554.
402. Almond PS, Matas AJ, Nakhleh RE, Morel P, Troppmann C, Najarian
JS et al. Renal transplantation for infantile cystinosis: long-term fol-
low-up. J Pediatr Surg 1993; 28: 232–238.
403. Schneider JA, Katz B, Melles RB. Cystinosis. AKF Nephrology Letter
1990; 7: 22–31.
404. Nissenson AR, Port FK. Outcome of end-stage renal disease in pa-
tients with rare causes of renal failure. I. Inherited and metabolic
disorders. Q J Med 1989; 73: 1055–1062.
405. Langlois RP, O’Regan S, Pelletier M, Robitaille P. Kidney transplan-
tation in uremic children with cystinosis. Nephron 1981; 28: 273–
275.
406. Ehrich JH, Brodehl J, Byrd DI, Hossfeld S, Hoyer PF, Leipert KP et
al. Renal transplantation in 22 children with nephropathic cystinosis.
Pediatr Nephrol 1991; 5: 708–714.
407. Kashtan CE, McEnery PT, Tejani A, Stablein DM. Renal allograft sur-
vival according to primary diagnosis: a report of the North American
2001; Suppl. 1: Vol. 2: 5–95
Pediatric Renal Transplant Cooperative Study. Pediatr Nephrol 1995;
9: 679–684.
408. Theodoropoulos DS, Krasnewich D, Kaiser-Kupfer MI, Gahl WA.
Classic nephropathic cystinosis as an adult disease. JAMA 1993;
270: 2200–2204.
409. Goodyer P, Langlois V, Geary D, Murray L, Champoux S, Hebert D et
al. Polyuria and proteinuria in cystinosis have no impact on renal
transplantation. A report of the North American Pediatric Renal
Transplant Cooperative Study. Plasmapheresis treatment for recur-
rent focal sclerosis in pediatric renal allografts. Pediatr Nephrol 2000;
15: 7–10.
410. Spence MW, MacKinnon KE, Burgess JK, d’Entremont DM, Belitsky
P, Lannon SG et al. Failure to correct the metabolic defect by renal
allotransplant ion in Fabry’s disease. Ann Intern Med 1976; 84: 13–
16.
411. Friedlaender MM, Kopolovic J, Rubinger D, Silver J, Drukker A, Ben
Gershon Z et al. Renal biopsy in Fabry’s disease eight years after
successful renal transplantation. Clin Nephrol 1987; 27: 206–211.
412. Popli S, Molnar ZV, Leehey DJ, Daugirdas JT, Roth DA, Adams MB
et al. Involvement of renal allograft by Fabry’s disease. Am J Nephrol
1987; 7: 316–318.
413. Mosnier JF, Degott C, Bedrossian J, Molas G, Degos F, Pruna A et
al. Recurrence of Fabry’s disease in a renal allograft eleven years
after successful renal transplantation. Transplantation 1991; 51:
759–762.
414. Gantenbein H, Bruder E, Burger HR, Briner J, Binswanger U. Recur-
rence of Fabry’s disease in a renal allograft 14 years after transplan-
tation. Nephrol Dial Transplant 1995; 10: 287–289.
415. Kramer W, Thormann J, Mueller K, Frenzel H. Progressive cardiac
involvement by Fabry’s disease despite successful renal allotrans-
plantation. Int J Cardiol 1985; 7: 72–75.
416. Jacky E. Fabrysche Erkrankung Angiokeratoma corporis diffusum un-
iversale.: gunstiger Verlauf nach Nierentransplantation [Fabry’s dis-
ease angiokeratoma corporis diffusum universale.: benign course
after kidney transplantation]. Schweiz Med Wochenschr 1976; 106:
703–709.
417. Erten Y, Ozdemir FN, Demirhan B, Karakayali H, Demirag A, Akkoc
H. A case of Fabry’s disease with normal kidney function at 10 years
after successful renal transplantation. Transplant Proc 1998; 30:
842–843.
418. Ojo A, Meier-Kriesche HU, Friedman G, Hanson J, Cibrik D, Leicht-
man A et al. Excellent outcome of renal transplantation in patients
with Fabry’s disease. Transplantation 2000; 69: 2337–2339.
419. Donati D, Novario R, Gastaldi L. Natural history and treatment of
uremia secondary to Fabry’s disease: A European experience. Neph-
ron 1987; 46: 353–359.
420. Takenaka T, Hendrickson CS, Tworek DM, Tudor M, Schiffmann R,
Brady RO et al. Enzymatic and functional correction along with long-
term enzyme secretion from transduced bone marrow hematopoi-
etic stem/progenitor and stromal cells derived from patients with Fa-
bry disease. Exp Hematol 1999; 27: 1149–1159.
421. Kursat S, Erkin E. The simultaneous appearance of Alport syndrome
in a renal transplant donor and the recipient as primary disease re-
currence. Nephron 1998; 79: 364.
422. Brainwood D, Kashtan C, Gubler MC, Turner AN. Targets of alloanti-
bodies in Alport anti-glomerular basement membrane disease after
renal transplantation. Kidney Int 1998; 53: 762–766.
423. Kalluri R, Torre A, Shield CF, III, Zamborsky ED, Werner MC, Suchin
E et al. Identification of alpha3; alpha4; and alpha5 chains of type
IV collagen as alloantigens for Alport posttransplant anti-glomerular
basement membrane antibodies. Transplantation 2000; 69: 679–
683.
424. Milliner DS, Pierides AM, Holley KE. Renal transplantation in Alport’s
syndrome. Mayo Clin Proc 1982; 57: 35–43.
77
Kasiske et al.
425. Diaz JI, Valenzuela R, Gephardt G, Novick A, Tubbs RR. Anti-glom-
erular and anti-tubular basement membrane nephritis in a renal allo-
graft recipient with Alport’s syndrome. Arch Pathol Lab Med 1994;
118: 728–731.
426. Ding J, Stitzel J, Berry P, Hawkins E, Kashtan CE. Autosomal reces-
sive Alport syndrome: mutation in the COL4A3 gene in a woman
with Alport syndrome and posttransplant antiglomerular basement
membrane nephritis. J Am Soc Nephrol 1995; 5: 1714–1717.
427. Peten E, Pirson Y, Cosyns J-P, Squifflet J-P, Alexandre GPJ, Nöel L-
H et al. Outcome of thirty patients with Alport’s syndrome after renal
transplantation. Transplantation 1991; 52: 823–826.
428. Miner DJ, Jorkasky DK, Perloff LJ, Grossman RA, Tomaszewski JE.
Recurrent sickle cell nephropathy in a transplanted kidney. Am J Kid-
ney Dis 1987; 10: 306–313.
429. Chatterjee SN. National study on natural history of renal allografts in
sickle cell disease or trait. Nephron 1980; 25: 199–201.
430. Ojo AO, Govaerts TC, Schmouder RL, Leichtman AB, Leavey SF,
Wolfe RA et al. Renal transplantation in end-stage sickle cell
nephropathy. Transplantation 1999; 67: 291–295.
431. Warady BA, Sullivan EK. Renal transplantation in children with sickle
cell disease: a report of the North American Pediatric Renal Transplant
Cooperative Study NAPRTCS. Pediatr Transplant 1998; 2: 130–133.
432. Thuraisingham RC, Roger SD, MacDougall IC, Cavill I, Stephens AD,
Baker LR et al. Improvement in anaemia following renal transplan-
tation but not after erythropoietin therapy in a patient with sickle-cell
disease. Nephrol Dial Transplant 1993; 8: 371–372.
433. Breen CP, MacDougall IC. Improvement of erythropoietin-resistant
anaemia after renal transplantation in patients with homozygous
sickle-cell disease. Nephrol Dial Transplant 1998; 13: 2949–2952.
434. Walters MC, Patience M, Leisenring W, Eckman JR, Scott JP, Mentz-
er WC et al. Bone marrow transplantation for sickle cell disease. N
Engl J Med 1996; 335: 369–376.
435. Vermylen C, Cornu G. Bone marrow transplantation for sickle cell
anemia. Curr Opin Hematol 1996; 3: 163–166.
436. Walters MC. Bone marrow transplantation for sickle cell disease:
where do we go from here? J Pediatr Hematol Oncol 1999; 21: 467–
474.
437. Pasternack A, Ahonen J, Kuhlbäck B. Renal transplantation in 45
patients with amyloidosis. Transplantation 1986; 42: 598–601.
438. Helin H, Pasternack A, Falck H, Kuhlback B. Recurrence of renal
amyloid and de novo membranous glomerulonephritis after trans-
plantation. Transplantation 1981; 32: 6–9.
439. Heering P, Kutkuhn B, Frenzel H, Linke RP, Grabensee B. Renal trans-
plantation in amyloid nephropathy. Int Urol Nephrol 1989; 21: 339–
347.
440. Heering P. Renal transplantation in secondary systemic amyloidosis.
Clin Transplant 1998; 12: 159–164.
441. Meier-Kriesche HU, Ojo AO, Cibrik DM, Hanson JA, Leichtman AB,
Magee JC et al. Relationship of recipient age and development of
chronic allograft failure. Transplantation 2000; 70: 306–310.
442. Livneh A, Zemer D, Siegal B, Laor A, Sohar E, Pras M. Colchicine
prevents kidney transplant amyloidosis in familial Mediterranean fe-
ver. Nephron 1992; 60: 418–422.
443. Sobh M, Refaie A, Moustafa F, Shokeir A, Hassan N, Sally S et al.
Study of live donor kidney transplantation outcome in recipients with
renal amyloidosis. Nephrol Dial Transplant 1994; 9: 704–708.
444. Gillmore JD, Booth DR, Rela M, Heaton ND, Rahman V, Stangou AJ
et al. Curative hepatorenal transplantation in systemic amyloidosis
caused by the Glu526Val fibrinogen alpha-chain variant in an English
family. QJM 2000; 93: 269–275.
445. Hiesse C, Bastuji-Garin S, Santelli G, Moulin B, Cantarovich M, Lantz
O et al. Recurrent essential mixed cryoglobulinemia in renal allo-
grafts. Report of two cases and review of the literature. Am J
Nephrol 1989; 9: 150–154.
78
446. Tarantino A, Moroni G, Banfi G, Manzoni C, Segagni S, Ponticelli C.
Renal replacement therapy in cryoglobulinaemic nephritis. Nephrol
Dial Transplant 1994; 9: 1426–1430.
447. Bradley JR, Thiru S, Bajallan N, Evans DB. Renal transplantation in
Waldenstrom’s macroglobulinaemia. Nephrol Dial Transplant 1988;
3: 214–216.
448. David-Neto E, Ianhez LE, Chocair PR, Saldanha LB, Sabbaga E, Arap
S. Renal transplantation in systemic light-chain deposition SLCD: a
44 month follow-up without recurrence. Transplant Proc 1989; 21:
2128–2129.
449. Gerlag PGG, Koene RAP, Berden JHM. Renal transplantation in light
chain nephropathy, case report and review of the literature. Clin
Nephrol 1986; 25: 101–104.
450. Lin JJ, Miller F, Waltzer W, Kaskel FJ, Arbeit L. Recurrence of im-
munoglobulin A-kappa crystalline deposition disease after kidney
transplantation. Am J Kidney Dis 1995; 25: 75–78.
451. Alpers CE, Rennke HG, Hopper J, Jr, Biava CG. Fibrillary glomeru-
lonephritis: an entity with unusual immunofluorescence features.
Kidney Int 1987; 31: 781–789.
452. Korbet SM, Rosenberg BF, Schwartz MM, Lewis EJ. Course of renal
transplantation in immunotactoid glomerulopathy. Am J Med 1990;
89: 91–95.
453. Woodhall PB, McCoy RC, Gunnells JC, Seigler HF. Apparent recur-
rence of progressive systemic sclerosis in a renal allograft. JAMA
1976; 236: 1032–1034.
454. Merino GE, Sutherland DE, Kjellstrand CM, Simmons RL, Najarian
JS. Renal transplantation for progressive systemic sclerosis with re-
nal failure: case report and review of previous experience. Am J Surg
1977; 133: 745–749.
455. Caplin NJ, Dikman S, Winston J, Spiera H, Uribarri J. Recurrence of
scleroderma in a renal allograft from an identical twin sister. Am J
Kidney Dis 1999; 33: e7.
456. Chang YJ, Spiera H. Renal transplantation in scleroderma. Medicine
Baltimore. 1999; 78: 382–385.
457. Martini A, Maccario R, Ravelli A, Montagna D, de Benedetti F, Bonetti
F et al. Marked and sustained improvement two years after auto-
logous stem cell transplantation in a girl with systemic sclerosis. Ar-
thritis Rheum 1999; 42: 807–811.
458. Clements PJ, Furst DE. Choosing appropriate patients with systemic
sclerosis for treatment by autologous stem cell transplantation. J
Rheumatol Suppl 1997; 48: 85–88.
459. Nash RA, McSweeney PA, Storb R, Nelson JL, Gauthier J, Furst DE
et al. Development of a protocol for allogeneic marrow transplan-
tation for severe systemic sclerosis: paradigm for autoimmune dis-
ease. J Rheumatol Suppl 1997; 48: 72–78.
460. Berg B, Groth CG, Magnusson G, Lundgren G, Ringden O. Gastroin-
testinal complications in 248 kidney transplant recipients. Scand J
Urol Nephrol 1975; 19–20.
461. Archibald SD, Jirsch DW, Bear RA. Gastrointestinal complications of
renal transplantation 2. The colon. Can Med Assoc J 1978; 119:
1301–1305, 1309.
462. Carson SD, Krom RA, Uchida K, Yokota K, West JC, Weil R, III. Colon
perforation after kidney transplantation. Ann Surg 1978; 188: 109–
113.
463. McCune TR, Nylander WA, van Buren DH, Richie RE, MacDonell RC,
Jr, Johnson HK et al. Colonic screening prior to renal transplantation
and its impact on post-transplant colonic complications. Clin Sci
1992; 6: 91–96.
464. Soravia C, Baldi A, Kartheuser A, Mourad M, Kestens PJ, Detry R et
al. Acute colonic complications after kidney transplantation. Acta
Chir Belg 1995; 95: 157–161.
465. Stelzner M, Vlahakos DV, Milford EL, Tilney NL. Colonic perforations
after renal transplantation. J Am Coll Surg 1997; 184: 63–69.
466. Koneru B, Selby R, OHair DP, Tzakis AG, Hakala TR, Starzl TE. Nonob-
2001; Suppl. 1: Vol. 2: 5–95
 The Evaluation of Renal Transplant Candidates: Clinical Practice Guidelines
structing colonic dilatation and colon perforations following renal
transplantation. Arch Surg 1990; 125: 610–613.
467. Bartolomeo RS, Calabrese PR, Taubin HL. Spontaneous perforation
of the colon. A potential complication of chronic renal failure. Am J
Dig Dis 1977; 22: 656–657.
468. Lipschutz DE, Easterling RE. Spontaneous perforation of the colon
in chronic renal failure. Arch Intern Med 1973; 132: 758–759.
469. Pirenne J, Lledo-Garcia E, Benedetti E, West M, Hakim NS, Suther-
land DE et al. Colon perforation after renal transplantation: a single-
institution review. Clin Sci 1997; 11: 88–93.
470. Lederman ED, Conti DJ, Lempert N, Singh TP, Lee EC. Complicated
diverticulitis following renal transplantation. Dis Colon Rectum 1998;
41: 613–618.
471. Dominguez FE, Albrecht KH, Heemann U, Kohnle M, Erhard J, Stobl-
en F et al. Prevalence of diverticulosis and incidence of bowel perfor-
ation after kidney transplantation in patients with polycystic kidney
disease. Transplant Int 1998; 11: 28–31.
472. Gordon EM, Johnson AG, Williams G. Gastric assessment of pros-
pective renal-transplant patients. Lancet 1972; 1: 226–229.
473. Linder MM, Bussmann JF, Kosters W, Rethel R. Preventive gastrec-
tomies before kidney transplantations. Fortschr Med 1977; 95:
2583–2587.
474. Uhlschmid G, Largiader F. Surgical prophylaxis of gastroduodenal
complications associated with renal allotransplantation. World J Surg
1977; 1: 397–405.
475. Launois B, Campion JP, Gosselin M, Cartier F. Prevention and treat-
ment of gastric and duodenal ulcers in renal transplant patients.
Gastroenterol Clin Biol 1977; 1: 23–27.
476. Doherty CC, McGeown MG. Prevention of upper gastrointestinal
complications after kidney transplantation. Proc Eur Dial Transplant
Assoc 1978; 15: 361–371.
477. Flatmark A. Prophylactic gastric operations in uremic patients prior
to renal transplantation. Invited commentary. World J Surg 1979; 3:
504.
478. Linder MM, Kosters W, Rethel R. Prophylactic gastric operations in
uremic patients prior to renal transplantation. World J Surg 1979; 3:
501–503.
479. Knechtle SJ, Kempf K, Bollinger RR. Peptic ulcer disease following
renal transplantation. Transplant Proc 1987; 19: 2233–2236.
480. Stuart FP, Reckard CR, Schulak JA, Ketel BL. Gastroduodenal compli-
cations in kidney transplant recipients. Ann Surg 1981; 194: 339–
344.
481. Brzowski R, Maldyk M, Talalaj M. Gastrointestinal and pancreatic
complications after kidney transplantation. Int Urol Nephrol 1983;
15: 93–101.
482. Milito G, Taccone-Gallucci M, Brancaleone C, Nardi F, Filingeri V,
Cesca D et al. Assessment of the upper gastrointestinal tract in
hemodialysis patients awaiting renal transplantation. Am J Gastro-
enterol 1983; 78: 328–331.
483. Feduska NJ, Amend WJ, Vincenti F, Melzer JS, Duca R, Garovoy MR
et al. Peptic ulcer disease in kidney transplant recipients. Am J Surg
1984; 148: 51–57.
484. Komorowski RA, Cohen EB, Kauffman HM, Adams MB. Gastrointes-
tinal complications in renal transplant recipients. Am J Clin Pathol
1986; 86: 161–167.
485. Lao A, Bach D. The UGI series in renal transplant candidates. Can
Assoc Radiol J 1988; 39: 195–197.
486. Ala-Kaila K. Upper gastrointestinal findings in chronic renal failure.
Scand J Gastroenterol 1987; 22: 372–376.
487. Reese J, Burton F, Lingle D, Lindsey L, Aridge D, Fairchild R et al.
Peptic ulcer disease following renal transplantation in the cyclospor-
ine era. Am J Surg 1991; 162: 558–562.
488. Benoit G, Moukarzel M, Verdelli G, Hiesse C, Buffet C, Bensadoun H
et al. Gastrointestinal complications in renal transplantation. Trans-
plant Int 1993; 6: 45–49.
2001; Suppl. 1: Vol. 2: 5–95
489. Skala I, Mareckova O, Vitko S, Matl I, Lacha J. Prophylaxis of acute
gastroduodenal bleeding after renal transplantation. Transplant Int
1997; 10: 375–378.
490. Troppman C, Papalois BE, Chiou A, Benedetti E, Dunn DL, Matas AJ
et al. Incidence, complications, treatment, and outcome of ulcers of
the upper gastrointestinal tract after renal transplantation during the
cyclosporine era. J Am Coll Surg 1995; 180: 433–443.
491. Teenan RP, Burgoyne M, Brown IL, Murray WR. Helicobacter pylori
in renal transplant recipients. Transplantation 1993; 56: 100–103.
492. Ozgur O, Boyacioglu S, Ozdogan M, Gur G, Telatar H, Haberal M.
Helicobacter pylori infection in haemodialysis patients and renal
transplant recipients. Nephrol Dial Transplant 1997; 12: 289–291.
493. Emir S, Bereket G, Boyacioglu S, Varan B, Tunali H, Haberal M. Gas-
troduodenal lesions and Helicobacter pylori in children with end-
stage renal disease. Pediatr Nephrol 2000; 14: 837–840.
494. Huang JJ, Huang CJ, Ruaan MK, Chen KW, Yen TS, Sheu BS. Diag-
nostic efficacy of 13C-urea breath test for Helicobacter pylori infec-
tion in hemodialysis patients. Am J Kidney Dis 2000; 36: 124–129.
495. Current European concepts in the management of Helicobacter py-
lori infection. The Maastricht Consensus Report. European Helico-
bacter Pylori Study Group. Gut 1997; 41: 8–13.
496. Hunt R, Thomson AB. Canadian Helicobacter pylori consensus con-
ference. Canadian Association of Gastroenterology. Can J Gastro-
enterol 1998; 12: 31–41.
497. Howden CW, Hunt RH. Guidelines for the management of Helico-
bacter pylori infection. Ad Hoc Committee on Practice Parameters
of the American College of Gastroenterology. Am J Gastroenterol
1998; 93: 2330–2338.
498. Hunt RH, Fallone CA, Thomson AB. Canadian Helicobacter pylori
Consensus Conference update: infections in adults. Canadian Hel-
icobacter Study Group. Can J Gastroenterol 1999; 13: 213–217.
499. Sherman P, Hassall E, Hunt RH, Fallone CA, Veldhuyzen VZ, Thom-
son AB. Canadian Helicobacter Study Group Consensus Conference
on the Approach to Helicobacter pylori Infection in Children and
Adolescents. Can J Gastroenterol 1999; 13: 553–559.
500. Diaz-Gonzalez de Ferris ME, Mendoza SA, Griswold WR, Strauch
LH, Reznik VM. Symptomatic cholelithiasis in pediatric renal trans-
plant recipients. Pediatr Nephrol 1991; 5: 15–17.
501. Lowell JA, Stratta RJ, Taylor RJ, Bynon JS, Larsen JL, Nelson NL.
Cholelithiasis in pancreas and kidney transplant recipients with dia-
betes. Surgery 1993; 114: 858–863, Discussion.
502. Hull D, Bartus SA, Perdrizet G, Schweizer RT. Management of choleli-
thiasis in heart and kidney transplant patients: with review of laparo-
scopic cholecystectomy. Conn Med 1994; 58: 643–647.
503. Graham SM, Flowers JL, Schweitzer E, Bartlett ST, Imbembo AL.
The utility of prophylactic laparoscopic cholecystectomy in transplant
candidates. Am J Surg 1995; 169: 44–48.
504. Greenstein SM, Katz S, Sun S, Glicklich D, Schechner R, Kutcher R
et al. Prevalence of asymptomatic cholelithiasis and risk of acute
cholecystitis after kidney transplantation. Transplantation 1997; 63:
1030–1032.
505. Melvin WS, Meier DJ, Elkhammas EA, Bumgardner GL, Davies EA,
Henry ML et al. Prophylactic cholecystectomy is not indicated fol-
lowing renal transplantation. Am J Surg 1998; 175: 317–319.
506. Pereira BJ. Hepatitis C infection and post-transplantation liver dis-
ease. Nephrol Dial Transplant 1995; 10 Suppl 1: 58–67.
507. Huang CC, Lai MK, Fong MT. Hepatitis B liver disease in cyclospor-
ine-treated renal allograft recipients. Transplantation 1990; 49: 540–
544.
508. Rao KV, Anderson WR, Kasiske BL, Dahl DC. Value of liver biopsy
in the evaluation and management of chronic liver disease in renal
transplant recipients. Am J Med 1993; 94: 241–250.
509. Allison MC, Mowat A, McCruden EA, McGregor E, Burt AD, Briggs
JD et al. The spectrum of chronic liver disease in renal transplant
recipients. Q J Med 1992; 83: 355–367.
79
Kasiske et al.
510. Parfrey PS, Farge D, Forbes RD, Dandavino R, Kenick S, Guttmann
RD. Chronic hepatitis in end-stage renal disease: comparison of
HBsAg-negative and HBsAg-positive patients. Kidney Int 1985; 28:
959–967.
511. Parfrey PS, Forbes RD, Hutchinson TA, Kenick S, Farge D, Dauphinee
WD et al. The impact of renal transplantation on the course of hepa-
titis B liver disease. Transplantation 1985; 39: 610–615.
512. Harnett JD, Zeldis JB, Parfrey PS, Kennedy M, Sircar R, Steinmann
TI et al. Hepatitis B disease in dialysis and transplant patients. Further
epidemiologic and serologic studies. Transplantation 1987; 44:
369–376.
513. Rao KV, Kasiske BL, Anderson WR. Variability in the morphological
spectrum and clinical outcome of chronic liver disease in hepatitis
B-positive and B-negative renal transplant recipients. Transplantation
1991; 51: 391–396.
514. Hiesse C, Buffet C, Neyrat N, Rieu P, Charpentier B, Etienne JP et al.
Impact of HBV antigenemia on long-term patient survival and
causes of death after renal transplantation. Clin Sci 1992; 46: 461–
467.
515. Mathurin P, Mouquet C, Poynard T, Sylla C, Benalia H, Fretz C et al.
Impact of hepatitis B and C virus on kidney transplantation outcome.
Hepatology 1999; 29: 257–263.
516. Pol S, Debure A, Degott C, Carnot F, Legendre C, Brechot C et al.
Chronic hepatitis in kidney allograft recipients. Lancet 1990; 335:
878–880.
517. Friedlaender MM, Kaspa RT, Rubinger D, Silver J, Popovtzer MM.
Renal transplantation is not contraindicated in asymptomatic carriers
of hepatitis B surface antigen. Am J Kidney Dis 1989; 14: 204–210.
518. Rostaing L, Izopet J, Cisterne JM, Arnaud C, Duffaut M, Rumeau JL
et al. Impact of hepatitis C virus duration and hepatitis C virus geno-
types on renal transplant patients: correlation with clinicopathologi-
cal features. Transplantation 1998; 65: 930–936.
519. Fornairon S, Pol S, Legendre C, Carnot F, Mamzer-Bruneel MF, Bre-
chot C et al. The long-term virologic and pathologic impact of renal
transplantation on chronic hepatitis B virus infection. Transplantation
1996; 62: 297–299.
520. Fairley CK, Mijch A, Gust ID, Nichilson S, Dimitrakakis M, Lucas CR.
The increased risk of fatal liver disease in renal transplant patients
who are hepatitis Be antigen and/or HBV DNA positive. Transplan-
tation 1991; 52: 497–500.
521. Wolfe RA, Ashby VB, Milford EL, Ojo AO, Ettenger RE, Agodoa LY
et al. Comparison of mortality in all patients on dialysis, patients on
dialysis awaiting transplantation, and recipients of a first cadaveric
transplant . N Engl J Med 1999; 341: 1725–1730.
522. Rostaing L, Henry S, Cisterne JM, Duffaut M, Icart J, Durand D.
Efficacy and safety of lamivudine on replication of recurrent hepatitis
B after cadaveric renal transplantation. Transplantation 1997; 64:
1624–1627.
523. Goffin E, Horsmans Y, Cornu C, Squifflet JP, Pirson Y. Lamivudine
inhibits hepatitis B virus replication in kidney graft recipients [letter].
Transplantation 1998; 66: 407–409.
524. Jung YO, Lee YS, Yang WS, Han DJ, Park JS, Park SK. Treatment
of chronic hepatitis B with lamivudine in renal transplant recipients.
Transplantation 1998; 66: 733–737.
525. Ben Ari Z, Broida E, Kittai Y, Chagnac A, Tur-Kaspa R. An open-label
study of lamivudine for chronic hepatitis B in six patients with chronic
renal failure before and after kidney transplantation. Am J Gastro-
enterol 2000; 95: 3579–3583.
526. Fontaine H, Thiers V, Chretien Y, Zylberberg H, Poupon RE, Brechot
C et al. HBV genotypic resistance to lamivudine in kidney recipients
and hemodialyzed patients. Transplantation 2000; 69: 2090–
2094.
527. Puchhammer-Stockl E, Mandl CW, Kletzmayr J, Holzmann H, Hof-
mann A, Aberle SW et al. Monitoring the virus load can predict the
80
emergence of drug-resistant hepatitis B virus strains in renal trans-
plantation patients during lamivudine therapy. J Infect Dis 2000;
181: 2063–2066.
528. Grob P. Hepatitis B vaccination of renal transplant and hemodialysis
patients. Scand J Infect Dis Suppl 1983; 38: 28–32.
529. Grob PJ, Binswanger U, Zaruba K, Joller-Jemelka HI, Schmid M,
Hacki W et al. Immunogenicity of a hepatitis B subunit vaccine in
hemodialysis and in renal transplant recipients. Antiviral Res 1983;
3: 43–52.
530. Peces R, de la TM, Alcazar R, Urra JM. Prospective analysis of the
factors influencing the antibody response to hepatitis B vaccine in
hemodialysis patients. Am J Kidney Dis 1997; 29: 239–245.
531. Miller ER, Alter MJ, Tokars JI. Protective effect of hepatitis B vaccine
in chronic hemodialysis patients. Am J Kidney Dis 1999; 33: 356–
360.
532. Mitwalli A. Responsiveness to hepatitis B vaccine in immunocom-
promised patients by doubling the dose scheduling. Nephron 1996;
73: 417–420.
533. Waite NM, Thomson LG, Goldstein MB. Successful vaccination with
intradermal hepatitis B vaccine in hemodialysis patients previously
nonresponsive to intramuscular hepatitis B vaccine. J Am Soc
Nephrol 1995; 5: 1930–1934.
534. Mettang T, Schenk U, Thomas S, Machleidt C, Kiefer T, Fischer FP
et al. Low-dose intradermal versus intramuscular hepatitis B vacci-
nation in patients with end-stage renal failure. A preliminary study.
Nephron 1996; 72: 192–196.
535. Chang PC, Schrander-van der Meer AM, van Dorp WT, van Leer E.
Intracutaneous versus intramuscular hepatitis B vaccination in pri-
mary non-responding haemodialysis patients. Nephrol Dial Trans-
plant 1996; 11: 191–193.
536. Fabrizi F, Andrulli S, Bacchini G, Corti M, Locatelli F. Intradermal versus
intramuscular hepatitis B re-vaccination in non- responsive chronic di-
alysis patients: a prospective randomized study with cost-effective-
ness evaluation. Nephrol Dial Transplant 1997; 12: 1204–1211.
537. Propst T, Propst A, Lhotta K, Vogel W, Konig P. Reinforced intradermal
hepatitis B vaccination in hemodialysis patients is superior in anti-
body response to intramuscular or subcutaneous vaccination. Am J
Kidney Dis 1998; 32: 1041–1045.
538. Kapoor D, Aggarwal SR, Singh NP, Thakur V, Sarin SK. Granulocyte-
macrophage colony-stimulating factor enhances the efficacy of
hepatitis B virus vaccine in previously unvaccinated haemodialysis
patients. J Viral Hepat 1999; 6: 405–409.
539. Anandh U, Bastani B, Ballal S, Vlassopoulos DA, Arvanitis DK, Lilis
DS et al. Granulocyte-macrophage colony-stimulating factor as an
adjuvant to hepatitis B vaccination in maintenance hemodialysis pa-
tientsLower long-term efficiency of intradermal hepatitis B vaccine
compared to the intramuscular route in hemodialysis patients. Am J
Nephrol 2000; 20: 53–56.
540. Vazquez G, Mendoza-Guevara L, Alvarez T, Aguilar A, Morales A,
Rodriguez F et al. Comparison of the response to the recombinant
vaccine against hepatitis B virus in dialyzed and nondialyzed children
with CRF using different doses and routes of administration. Adv
Perit Dial 1997; 13: 291–296.
541. Pereira BJG, Wright TL, Schmid CH, Levey AS. The impact of pre-
transplantation hepatitis C infection on the outcome of renal trans-
plantation. Transplantation 1995; 60: 799–805.
542. Cosio FG, Sedmak DD, Henry ML, Al Haddad C, Falkenhain ME,
Elkhammas EA et al. The high prevalence of severe early posttrans-
plant renal allograft pathology in hepatitis C positive recipients. Trans-
plantation 1996; 62: 1054–1059.
543. Hestin D, Guillemin F, Castin N, Le Faou A, Champigneulles J, Kessler
M. Pretransplant hepatitis C virus infection: a predictor of proteinuria
after renal transplantation. Transplantation 1998; 65: 741–744.
544. Fritsche C, Brandes JC, Delaney SR, Gallagher-Lepak S, Menitove
2001; Suppl. 1: Vol. 2: 5–95
 The Evaluation of Renal Transplant Candidates: Clinical Practice Guidelines
JE, Rich L et al. Hepatitis C is a poor prognostic indicator in black
kidney transplant recipients. Transplantation 1993; 55: 1283–87.
545. Bouthot BA, Murthy BV, Schmid CH, Levey AS, Pereira BJ. Long-
term follow-up of hepatitis C virus infection among organ transplant
recipients: implications for policies on organ procurement. Trans-
plantation 1997; 63: 849–853.
546. Hanafusa T, Ichikawa Y, Kishikawa H, Kyo M, Fukunishi T, Kokado Y
et al. Retrospective study on the impact of hepatitis C virus infection
on kidney transplant patients over 20 years. Transplantation 1998;
66: 471–476.
547. Legendre C, Garrigue V, Le Bihan C, Mamzer-Bruneel MF, Chaix ML,
Landais P et al. Harmful long-term impact of hepatitis C virus infec-
tion in kidney transplant recipients. Transplantation 1998; 65: 667–
670.
548. Mahmoud IM, Sobh MA, Amer GM, el Chenawy FA, Gazareen SH,
el Sherif A et al. A prospective study of hepatitis C viremia in renal
allograft recipients. Am J Nephrol 1999; 19: 576–585.
549. Gentil MA, Rocha JL, Rodriguez-Algarra G, Pereira P, Lopez R, Bernal
G et al. Impaired kidney transplantsurvival in patients with antibodies
to hepatitis C virus. Nephrol Dial Transplant 1999; 14: 2455–2460.
550. Ponz E, Campistol JM, Bruguera M, Barrera JM, Gil C, Pinto JB et
al. Hepatitis C virus infection among kidney transplant recipients. Kid-
ney Int 1991; 40: 748–751.
551. Klauser R, Franz M, Traindl O, Pidlich J, Hay U, Watschinger B et al.
Hepatitis C antibody in renal transplant patients. Transplant Proc
1992; 24: 286–288.
552. Ynares C, Johnson HK, Kerlin T, Crowe D, MacDonell R, Richie R.
Impact of pretransplant hepatitis C antibody status upon long-term
patient and renal allograft survival–a 5- and 10-year follow-up. Trans-
plant Proc 1993; 25: 1466–1468.
553. Stempel CA, Lake J, Kuo G, Vincenti F. Hepatitis C – its prevalence
in end-stage renal failure patients and clinical course after kidney
transplantation. Transplantation 1993; 55: 273–276.
554. Vincenti F, Weber P, Kuo G, Forsell J, Hunt S, Melzer J et al. Hepatitis
C virus in cadaver organ donors: prevalence and risk of transmission
to transplant recipients. Transplant Proc 1991; 23: 2651–2652.
555. Roth D, Zucker K, Cirocco R, DeMattos A, Burke GW, Nery J et al.
The impact of hepatitis C virus infection on renal allograft recipients.
Kidney Int 1994; 45: 238–244.
556. Orloff SL, Stempel CA, Wright TL, Tomlanovich SJ, Amend WJ, Stock
PG et al. Long-term outcome in kidney transplant patients with hepa-
titis C HCV. infection. Clin Sci 1995; 9: 119–124.
557. Roth D, Zucker K, Cirocco R, Burke G, Ciancio G, Esquenazi V et al.
A prospective study of hepatitis C virus infection in renal allograft
recipients. Transplantation 1996; 61: 886–889.
558. Kliem V, van den HU, Brunkhorst R, Tillmann HL, Flik J, Manns MP
et al. The long-term course of hepatitis C after kidney transplantation.
Transplantation 1996; 62: 1417–1421.
559. Natov SN, Lau JY, Ruthazer R, Schmid CH, Levey AS, Pereira BJ.
Hepatitis C virus genotype does not affect patient survival among
renal transplant candidates. The New England Organ Bank Hepatitis
C Study Group. Kidney Int 1999; 56: 700–706.
560. Rostaing L, Izopet J, Arnaud C, Cisterne JM, Alric L, Rumeau JL et al.
Long-term impact of superinfection by hepatitis G virus in hepatitis C
virus-positive renal transplant patients. Transplantation 1999; 67:
556–560.
561. Nakayama E, Akiba T, Marumo F, Sato C. Prognosis of anti-hepatitis
C virus antibody-positive patients on regular hemodialysis therapy. J
Am Soc Nephrol 2000; 11: 1896–1902.
562. Knoll GA, Tankersley MR, Lee JY, Julian BA, Curtis JJ. The impact of
renal transplantation on survival in hepatitis C-positive end-stage re-
nal disease patients. Am J Kidney Dis 1997; 29: 608–614.
563. Pereira BJ, Natov SN, Bouthot BA, Murthy BV, Ruthazer R, Schmid
CH et al. Effects of hepatitis C infection and renal transplantation on
2001; Suppl. 1: Vol. 2: 5–95
survival in end-stage renal disease. The New England Organ Bank
Hepatitis C Study Group. Kidney Int 1998; 53: 1374–1381.
564. Ozdogan M, Ozgur O, Gur G, Boyacioglu S, Ozderin Y, Demirhan B
et al. Histopathological impacts of hepatitis virus infection in hemo-
dialysis patients: should liver biopsy be performed before renal trans-
plantation? Artif Organs 1997; 21: 355–358.
565. Martin P, Carter D, Fabrizi F, Dixit V, Conrad AJ, Artinian L et al. Histo-
pathological features of hepatitis C in renal transplant candidates.
Transplantation 2000; 69: 1479–1484.
566. Koenig P, Vogel W, Umlauft F, Weyrer K, Prommegger R, Lhotta K et
al. Interferon treatment for chronic hepatitis C virus infection in urem-
ic patients. Kidney Int 1994; 45: 1507–1509.
567. Raptopoulou-Gigi M, Spaia S, Garifallos A, Xenou P, Orphanou H,
Zarafidou E et al. Interferon-alpha 2b treatment of chronic hepatitis
C in haemodialysis patients. Nephrol Dial Transplant 1995; 10:
1834–1837.
568. Pol S, Thiers V, Carnot F, Zins B, Romeo R, Berthelot P et al. Efficacy
and tolerance of alpha-2b interferon therapy on HCV infection of
hemodialyzed patients. Kidney Int 1995; 47: 1412–1418.
569. Fernandez JL, Rendo P, del Pino N, Viola L. A double-blind controlled
trial of recombinant interferon-alpha 2b in haemodialysis patients
with chronic hepatitis C virus infection and abnormal aminotransfer-
ase levels. Nephrologists’ Group for the Study of HCV infection. J
Viral Hepat 1997; 4: 113–119.
570. Chan TM, Wu PC, Lau JY, Lok AS, Lai CL, Cheng IK. Interferon treat-
ment for hepatitis C virus infection in patients on haemodialysis.
Nephrol Dial Transplant 1997; 12: 1414–1419.
571. Izopet J, Rostaing L, Moussion F, Alric L, Dubois M, That HT et al.
High rate of hepatitis C virus clearance in hemodialysis patients after
interferon-alpha therapy. J Infect Dis 1997; 176: 1614–1617.
572. Uchihara M, Izumi N, Sakai Y, Yauchi T, Miyake S, Sakai T et al.
Interferon therapy for chronic hepatitis C in hemodialysis patients:
increased serum levels of interferon. Nephron 1998; 80: 51–56.
573. Benci A, Caremani M, Menchetti D, Sasdelli M, Giusti PB. Low-dose
leukocyte interferon-alpha therapy in dialysed patients with chronic
hepatitis C. Curr Med Res Opin 1998; 14: 141–144.
574. Campistol JM, Esforzado N, Martinez J, Rosello L, Veciana L, Modol
J et al. Efficacy and tolerance of interferon-alpha2b. in the treatment
of chronic hepatitis C virus infection in haemodialysis patients. Pre-
and post-renal transplantation assessment. Nephrol Dial Transplant
1999; 14: 2704–2709.
575. Huraib S, Tanimu D, Romeh SA, Quadri K, Al Ghamdi G, Iqbal A et
al. Interferon-alpha in chronic hepatitis C infection in dialysis patients.
Am J Kidney Dis 1999; 34: 55–60.
576. Rostaing L, Chatelut E, Payen JL, Izopet J, Thalamas C, Ton-That H
et al. Pharmacokinetics of alphaIFN-2b in chronic hepatitis C virus
patients undergoing chronic hemodialysis or with normal renal func-
tion: clinical implications. J Am Soc Nephrol 1998; 9: 2344–2348.
577. Zeuzem S, Feinman SV, Rasenack J, Heathcote EJ, Lai MY, Gane E
et al. Peginterferon Alpha-2a in Patients with Chronic Hepatitis C. N
Engl J Med 2000; 343: 1666–1672.
578. Heathcote EJ, Shiffman ML, Cooksley WG, Dusheiko GM, Lee SS,
Balart L et al. Peginterferon Alpha-2a in Patients with Chronic Hepa-
titis C and Cirrhosis. N Engl J Med 2000; 343: 1673–1680.
579. Di Bisceglie AM, Conjeevaram HS, Fried MW, Sallie R, Park Y, Yur-
daydin C et al. Ribavirin as therapy for chronic hepatitis C. A ran-
domized, double- blind, placebo-controlled trial. Ann Intern Med
1995; 123: 897–903.
580. Dusheiko G, Main J, Thomas H, Reichard O, Lee C, Dhillon A et al.
Ribavirin treatment for patients with chronic hepatitis C: results of a
placebo-controlled study. J Hepatol 1996; 25: 591–98.
581. Lai MY, Kao JH, Yang PM, Wang JT, Chen PJ, Chan KW et al. Long-
term efficacy of ribavirin plus interferon alpha in the treatment of
chronic hepatitis C. Gastroenterology 1996; 111: 1307–1312.
81
Kasiske et al.
582. Reichard O, Norkrans G, Fryden A, Braconier JH, Sonnerborg A, Wei-
land O. Randomized, double-blind, placebo-controlled trial of inter-
feron alpha- 2b with and without ribavirin for chronic hepatitis C. The
Swedish Study Group. Lancet 1998; 351: 83–87.
583. Poynard T, Marcellin P, Lee SS, Niederau C, Minuk GS, Ideo G et al.
Randomised trial of interferon alpha2b plus ribavirin for 48 weeks or
for 24 weeks versus interferon alpha2b plus placebo for 48 weeks
for treatment of chronic infection with hepatitis C virus. International
Hepatitis Interventional Therapy Group IHIT.]. Lancet 1998; 352:
1426–1432.
584. McHutchison JG, Gordon SC, Schiff ER, Shiffman ML, Lee WM,
Rustgi VK et al. Interferon alpha-2b alone or in combination with
ribavirin as initial treatment for chronic hepatitis C. Hepatitis Inter-
ventional Therapy Group. N Engl J Med 1998; 339: 1485–1492.
585. Schalm SW, Weiland O, Hansen BE, Milella M, Lai MY, Hollander A et
al. Interferon-ribavirin for chronic hepatitis C with and without cir-
rhosis: analysis of individual patient data of six controlled trials. Euro-
hep Study Group for Viral Hepatitis. Gastroenterology 1999; 117: 408–
413.
586. el Zayadi A, Selim O, Haddad S, Simmonds P, Hamdy H, Badran HM
et al. Combination treatment of interferon alpha-2b and ribavirin in
comparison to interferon monotherapy in treatment of chronic hepa-
titis C genotype 4 patients. Ital J Gastroenterol Hepatol 1999; 31: 472–
475.
587. Davis GL, Esteban-Mur R, Rustgi V, Hoefs J, Gordon SC, Trepo C et al.
Interferon alpha-2b alone or in combination with ribavirin for the treat-
ment of relapse of chronic hepatitis C. International Hepatitis Inter-
ventional Therapy Group. N Engl J Med 1998; 339: 1493–1499.
588. Bell H, Hellum K, Harthug S, Myrvang B, Ritland S, Maeland A et al.
Treatment with interferon-alpha2a alone or interferon-alpha2a plus
ribavirin in patients with chronic hepatitis C previously treated with
interferon-alpha2a. CONSTRUCT Group. Scand J Gastroenterol
1999; 34: 194–198.
589. Milella M, Santantonio T, Pietromatera G, Maselli R, Casalino C,
Mariano N et al. Retreatment of non-responder or relapser chronic
hepatitis C patients with interferon plus ribavirin vs interferon alone.
Ital J Gastroenterol Hepatol 1999; 31: 211–215.
590. Barbaro G, Di Lorenzo G, Belloni G, Ferrari L, Paiano A, del Poggio P et al.
Interferon alpha-2B and ribavirin in combination for patients with
chronic hepatitis C who failed to respond to, or relapsed after, interferon
alpha therapy: a randomized trial. Am J Med 1999; 107: 112–118.
591. Kletzmayr J, Watschinger B, Muller C, Demetriou D, Stockl E, Ferenci
P et al. Twelve months of lamivudine treatment for chronic hepatitis
B virus infection in renal transplant recipients. Transplantation 2000;
70: 1404–1407.
592. Bellobuono A, Mondazzi L, Tempini S, Silini E, Vicari F, Ideo G. Ribavi-
rin and interferon-alpha combination therapy vs interferon-alpha
alone in the retreatment of chronic hepatitis C: a randomized clinical
trial. J Viral Hepat 1997; 4: 185–191.
593. Barbaro G, Di Lorenzo G, Soldini M, Giancaspro G, Bellomo G, Belloni
G et al. Interferon-alpha-2B and ribavirin in combination for chronic
hepatitis C patients not responding to interferon-alpha alone: an Ital-
ian multicenter, randomized, controlled, clinical study. Am J Gastro-
enterol 1998; 93: 2445–2451.
594. Andreone P, Gramenzi A, Cursaro C, Sbolli G, Fiorino S, Di Giammari-
no L et al. Interferon-alpha plus ribavirin in chronic hepatitis C resis-
tant to previous interferon-alpha course: results of a randomized
multicenter trial. J Hepatol 1999; 30: 788–793.
595. Pol S, Couzigou P, Bourliere M, Abergel A, Combis JM, Larrey D et
al. A randomized trial of ribavirin and interferon-alpha vs. interferon-
alpha alone in patients with chronic hepatitis C who were non-re-
sponders to a previous treatment. Multicenter Study Group under
the coordination of the Necker Hospital, Paris, France. J Hepatol
1999; 31: 1–7.
82
596. Salmeron J, Ruiz-Extremera A, Torres C, Rodriguez-Ramos L, Lavin
I, Quintero D et al. Interferon versus ribavirin plus interferon in chronic
hepatitis C previously resistant to interferon: a randomized trial. Liver
1999; 19: 275–280.
597. Kramer TH, Gaar GG, Ray CG, Minnich L, Copeland JG, Connor JD.
Hemodialysis clearance of intravenously administered ribavirin. Anti-
microb Agents Chemother 1990; 34: 489–490.
598. Kiberd BA. Should hepatitis C-infected kidneys be transplanted in
the United States? Transplantation 1994; 57: 1068–1072.
599. Mandal AK, Kraus ES, Samaniego M, Rai R, Humphreys SL, Ratner
LE et al. Shorter waiting times for hepatitis C virus seropositive recipi-
ents of cadaveric renal allografts from hepatitis C virus seropositive
donors. Clin Transplant 2000; 14: 391–396.
600. Morales JM, Campistol JM, Castellano G, Andres A, Colina F, Fuertes
A et al. transplantation of kidneys from donors with hepatitis C anti-
body into recipients with pre-transplantation anti-HCVS. Kidney Int
1995; 47: 236–240.
601. Smetana GW. Preoperative pulmonary evaluation. N Engl J Med
1999; 340: 937–944.
602. Ferguson MK. Preoperative assessment of pulmonary risk. Chest
1999; 115: 58S-63S.
603. Williams C.D, Brenowitz Jerold B. ‘‘Prohibitive’’ lung function and
major surgical procedures. Am J Surg 1978; 132: 763–766.
604. Gracey DR, Divertie MB, Dider EP. Preoperative Pulmonary prepara-
tion of Patients with Chronci Obstructive Pulmonar. Chest 1979; 76:
123–129.
605. Tisi GM. Preoperative evaluation of pulmonary function. Am Rev
Respir Dis 1979; 119: 293–310.
606. Okeson GC. Pulmonary dysfunction and surgical risk. How to assess
and minimize the hazards. Postgrad Med 1983; 74: 75–83.
607. Kingston GG, Hirshman CA. Perioperative Management on the pa-
tient with asthma. Anesth Analg 1984; 63: 844–855.
608. Gass GD, Olsen GN. Clinical Significance of Pulmonary function
tests. Preoperative pulmonary funct testing to predict postoperative
morbidity and mortality. Chest 1986; 89: 127–134.
609. Jackson CVS. Preoperative pulmonary evaluation. Arch Intern Med
1988; 148: 2120–2127.
610. Wiener-Kronish JP, Matthay MA. Preoperative evaluation. In: Murray
JS, Nadel JA, eds. Philadelphia: W.B. Saunders, 1988: 683–698.
611. Sykes LA, Bowe EA. Cardiorespiratory Effects of Anesthesia. Clin
Chest Med 1993; 14: 211–226.
612. Zibrak JD, O’Donnell CR. Indications for Preoperative Pulmonary
Function Testing. Clin Chest Med 1993; 14: 227–236.
613. Mitchell CK, Smoger SH, Pfeifer MP, Vogel RL, Pandit MK, Donnelly
PJ et al. Multivariate analysis of factors associated with postoperative
pulmonary complications following general elective surgery. Arch
Surg 1998; 133: 194–198.
614. Bluman LG, Mosca L, Newman N, Simon DG. Preoperative smoking
habits and postoperative pulmonary complications. Chest 1998; 113:
883–889.
615. Johnson CP, Kuhn EM, Hariharan S, Hartz AJ, Roza AM, Adams MB.
Pre-transplant identification of risk factors that adversely affect
length of stay and charges for renal transplantation. Clin Sci 1999;
13: 168–175.
616. Kasiske BL. Risk factors for accelerated atherosclerosis in renal trans-
plant recipients. Am J Med 1988; 84: 985–992.
617. Lemmers MJ, Barry JM. Major role for arterial disease in morbidity
and mortality after kidney transplantation in diabetic recipients. Dia-
betes Care 1991; 14: 295–301.
618. Lindholm A, Albrechtsen D, Frodin L, Tufveson G, Persson NH,
Lundgren G. Ischemic heart disease–major cause of death and graft
loss after renal transplantation in Scandinavia. Transplantation 1995;
60: 451–457.
619. Kasiske BL, Guijarro C, Massy ZA, Wiederkehr MR, Ma JZ. Cardio-
2001; Suppl. 1: Vol. 2: 5–95
 The Evaluation of Renal Transplant Candidates: Clinical Practice Guidelines
vascular disease after renal transplantation. J Am Soc Nephrol 1996;
7: 158–165.
620. Ojo AO, Hanson JA, Wolfe RA, Leichtman AB, Agodoa LY, Port FK.
Long-term survival in renal transplant recipients with graft function.
Kidney Int 2000; 57: 307–313.
621. Manske CL, Wang Y, Rector T, Wilson RF, White CW. Coronary revas-
cularisation in insulin-dependent diabetic patients with chronic renal
failure. Lancet 1992; 340: 998–1002.
622. Goldman L, Caldera DL, Nussbaum SR, Southwick FS, Krogstad D,
Murray B et al. Multifactorial index of cardiac risk in noncardiac surgi-
cal procedures. N Engl J Med 1977; 297: 845–850.
623. Goldman L. Assessment of the patient with known or suspected
ischaemic heart disease for non-cardiac surgery. Br J Anaesth 1988;
61: 38–43.
624. Goldman L. Multifactorial index of cardiac risk in noncardiac surgery:
ten- year status report. J Cardiothorac Anesth 1987; 1: 237–244.
625. Jeffrey CC, Kunsman J, Cullen DJ, Brewster DC. A prospective evalu-
ation of cardiac risk index. Anesthesiology 1983; 58: 462–464.
626. Carliner NH, Fisher ML, Plotnick GD, Garbart H, Rapoport A, Kelemen
MH et al. Routine preoperative exercise testing in patients under-
going major noncardiac surgery. Am J Cardiol 1985; 56: 51–58.
627. Gerson MC, Hurst JM, Hertzberg VS, Doogan PA, Cochran MB, Lim
SP et al. Cardiac prognosis in noncardiac geriatric surgery. Ann Intern
Med 1985; 103: 832–837.
628. Meguid MM, Mughal MM, Meguid V, Terz JJ. Risk-benefit analysis
of malnutrition and perioperative nutritional support: a review. Nu-
trition International 1987; 3: 25–34.
629. Hensle TW, Askanazi J. Metabolism and nutrition in the perioperative
period. J Urol 1988; 139: 229–239.
630. Goldman L, Caldera DL. Risks of general anesthesia and elective op-
eration in the hypertensive patient. Anesthesiology 1979; 50: 285–
292.
631. Charlson ME, MacKenzie CR, Gold JP, Ales KL, Topkins M, Shires
GT. Preoperative characteristics predicting intraoperative hypotension
and hypertension among hypertensives and diabetics undergoing
noncardiac surgery. Ann Surg 1990; 212: 66–81.
632. Detsky AS, Abrams HB, McLaughlin JR, Drucker DJ, Sasson Z,
Johnston N et al. Predicting cardiac complications in patients under-
going non-cardiac surgery. J Gen Intern Med 1986; 1: 211–219.
633. Palda VA, Detsky AS. Perioperative assessment and management of
risk from coronary artery disease. Ann Intern Med 1997; 127: 313–
328.
634. American College of Physicians. Guidelines for assessing and man-
aging the perioperative risk from coronary artery disease associated
with major noncardiac surgery. Ann Intern Med 1997; 127: 309–
312.
635. Eagle KA, Brundage BH, Chaitman BR, Ewy GA, Fleisher LA, Hertzer
NR et al. Guidelines for perioperative cardiovascular evaluation for
noncardiac surgery. Report of the American College of Cardiology/
American Heart Association Task Force on Practice Guidelines. Com-
mittee on Perioperative Cardiovascular Evaluation for Noncardiac. Cir-
culation 1996; 93: 1278–1317.
636. Whiteley MS, Prytherch DR, Higgins B, Weaver PC, Prout WG. An
evaluation of the POSSUM surgical scoring system. Br J Surg 1996;
83: 812–815.
637. Brunelli A, Fianchini A, Xiume F, Gesuita R, Mattei A, Carle F. Evalu-
ation of the POSSUM scoring system in lung surgery. Physiological
and Operative Severity Score for the enUmeration of Mortality and
Morbidity. Thorac Cardiovasc Surg 1998; 46: 141–146.
638. Wijesinghe LD, Mahmood T, Scott DJ, Berridge DC, Kent PJ, Kester
RC. Comparison of POSSUM and the Portsmouth predictor equation
for predicting death following vascular surgery. Br J Surg 1998; 85:
209–212.
639. Prytherch DR, Whiteley MS, Higgins B, Weaver PC, Prout WG, Powell
2001; Suppl. 1: Vol. 2: 5–95
SJ. POSSUM and Portsmouth POSSUM for predicting mortality.
Physiological and Operative Severity Score for the enUmeration of
Mortality and morbidity. Br J Surg 1998; 85: 1217–1220.
640. Midwinter MJ, Tytherleigh M, Ashley S. Estimation of mortality and
morbidity risk in vascular surgery using POSSUM and the Ports-
mouth predictor equation. Br J Surg 1999; 86: 471–474.
641. Tekkis P, Trotter G, South LM. Comparison of POSSUM and the
Portsmouth predictor equation for predicting death following vascu-
lar surgery. Br J Surg 1999; 86: 713–714.
642. Gilbert K, Larocque BJ, Patrick LT. Prospective evaluation of cardiac
risk indices for patients undergoing noncardiac surgery. Ann Intern
Med 2000; 133: 356–359.
643. Lewis MS, Wilson RA, Walker K, Stegeman-Olsen J, Norman DJ,
Barry JM et al. Factors in cardiac risk stratification of candidates for
renal transplant . J Cardiovasc Risk 1999; 6: 251–255.
644. Heule H, Keusch G, Uhlschmid G, Largiadër F, Binswanger U. [Car-
diovascular disease after kidney transplantation: an analysis of pre-
disposing factors]. Schweiz Med Wochenschr 1981; 111: 709–716.
645. Rimmer JM, Sussman M, Foster R, Gennari FJ. Renal transplantation
in diabetes mellitus. Influence of preexisting vascular disease on out-
come. Nephron 1986; 42: 304–310.
646. Rischen-Vos J, van der Woude FJ, Tegzess AM, Zwinderman AH,
Gooszen HC, van den Akker PJ et al. Increased morbidity and mor-
tality in patients with diabetes mellitus after kidney transplantation
as compared with non- diabetic patients. Nephrol Dial Transplant
1992; 7: 433–437.
647. Bennett WM, Kloster F, Rosch J, Barry J, Porter GA. Natural history
of asymptomatic coronary arteriographic lesions in diabetic patients
with end-stage renal disease. Am J Med 1978; 65: 779–784.
648. Weinrauch LA, D’elia JA, Healy RW, Gleason RE, Takacs FJ, Libertino
JA et al. Asymptomatic coronary artery disease: angiography in dia-
betic patients before renal transplantation. Relation of findings to
postoperative survival. Ann Intern Med 1978; 88: 346–348.
649. Braun WE, Phillips DF, Vidt DG, Novick AC, Nakamoto S, Popowniak
KL et al. Coronary artery disease in 100 diabetics with end-stage
renal failure. Transplant Proc 1984; 16: 603–607.
650. Lorber MI, van Buren CT, Flechner SM, Cameron L, Leatherwood J,
Walker WE et al. Pretransplant coronary arteriography for diabetic
renal transplant recipients. Transplant Proc 1987; 19: 1539–1541.
651. Manske CL, Wilson RF, Wang Y, Thomas W. Prevalence of, and risk
factors for, angiographically determined coronary artery disease in
type I-diabetic patients with nephropathy. Arch Intern Med 1992;
152: 2450–2455.
652. Manske CL, Wilson RF, Wang Y, Thomas W. Atherosclerotic vascular
complications in diabetic transplant candidates. Am J Kidney Dis
1997; 29: 601–607.
653. Heston TF, Norman DJ, Barry JM, Bennett WM, Wilson RA. Cardiac
risk stratification in renal transplantation using a form of artificial in-
telligence. Am J Cardiol 1997; 79: 415–417.
654. Expert Panel on Detection, Evaluation and Treatment of High Blood
Cholesterol in Adults. Summary of the Second Report of the National
Cholesterol Education Program (NCEP) (Adult Treatment Panel II).
JAMA 1993; 269: 3015–3023.
655. McPhail N, Calvin JE, Shariatmadar A, Barber GG, Scobie TK. The
use of preoperative exercise testing to predict cardiac complications
after arterial reconstruction. J Vasc Surg 1988; 7: 60–68.
656. Raby KE, Barry J, Creager MA, Cook EF, Weisberg MC, Goldman L.
Detection and significance of intraoperative and postoperative myo-
cardial ischemia in peripheral vascular surgery. JAMA 1992; 268:
222–227.
657. Raby KE, Goldman L, Creager MA, Cook EF, Weisberg MC, Whitte-
more AD et al. Correlation between preoperative ischemia and major
cardiac events after peripheral vascular surgery. N Engl J Med 1989;
321: 1296–1300.
83
Kasiske et al.
658. Baron J-F, Mundler O, Bertrand M, Vicaut E, Barré E, Godet G et al.
Dipyridamole-thallium scintigraphy and gated radionuclide angiogra-
phy to assess cardiac risk before abdominal aortic surgery. N Engl J
Med 1994; 330: 663–669.
659. Pasternack PF, Imparato AM, Bear G, Riles TS, Baumann FG, Benja-
min D et al. The value of radionuclide angiography as a predictor of
perioperative myocardial infarction in patients undergoing abdominal
aortic aneurysm resection. J Vasc Surg 1984; 1: 320–325.
660. Manning WJ, Li W, Edelman RR. A preliminary report comparing
magnetic resonance coronary angiography with conventional angio-
graphy. N Engl J Med 1993; 328: 828–832.
661. Fleischmann KE, Hunink MG, Kuntz KM. Exercise echocardiography
or exercise SPECT imaging? A meta-analysis of diagnostic test per-
formance. JAMA 1998; 280: 913–920.
662. Marwick TH, Shan K, Go RT, MacIntyre WJ, Lauer MS. Use of posi-
tron emission tomography for prediction of perioperative and late
cardiac events before vascular surgery. Am Heart J 1995; 130:
1196–1202.
663. Achenbach S, Moshage W, Ropers D, Nossen J, Daniel WG. Value
of electron-beam computed tomography for the noninvasive detec-
tion of high-grade coronary-artery stenoses and occlusions. N Engl
J Med 1998; 339: 1964–1971.
664. Shavelle DM, Budoff MJ, LaMont DH, Shavelle RM, Kennedy JM,
Brundage BH. Exercise testing and electron beam computed tomo-
graphy in the evaluation of coronary artery disease. J Am Coll Cardiol
2000; 36: 32–38.
665. He ZX, Hedrick TD, Pratt CM, Verani MS, Aquino V, Roberts R et al.
Severity of coronary artery calcification by electron beam computed
tomography predicts silent myocardial ischemia. Circulation 2000;
101: 244–251.
666. Wong ND, Hsu JC, Detrano RC, Diamond G, Eisenberg H, Gardin
JM. Coronary artery calcium evaluation by electron beam computed
tomography and its relation to new cardiovascular events. Am J Car-
diol 2000; 86: 495–498.
667. Arad Y, Spadaro LA, Goodman K, Newstein D, Guerci AD. Prediction
of coronary events with electron beam computed tomography. J Am
Coll Cardiol 2000; 36: 1253–1260.
668. O’Malley PG, Taylor AJ, Jackson JL, Doherty TM, Detrano RC. Prog-
nostic value of coronary electron-beam computed tomography for
coronary heart disease events in asymptomatic populations. Am J
Cardiol 2000; 85: 945–948.
669. Boucher CA, Brewster DC, Darling RC, Okada RD, Strauss HW, Po-
host GM. Determination of cardiac risk by dipyridamole-thallium im-
aging before peripheral vascular surgery. N Engl J Med 1985; 312:
389–394.
670. Eagle KA, Singer DE, Brewster DC, Darling RC, Mulley AG, Boucher
CA. Dipyridamole-thallium scanning in patients undergoing vascular
surgery. JAMA 1987; 257: 2185–2189.
671. Cutler BS, Leppo JA. Dipyridamole thallium 201 scintigraphy to de-
tect coronary artery disease before abdominal aortic surgery. J Vasc
Surg 1987; 5: 91–100.
672. Eagle KA, Coley CM, Newell JB, Brewster DC, Darling RC, Strauss
HW et al. Combining clinical and thallium data optimizes preopera-
tive assessment of cardiac risk before major vascular surgery. Ann
Intern Med 1989; 110: 859–866.
673. Le A, Wilson R, Douek K, Pullian L, Tolzman D, Norman D et al.
Prospective risk stratification in renal transplant candidates for car-
diac death. Am J Kidney Dis 1994; 24: 65–71.
674. de Virgilio C, Toosie K, Elbassir M, Donayre C, Baker JD, Narahara
K et al. Dipyridamole-thallium/sestamibi before vascular surgery: a
prospective blinded study in moderate-risk patients. J Vasc Surg
2000; 32: 77–89.
675. Poldermans D, Fioretti PM, Forster T, Thomson IR, Boersma E, el-
Said E-SM et al. Dobutamine stress echocardiography for assess-
84
ment of perioperative cardiac risk in patients undergoing major vas-
cular surgery. Circulation 1993; 87: 1506–1512.
676. Marwick T, D’Hondt AM, Baudhuin T, Willemart B, Wijns W, Detry
JM et al. Optimal use of dobutamine stress for the detection and
evaluation of coronary artery disease: combination with echocar-
diography or scintigraphy, or both? J Am Coll Cardiol 1993; 22: 159–
167.
677. Weinrauch LA, D’elia JA, Monaco AP, Gleason RE, Welty F, Nishan
PC et al. Preoperative evaluation for diabetic renal transplantation:
impact of clinical, laboratory, and echocardiographic parameters on
patient and allograft survival. Am J Med 1992; 93: 19–28.
678. Mueller-Brand J, Pfisterer M, Cottier C, Thiel G. Role of radionuclide
ventriculography in the management of kidney transplant candi-
dates. Contrib Nephrol 1987; 56: 186–190.
679. Bullock RE, Amer HA, Simpson I, Ward MK, Hall RJC. Cardiac abnor-
malities and exercise tolerance in patients receiving renal replace-
ment therapy. Br Med J Clin Res Ed. 1984; 289: 1479–1484.
680. Marwick TH, Steinmuller DR, Underwood DA, Hobbs RE, Go RT,
Swift C et al. Ineffectiveness of dipyridamole spect thallium imaging
as a screening technique for coronary artery disease in patients with
end-stage renal failure. Transplantation 1990; 49: 100–103.
681. Detrano RC, Wong ND, Doherty TM, Shavelle RM, Tang W, Ginzton
LE et al. Coronary calcium does not accurately predict near-term
future coronary events in high-risk adults. Circulation 1999; 99:
2633–2638.
682. Braun J, Oldendorf M, Moshage W, Heidler R, Zeitler E, Luft FC.
Electron beam computed tomography in the evaluation of cardiac
calcification in chronic dialysis patients. Am J Kidney Dis 1996; 27:
394–401.
683. Goodman WG, Goldin J, Kuizon BD, Yoon C, Gales B, Sider D et al.
Coronary-artery calcification in young adults with end-stage renal
disease who are undergoing dialysis. N Engl J Med 2000; 342:
1478–1483.
684. Stratmann HG, Younis LT, Wittry MD, Amato M, Mark AL, Miller DD.
Dipyridamole technetium 99m sestamibi myocardial tomography for
preoperative cardiac risk stratification before major or minor nonvas-
cular surgery. Am Heart J 1996; 132: 536–541.
685. Mangano DT, London MJ, Tubau JF, Browner WS, Hollenberg M,
Krupski W et al. Dipyridamole thallium-201 scintigraphy as a pre-
operative screening test – a reexamination of its predictive potential.
Circulation 1991; 84: 493–502.
686. Goldman L. Assessment of perioperative cardiac risk. N Engl J Med
1994; 330: 707–709.
687. Boudreau RJ, Strony JT, du Cret RP, Kuni CC, Wang Y, Wilson RF et
al. Perfusion thallium imaging of type I diabetes patients with end-
stage renal disease: comparison of oral and intravenous dipyrida-
mole administration. Radiology 1990; 175: 103–105.
688. Mistry BM, Bastani B, Solomon H, Hoff J, Aridge DL, Lindsey LM et al.
Prognostic value of dipyridamole thallium-201 screening to minimize
perioperative cardiac complications in diabetics undergoing kidney or
kidney-pancreas transplantation. Clin Sci 1998; 12: 130–135.
689. Morrow CE, Schwartz JS, Sutherland DER, Simmons RL, Ferguson
RM, Kjellstrand CM et al. Predictive value of thallium stress testing
for coronary and cardiovascular events in uremic diabetic patients
before renal transplantation. Am J Surg 1983; 146: 331–335.
690. Brown KA, Rimmer J, Haisch C. Noninvasive cardiac risk stratification
of diabetic and nondiabetic uremic renal allograft candidates using
dipyridamole- thallium-201 imaging and radionuclide ventriculogra-
phy. Am J Cardiol 1989; 64: 1017–1021.
691. Marcen R, Lamas S, Orofino L, Quereda C, Barcia F, Castro JM et al.
Dipyridamole thallium-201 perfusion imaging for the study of ische-
mic heart diease in hemodialysis patients. Int J Artif Organs 1989;
12: 773–777.
692. Camp AD, Garvin PJ, Hoff J, Marsh J, Byers SL, Chaitman BR. Prog-
2001; Suppl. 1: Vol. 2: 5–95
 The Evaluation of Renal Transplant Candidates: Clinical Practice Guidelines
nostic value of intravenous dipyridamole thallium imaging in patients
with diabetes mellitus considered for renal transplantation. Am J Car-
diol 1990; 65: 1459–1463.
693. Brown, J. H, Vites, N. P, Testa, H. J, Prescott, M. C, Hunt, L, Cotter,
L, Gokal, R, and Mallick, N. P. Thallium myocardial perfusion imaging
and echocardiography as prospective screening investigations for
cardiovascular disease in dialysis patients [abstract]. J Am Soc
Nephrol 1991; 2: 233.
694. Derfler K, Kletter K, Balcke P, Heinz G, Dudczak R. Predictive value of
thallium-201-dipyridamole myocardial stress scintigraphy in chronic
hemodialysis patients and transplant recipients. Clin Nephrol 1991;
36: 192–202.
695. Brown JH, Vites NP, Testa HJ, Prescott MC, Hunt LP, Gokal R et
al. Value of thallium myocardial imaging in the prediction of future
cardiovascular events in patients with end-stage renal failure.
Nephrol Dial Transplant 1993; 8: 433–437.
696. Russell, J. D, Stanton, E. B, Lambert, K, Carlisle, E. J. F, Thorpe, K,
Ludwin, D, and Churchill, D. N. Risk stratification for cardiovascular
disease in renal transplant candidates: the role of dipyridamole thal-
lium scintigraphy [abstract]. J Am Soc Nephrol 1993; 4: 960.
697. Dahan M, Viron BM, Faraggi M, Himbert DL, Lagallicier BJ, Kolta
AM et al. Diagnostic accuracy and prognostic value of combined
dipyridamole-exercise thallium imaging in hemodialysis patients.
Kidney Int 1998; 54: 255–262.
698. Nally, J, Mairesse, G, Grimm, R, D’Hondt, A, Veneverschelde, J,
Braun, W, and Marwick, T. Dobutamine echocardiography is an ef-
fective screening tool for coronary artery disease in ESRD [abstract].
J Am Soc Nephrol 1993; 4: 255.
699. Reis G, Marcovitz PA, Leichtman AB, Merion RM, Fay WP, Werns
SW et al. Usefulness of dobutamine stress echocardiography in de-
tecting coronary artery disease in end-stage renal disease. Am J
Cardiol 1995; 75: 707–710.
700. Bates JR, Sawada SG, Segar DS, Spaedy AJ, Petrovic O, Fineberg
NS et al. Evaluation using dobutamine stress echocardiography in
patients with insulin-dependent diabetes mellitus before kidney and/
or pancreas transplantation. Am J Cardiol 1996; 77: 175–179.
701. Herzog CA, Marwick TH, Pheley AM, White CW, Rao VK, Dick CD.
Dobutamine stress echocardiography for the detection of significant
coronary artery disease in renal transplant candidates. Am J Kidney
Dis 1999; 33: 1080–1090.
702. Smart SC, Bhatia A, Hellman R, Stoiber T, Krasnow A, Collier BD et
al. Dobutamine-atropine stress echocardiography and dipyridamole
sestamibi scintigraphy for the detection of coronary artery disease:
limitations and concordance. J Am Coll Cardiol 2000; 36: 1265–
1273.
703. Chawla R, Gailiunas P, Jr, Lazarus JM, Gottlieb MN, Lowrie EG, Col-
lins JJ et al. Cardiopulmonary bypass surgery in chronic hemo-
dialysis and transplant patients. Trans Am Soc Artif Intern Organs
1977; 23: 694–697.
704. Kimbler RW, Zincke H, Woods JE, Roses J, Pluth JR. Renal trans-
plantation: patients with previous saphenous vein- coronary artery
bypass grafts. Eur Urol 1979; 5: 103–105.
705. Rottembourg J, Mussat T, Gandjbakhch I, Barthelemy A, Toledano
D, Gahl GM et al. Open heart surgery in patients with end-stage
renal disease. Proc Eur Dial Transplant Assoc 1983; 20: 169–175.
706. Laws KH, Merrill WH, Hammon JW, Jr, Prager RL, Bender HW, Jr.
Cardiac surgery in patients with chronic renal disease. Ann Thorac
Surg 1986; 42: 152–157.
707. Marshall WG, Jr, Rossi NP, Meng RL, Wedige-Stecher T. Coronary
artery bypass grafting in dialysis patients. Ann Thorac Surg 1986;
42: S12-S15.
708. Opsahl JA, Husebye DG, Helseth HK, Collins AJ. Coronary artery
bypass surgery in patients on maintenance dialysis: Long-term sur-
vival. Am J Kidney Dis 1988; 12: 271–274.
2001; Suppl. 1: Vol. 2: 5–95
709. Rostand SG, Kirk KA, Rutsky EA, Pacifico AD. Results of coronary
artery bypass grafting in end-stage renal disease. Am J Kidney Dis
1988; 12: 266–270.
710. Blakeman BM, Pifarre R, Sullivan HJ, Montoya A, Bakhos M. Cardiac
surgery for chronic renal dialysis patients. Chest 1989; 95: 509–511.
711. Deutsch E, Bernstein RC, Addonizio VP, Kussmaul WG, III. Coronary
artery bypass surgery in patients on chronic hemodialysis. Ann Intern
Med 1989; 110: 369–372.
712. Batiuk TD, Kurtz SB, Oh JK, Orszulak TA. Coronary artery bypass
operation in dialysis patients. Mayo Clin Proc 1991; 66: 45–53.
713. de Meyer M, Wyns W, Dion R, Khoury G, Pirson Y, van Ypersele de
Strihou C. Myocardial revascularization in patients on renal replace-
ment therapy. Clin Nephrol 1991; 36: 147–151.
714. Herzog CA, Ma JZ, Collins AJ. Long-term outcome of dialysis pa-
tients in the United States with coronary revascularization pro-
cedures. Kidney Int 1999; 56: 324–332.
715. Agirbasli M, Weintraub WS, Chang GL, King SB, Guyton RA, Thomp-
son TD et al. Outcome of coronary revascularization in patients on
renal dialysis. Am J Cardiol 2000; 86: 395–399.
716. Franga DL, Kratz JM, Crumbley AJ, Zellner JL, Stroud MR, Crawford
FA. Early and long-term results of coronary artery bypass grafting in
dialysis patients. Ann Thorac Surg 2000; 70: 813–818.
717. Liu JY, Birkmeyer NJ, Sanders JH, Morton JR, Henriques HF, Lahey
SJ et al. Risks of morbidity and mortality in dialysis patients under-
going coronary artery bypass surgery. Circulation 2000; 102: 2973–
2977.
718. Batist G, Blaker M, Kosinski E, Brown E, Christlieb R, Leland OS, Jr.
et al. Coronary bypass survery in juvenile onset diabetes. Am Heart
J 1983; 106: 51–55.
719. Gersh BJ, Kronmal RA, Schaff HV, Frye RL, Ryan TJ, Myers WO et
al. Long-term 5 year results of coronary bypass surgery in patients
65 years old or older: a report from the Coronary Artery Surgery
Study. Circulation 1983; 68 suppl II: 190–199.
720. Hall RJ, Elayda MA, Gray A, Mathur VS, Garcia E, de Castro CM et al.
Coronary artery bypass: long-term follow-up of 22,284 consecutive
patients. Circulation 1983; 68 suppl II: 20–26.
721. Salomon NW, Page US, Okies JE, Stephens J, Krause AH, Bigelow
JC. Diabetes mellitus and coronary artery bypass: Short-term risk
and long-term prognosis. J Thorac Cardiovasc Surg 1983; 85: 264–
271.
722. Williams JS, Crawford FA, Jr, Kratz JM, Riley JB. Cardiac surgery for
patients maintained on chronic hemodialysis. J S C Med Assoc
1991; 87: 569–573.
723. Manske CL, Nelluri S, Thomas W, Shumway SJ. Outcome of coro-
nary artery bypass surgery in diabetic transplant candidates. Clin
Transplant 1998; 12: 73–79.
724. Beauchamp GD, Sharma JN, Crouch T, Reed W, Killen DA, McCallis-
ter BD et al. Coronary bypass surgery after renal transplantation. Am
J Cardiol 1976; 37: 1107–1110.
725. Hueb WA, Oliveira SA, Bittencourt D, Bellotti G, Jatene AD, Pileggi
F. Coronary bypass surgery for patients with renal transplantation.
Cardiology 1986; 73: 151–155.
726. Shafei H, Briggs JD, Bain WH. Follow-up after coronary revascularis-
ation in patients with renal transplants. Eur J Cardiothorac Surg
1989; 3: 262–266.
727. Herzog, C. A, Ma, J. Z, and Collins, A. J. Three-year survival of renal
transplant recipients in the US after coronary artery bypass surgery,
coronary angioplasty and coronary stenting [abstract]. J Am Soc
Nephrology 2000; 11: 719A.
728. Kahn JK, Rutherford BD, McConahay DR, Johnson WL, Giorgi LV,
Hartzler GO. Short- and long-term outcome of percutaneous translu-
minal coronary angioplasty in chronic dialysis patients. Am Heart J
1990; 1193 Pt 1: 484–489.
729. Takeshita S, Yamaguchi T, Isshiki T, Ikari Y, Maemura K, Furuta Y
85
Kasiske et al.
et al. Percutaneous transluminal coronary angioplasty and coronary
bypass grafting for refractory angina in chronic dialysis patients. J
Cardiol 1992; 22: 383–390.
730. Azar RR, Prpic R, Ho KK, Kiernan FJ, Shubrooks SJ, Jr, Baim DS et
al. Impact of end-stage renal disease on clinical and angiographic
outcomes after coronary stenting. Am J Cardiol 2000; 86: 485–
489.
731. Rubenstein MH, Harrell LC, Sheynberg BV, Schunkert H, Bazari H,
Palacios IF. Are patients with renal failure good candidates for percu-
taneous coronary revascularization in the new device Era? Circulation
2000; 102: 2966–2972.
732. Detre KM, Lombardero MS, Brooks MM, Hardison RM, Holubkov R,
Sopko G et al. The effect of previous coronary-artery bypass surgery
on the prognosis of patients with diabetes who have acute myocar-
dial infarction. Bypass Angioplasty Revascularization Investigation In-
vestigators. N Engl J Med 2000; 342: 989–997.
733. The sixth report of the Joint National Committee on prevention, de-
tection, evaluation, and treatment of high blood pressure. Arch Intern
Med 1997; 157: 2413–2446.
734. Levey, A. S. and Editor. Controlling the epidemic of cardiovascular
disease in chronic renal disease: What do we know? What do we
need to know? Where do we go from here? Special report for the
National Kidney Foundation Task Force on Cardiovascular Disease.
American Journal of Kidney Diseases 1998; 32 Suppl 3: S1-S199.
735. Marwick TH, Lauer MS, Lobo A, Nally J, Braun W. Use of dobuta-
mine echocardiography for cardiac risk stratification of patients with
chronic renal failure. J Intern Med 1998; 244: 155–161.
736. Foley RN, Parfrey PS, Harnett JD, Kent GM, Murray DC, Barre PE.
The prognostic importance of left ventricular geometry in uremic car-
diomyopathy. J Am Soc Nephrol 1995; 5: 2024–2031.
737. Mitsnefes MM, Daniels SR, Schwartz SM, Meyer RA, Khoury P, Strife
CF. Severe left ventricular hypertrophy in pediatric dialysis: preva-
lence and predictors. Pediatr Nephrol 2000; 14: 898–902.
738. Silaruks S, Sirivongs D, Chunlertrith D. Left ventricular hypertrophy
and clinical outcome in CAPD patients. Perit Dial Int 2000; 20: 461–
466.
739. Peteiro J, Alvarez N, Calvino R, Penas M, Ribera F, Castro BA.
Changes in left ventricular mass and filling after renal transplantation
are related to changes in blood pressure: an echocardiographic and
pulsed Doppler study. Cardiology 1994; 85: 273–283.
740. Parfrey PS, Harnett JD, Foley RN, Kent GM, Murray DC, Barre PE et
al. Impact of renal transplantation on uremic cardiomyopathy. Trans-
plantation 1995; 60: 908–914.
741. McGregor E, Jardine AG, Murray LS, Dargie HJ, Rodger RS, Junor
BJ et al. Pre-operative echocardiographic abnormalities and adverse
outcome following renal transplantation. Nephrol Dial Transplant
1998; 13: 1499–1505.
742. McGregor E, Stewart G, Rodger RS, Jardine AG. Early echocardio-
graphic changes and survival following renal transplantation. Nephrol
Dial Transplant 2000; 15: 93–98.
743. Parfrey PS, Foley RN, Harnett JD, Kent GM, Murray DC, Barre PE.
Outcome and risk factors for left ventricular disorders in chronic ur-
aemia. Nephrol Dial Transplant 1996; 11: 1277–1285.
744. Cannella G, Paoletti E, Ravera G, Cassottana P, Araghi P, Mulas D et
al. Inadequate diagnosis and therapy of arterial hypertension as
causes of left ventricular hypertrophy in uremic dialysis patients. Kid-
ney Int 2000; 58: 260–268.
745. Sikole A, Polenakovic M, Spirovska V, Polenakovic B, Masin G. Analy-
sis of heart morphology and function following erythropoietin treat-
ment of anemic dialysis patients. Artif Organs 1993; 17: 977–984.
746. Ma JZ, Ebben J, Xia H, Collins AJ. Hematocrit level and associated
mortality in hemodialysis patients. J Am Soc Nephrol 1999; 10: 610–
619.
747. Hayashi T, Suzuki A, Shoji T, Togawa M, Okada N, Tsubakihara Y et
86
al. Cardiovascular effect of normalizing the hematocrit level during
erythropoietin therapy in predialysis patients with chronic renal fail-
ure. Am J Kidney Dis 2000; 35: 250–256.
748. Besarab A, Bolton WK, Browne JK, Egrie JC, Nissenson AR, Okamo-
to DM et al. The effects of normal as compared with low hematocrit
values in patients with cardiac disease who are receiving hemo-
dialysis and epoetin. N Engl J Med 1998; 339: 584–590.
749. NKF-DOQI clinical practice guidelines for the treatment of anemia of
chronic renal failure. National Kidney Foundation-Dialysis Outcomes
Quality Initiative. Am J Kidney Dis 1997; 30: S192-S240.
750. Cannella G, Paoletti E, Delfino R, Peloso G, Molinari S, Traverso GB.
Regression of left ventricular hypertrophy in hypertensive dialyzed
uremic patients on long-term antihypertensive therapy. Kidney Int
1993; 44: 881–886.
751. Dyadyk AI, Bagriy AE, Lebed IA, Yarovaya NF, Schukina EV, Taradin
GG. ACE inhibitors captopril and enalapril induce regression of left
ventricular hypertrophy in hypertensive patients with chronic renal
failure. Nephrol Dial Transplant 1997; 12: 945–951.
752. Cannella G, Paoletti E, Delfino R, Peloso G, Rolla D, Molinari S. Pro-
longed therapy with ACE inhibitors induces a regression of left ven-
tricular hypertrophy of dialyzed uremic patients independently from
hypotensive effects. Am J Kidney Dis 1997; 30: 659–664.
753. Longenecker JC, Coresh J, Klag MJ, Levey AS, Martin AA, Fink NE et
al. Validation of comorbid conditions on the end-stage renal disease
medical evidence report: the CHOICE study. Choices for Healthy Out-
comes in Caring for ESRD. J Am Soc Nephrol 2000; 11: 520–529.
754. Rahman M, Fu P, Sehgal AR, Smith MC. Interdialytic weight gain,
compliance with dialysis regimen, and age are independent predic-
tors of blood pressure in hemodialysis patients. Am J Kidney Dis
2000; 35: 257–265.
755. Parfrey PS, Harnett JD, Griffiths S, Gault MH, Barre PE, Guttmann.
Low-output left ventricular failure in end-stage renal disease. Am J
Nephrol 1987; 7: 184–191.
756. Foley RN, Parfrey PS, Kent GM, Harnett JD, Murray DC, Barre PE.
Serial change in echocardiographic parameters and cardiac failure
in end-stage renal disease. J Am Soc Nephrol 2000; 11: 912–916.
757. Ikäheimo M, Linnaluoto M, Huttunen K, Takkunen J. Effects of renal
transplantation on left ventricular size and function. Br Heart J 1982;
47: 155–160.
758. Lai KN, Barnden L, Mathew TH. Effect of renal transplantation on left
ventricular function in hemodialysis patients. Clin Nephrol 1982; 18:
74–78.
759. Cueto-Garcia L, Herrera J, Arriaga J, Laredo C, Meaney E. Echo-
cardiographic changes after successful renal transplantation in
young nondiabetic patients. Chest 1983; 83: 56–62.
760. Larsson O, Attman P-O, Beckman-Suurküla M, Wallentin I, Wikstrand
J. Left ventricular function before and after kidney transplantation. A
prospective study in patients with juvenile- onset diabetes mellitus.
Eur Heart J 1986; 7: 779–791.
761. Colan SD, Sanders SP, Ingelfinger JR, Harmon W. Left ventricular
mechanics and contractile state in children and young adults with
end-stage renal disease: effect of dialysis and renal transplantation.
J Am Coll Cardiol 1987; 10: 1085–1094.
762. Teruel JL, Rodriguez Padial L, Quereda C, Yuste P, Marcen R, Ortuño
J. Regression of left ventricular hypertrophy after renal transplan-
tation. A prospective study. Transplantation 1987; 43: 307–309.
763. Himelman RB, Landzberg JS, Simonson JS, Amend W, Bouchard A,
Merz R et al. Cardiac consequences of renal transplantation:
changes in left ventricular morphology and function. J Am Coll Cardi-
ol 1988; 12: 915–923.
764. Burt RK, Gupta-Burt S, Suki WN, Barcenas CG, Ferguson JJ, van
Buren CT. Reversal of left ventricular dysfunction after renal trans-
plantation. Ann Intern Med 1989; 111: 635–640.
765. Arce Salinas CA, Bolaños Ulloa F, Delgado Toledano MA, Caballero
2001; Suppl. 1: Vol. 2: 5–95
 The Evaluation of Renal Transplant Candidates: Clinical Practice Guidelines
Hermosillo JA, Alvarez Amador L, Martinez-Reding JO. Modifica-
ciones de la masa y funcion del ventriculo izquierdo despues de
transplant e renal. Arch Inst Cardiol Mex 1991; 61: 527–532.
766. Adams HP, Jr, Dawson G, Coffman TJ, Corry RJ. Stroke in renal trans-
plant recipients. Arch Neurol 1986; 43: 113–115.
767. Aakhus S, Dahl K, Wideroe TE. Cardiovascular morbidity and risk
factors in renal transplant patients. Nephrol Dial Transplant 1999; 14:
648–654.
768. Massy ZA, Mamzer-Bruneel MF, Chevalier A, Millet P, Helenon O,
Chadefaux-Vekemans B et al. Carotid atherosclerosis in renal trans-
plant recipients. Nephrol Dial Transplant 1998; 13: 1792–1798.
769. Barbagallo CM, Pinto A, Gallo S, Parrinello G, Caputo F, Sparacino V
et al. Carotid atherosclerosis in renal transplant recipients: relation-
ships with cardiovascular risk factors and plasma lipoproteins. Trans-
plantation 1999; 67: 366–371.
770. Heyman A, Wilkinson WE, Heyden S, Helms MJ, Bartel AG, Karp HR
et al. Risk of stroke in asymptomatic persons with cervical arterial
bruits: a population study in Evans County, Georgia. N Engl J Med
1980; 302: 838–841.
771. Van Ruiswyk J, Noble H, Sigmann P. The natural history of carotid
bruits in elderly persons. Ann Intern Med 1990; 112: 340–343.
772. Reed GL, Singer DE, Picard EH, de Sanctis RW. Stroke following
coronary-artery bypass surgery. A case-control estimate of the risk
from carotid bruits. N Engl J Med 1988; 319: 1246–1250.
773. Biller J, Feinberg WM, Castaldo JE, Whittemore AD, Harbaugh RE,
Dempsey RJ et al. Guidelines for carotid endarterectomy. A State-
ment for healthcare professionals from a special writing group of
the stroke council, American Heart Association. Circulation 1998; 97:
501–509.
774. Executive Committee for the Asymptomatic Carotid Atherosclerosis
Study. Endarterectomy for asymptomatic carotid artery stenosis.
JAMA 1995; 273: 1421–1428.
775. Benavente O, Moher D, Pham B. Carotid endarterectomy for asympto-
matic carotid stenosis: a meta- analysis. BMJ 1998; 317: 1477–1480.
776. Wennberg DE, Lucas FL, Birkmeyer JD, Bredenberg CE, Fisher ES.
Variation in carotid endarterectomy mortality in the Medicare popula-
tion: trial hospitals, volume, and patient characteristics. JAMA 1998;
279: 1278–1281.
777. Brown MM, Humphrey PR. Carotid endarterectomy: recommenda-
tions for management of transient ischaemic attack and ischaemic
stroke. BMJ 1992; 305: 1071–1074.
778. Kistler JP, Buonanno FS, Gress DR. Carotid endarterectomy–specific
therapy based on pathophysiology. N Engl J Med 1991; 325: 505–
507.
779. North American Symptomatic Carotid Endarterectomy Trial Collabor-
ators. Beneficial effect of carotid endarterectomy in symptomatic pa-
tients with high-grade carotid stenosis. N Engl J Med 1991; 325:
445–453.
780. MRC European Carotid Surgery Trial: interim results for symptomatic
patients with severe 70–99% or with mild 0–29% carotid stenosis.
Lancet 1991; 337: 1235–1243.
781. Barnett HJ, Taylor DW, Eliasziw M, Fox AJ, Ferguson GG, Haynes RB
et al. Benefit of carotid endarterectomy in patients with symptomatic
moderate or severe stenosis. North American Symptomatic Carotid
Endarterectomy Trial Collaborators. N Engl J Med 1998; 339: 1415–
1425.
782. Randomised trial of endarterectomy for recently symptomatic carotid
stenosis: final results of the MRC European Carotid Surgery Trial
ECST. Lancet 1998; 351: 1379–1387.
783. Petersen P, Boysen G, Godtfredsen J, Andersen ED, Andersen B.
Placebo-controlled, randomised trial of warfarin and aspirin for pre-
vention of thromboembolic complications in chronic atrial fibrillation.
The Copenhagen AFASAK study. Lancet 1989; i: 175–179.
784. The effect of low-dose warfarin on the risk of stroke in patients with
2001; Suppl. 1: Vol. 2: 5–95
nonrheumatic atrial fibrillation. The Boston Area Anticoagulation Trial
for Atrial Fibrillation Investigators. N Engl J Med 1990; 323: 1505–
1511.
785. Connolly SJ, Laupacis A, Gent M, Roberts RS, Cairns JA, Joyner C.
Canadian Atrial Fibrillation Anticoagulation CAFA. Study. J Am Coll
Cardiol 1991; 18: 349–355.
786. Stroke prevention in atrial fibrillation study. Final results. Circulation
1991; 84: 527–39.
787. Ezekowitz MD, Bridgers SL, James KE, Carliner NH, Colling CL, Gor-
nick CC et al. Warfarin in the prevention of stroke associated with
nonrheumatic atrial fibrillation. Veterans Affairs Stroke Prevention in
Nonrheumatic Atrial Fibrillation Investigators. N Engl J Med 1992;
327: 1406–1412.
788. Warfarin versus aspirin for prevention of thromboembolism in atrial
fibrillation: Stroke Prevention in Atrial Fibrillation II Study. Lancet
1994; 343: 687–691.
789. Optimal oral anticoagulant therapy in patients with nonrheumatic at-
rial fibrillation and recent cerebral ischemia. The European Atrial Fib-
rillation Trial Study Group. N Engl J Med 1995; 333: 5–10.
790. Adjusted-dose warfarin versus low-intensity, fixed-dose warfarin
plus aspirin for high-risk patients with atrial fibrillation: Stroke Preven-
tion in Atrial Fibrillation III randomised clinical trial. Lancet 1996;
348: 633–638.
791. Ezekowitz MD, Levine JA. Preventing stroke in patients with atrial
fibrillation. JAMA 1999; 281: 1830–1835.
792. Hart RG, Benavente O, McBride R, Pearce LA. Antithrombotic ther-
apy to prevent stroke in patients with atrial fibrillation: a meta-analy-
sis. Ann Intern Med 1999; 131: 492–501.
793. Segal JB, McNamara RL, Miller MR, Kim N, Goodman SN, Powe NR
et al. Prevention of thromboembolism in atrial fibrillation. A meta-
analysis of trials of anticoagulants and antiplatelet drugs. J Gen In-
tern Med 2000; 15: 56–67.
794. Benavente O, Hart R, Koudstaal P, Laupacis A, McBride R. Oral anti-
coagulants for preventing stroke in patients with non-valvular atrial
fibrillation and no previous history of stroke or transient ischemic
attacks. Cochrane Database Syst Revs 2000; CD001927.
795. Green CJ, Hadorn DC, Bassett K, Kazanjian A. Anticoagulation in
chronic nonvalvular atrial fibrillation: a critical appraisal and meta-
analysis. Can J Cardiol 1997; 13: 811–815.
796. Hirsh J, Fuster VS. Guide to anticoagulant therapy. Part 2: Oral anti-
coagulants. American Heart Association. Circulation 1994; 89:
1469–1480.
797. Guidelines for medical treatment for stroke prevention. American
College of Physicians. Ann Intern Med 1994; 121: 54–55.
798. Practice parameter: Stroke prevention in patients with nonvalvular
atrial fibrillation. Report of the Quality Standards Subcommittee of
the American Academy of Neurology. Neurology 1998; 51: 671–673.
799. Chapman AB, Rubinstein D, Hughes R, Stears JC, Earnest MP, John-
son AM et al. Intracranial aneurysms in autosomal dominant poly-
cystic kidney disease. N Engl J Med 1992; 327: 916–920.
800. Huston J, Torres VE, Sulivan PP, Offord KP, Wiebers DO. Value of
magnetic resonance angiography for the detection of intracranial
aneurysms in autosomal dominant polycystic kidney disease. J Am
Soc Nephrol 1993; 3: 1871–1877.
801. Wiebers DO, Torres VE. Screening for unruptured intracranial aneu-
rysms in autosomal dominant polycystic kidney disease. N Engl J
Med 1992; 327: 953–955.
802. Chapman AB, Johnson AM, Gabow PA. Intracranial aneurysms in
patients with autosomal dominant polycystic kidney disease: how to
diagnose and who to screen. Am J Kidney Dis 1993; 22: 526–531.
803. Chauveau D, Pirson Y, Verellen-Dumoulin C, MacNicol A, Gonzalo A,
Grünfeld J-P. Intracranial aneurysms in autosomal dominant poly-
cystic kidney disease. Kidney Int 1994; 45: 1140–1146.
804. Levey AS, Pauker SG, Kassirer JP. Occult intracranial aneurysms in
87
Kasiske et al.
polycystic kidney disease. When is cerebral arteriography indicated?
N Engl J Med 1983; 308: 986–994.
805. Schievink WI, Torres VE, Piepgras DG, Wiebers DO. Saccular intra-
cranial aneurysms in autosomal dominant polycystic kidney disease.
J Am Soc Nephrol 1992; 3: 88–95.
806. The International Study of Unruptured Intracranial Aneurysms Inves-
tigators. Unruptured intracranial aneurysms – risk of rupture and
risks of surgical invervention. New Engl J Med 1998; 33924: 1725–
1733.
807. Ibels LS, Stewart JH, Mahony JF, Neale FC, Sheil AGR. Occlusive
arterial disease in uraemic and haemodialysis patients and renal
transplant recipients. A study of the incidence of arterial disease and
of the prevalence of risk factors implicated in the pathogenesis of
arteriosclerosis. Q J Med 1977; 46: 197–214.
808. Webb AT, Franks PJ, Reaveley DA, Greenhalgh RM, Brown EA. Preva-
lence of intermittent claudication and risk factors for its development
in patients on renal replacement therapy. Eur J Vasc Surg 1993; 7:
523–527.
809. Eggers PW, Gohdes D, Pugh J. Nontraumatic lower extremity ampu-
tations in the Medicare end-stage renal disease population. Kidney
Int 1999; 56: 1524–1533.
810. Sung RS, Althoen M, Howell TA, Merion RM. Peripheral vascular oc-
clusive disease in renal transplant recipients: risk factors and impact
on kidney allograft survival. Transplantation 2000; 70: 1049–1054.
811. Makisalo H, Lepantalo M, Halme L, Lund T, Peltonen S, Salmela K et
al. Peripheral arterial disease as a predictor of outcome after renal
transplantation. Transplant Int 1998; 11 Suppl 1: S140-S143.
812. Brekke IB, Lien B, S: dal G, Jakobsen A, Bentdal O, Pfeffer P et
al. Aortoiliac reconstruction in preparation for renal transplantation.
Transplant Int 1993; 6: 161–163.
813. Cerilli J, Evans WE, Vaccaro PS. Successful simultaneous renal trans-
plantation and abdominal aortic aneurysmectomy. Arch Surg 1977;
112: 1218–1219.
814. Piquet P, Berland Y, Coulange C, Olmer M, Mercier C, Rampal M.
Aortoiliac reconstruction and renal transplantation: staged or simul-
taneous. Ann Vasc Surg 1989; 3: 251–256.
815. Wright JG, Tesi RJ, Massop DW, Henry ML, Durham JR, Ferguson
RM et al. Safety of simultaneous aortic reconstruction and renal
transplantation. Am J Surg 1991; 162: 126–130.
816. Gouny P, Lenot B, Decaix B, Rondeau E, Kitzis M, Lacave R et al.
Aortoiliac surgery and kidney transplantation. Ann Vasc Surg 1991;
5: 26–31.
817. van der Vliet JA, Naafs DB, van Bockel JH, Kootstra G, Boll AP, Bar-
endregt WB et al. Fate of renal allografts connected to vascular pros-
theses. Clin Sci 1996; 10: 199–202.
818. Mestres CA, Talbot-Wright R, Carretero P. Simultaneous aortorenal
homograft transplantation: expanding the indications for renal and
vascular replacement. Br J Surg 1996; 83: 918.
819. Talbot-Wright R, Mestres CA, Campistol JM, Alcaraz A, Oppenheim-
er F, Carretero P. Simultaneous aortic bifurcation graft and kidney
transplantation from the same multi-organ donor: a new therapeutic
tool in complex renal transplantation. J Urol 1996; 156: 2000–2001.
820. Pittaluga P, Hassen-Khodja R, Cassuto-Viguier E, Batt M, Declemy S,
Bariseel H et al. Aortoiliac reconstruction and kidney transplantation:
a multicenter study. Ann Vasc Surg 1998; 12: 529–36.
821. Flechner SM, Hafez K. Use of a cadaveric donor aorta for vascular
replacement in kidney transplantation. J Urol 1999; 161: 909–910.
822. Levenson JL, Olbrisch ME. Psychosocial evaluation of organ trans-
plant candidates. A comparative survey of process, criteria, and out-
comes in heart, liver, and kidney transplantation. Psychosomatics
1993; 34: 314–323.
823. Sehgal AR, Grey SF, DeOreo PB, Whitehouse PJ. Prevalence, recog-
nition, and implications of mental impairment among hemodialysis
patients. Am J Kidney Dis 1997; 30: 41–49.
88
824. Pliskin NH, Yurk HM, Ho LT, Umans JG. Neurocognitive function in
chronic hemodialysis patients. Kidney Int 1996; 49: 1435–1440.
825. Kramer L, Madl C, Stockenhuber F, Yeganehfar W, Eisenhuber E,
Derfler K et al. Beneficial effect of renal transplantation on cognitive
brain function. Kidney Int 1996; 49: 833–838.
826. Benedetti E, Asolati M, Dunn T, Walczak DA, Papp P, Bartholomew
AM et al. Kidney transplantation in recipients with mental retardation:
clinical results in a single-center experience. Am J Kidney Dis 1998;
31: 509–512.
827. Stuber ML. Psychiatric aspects of organ transplantation in children
and adolescents. Psychosomatics 1993; 34: 379–387.
828. Fielding D, Brownbridge G. Factors related to psychosocial adjust-
ment in children with end-stage renal failure. Pediatr Nephrol 1999;
13: 766–770.
829. Mongeau JG, Clermont MJ, Robitaille P, Plante A, Jequier JC, God-
bout C et al. Study of psychosocial parameters related to the survival
rate of renal transplantation in children. Pediatr Nephrol 1997; 11:
542–546.
830. Mendley SR, Zelko FA. Improvement in specific aspects of neuroc-
ognitive performance in children after renal transplantation. Kidney
Int 1999; 56: 318–323.
831. Baqi N, Tejani A, Sullivan EK. Renal transplantation in Down syn-
drome: a report of the North American Pediatric Renal Transplant
Cooperative Study. Pediatr Transplant 1998; 2: 211–215.
832. RundelL JR, Hall RC. Psychiatric characteristics of consecutively
evaluated outpatient renal transplant candidates and comparisons
with consultation-liaison inpatients. Psychosomatics 1997; 38: 269–
276.
833. Kimmel PL, Peterson RA, Weihs KL, Simmens SJ, Boyle DH, Umana
WO et al. Psychologic functioning, quality of life, and behavioral
compliance in patients beginning hemodialysis. J Am Soc Nephrol
1996; 7: 2152–2159.
834. Kimmel PL, Weihs K, Peterson RA. Survival in hemodialysis patients:
the role of depression. J Am Soc Nephrol 1993; 4: 12–27.
835. Surman OS. Psychiatric aspects of organ transplantation. Am J Psy-
chiatry 1989; 146: 972–982.
836. Surman OS. Hemodialysis and renal transplantation. In: Hackett TP,
Cassem NH, eds. Massachusetts General Hospital Handbook of
General Hospital Psychiatry. Littleton, MA: PSG Publishing; 1991. p.
401–430.
837. Rodin G, Abbey S. Kidney transplantation. In: Craven J, Rodin GM,
eds. Psychiatric Aspects of Organ transplantation. Oxford: Oxford
University Press, 1992: 145–163.
838. Freeman A, Davies L, Webb JW, Craven J. Assessment of transplant
candidates and prediction of outcome. In: Craven J, Rodin GM, eds.
Psychiatric Aspects of Organ transplantation. Oxford: Oxford Univer-
sity Press, 1992: 9–21.
839. DiMartini A, Twillman R. Organ transplantation and paranoid schizo-
phrenia. Psychosomatics 1994; 35: 159–161.
840. Krahn LE, Santoscoy G, Van Loon JA. A schizophrenic patient’s
attempt to resume dialysis following renal transplantation. Psycho-
somatics 1998; 39: 470–473.
841. Greenstein S, Siegal B. Compliance and noncompliance in patients
with a functioning renal transplant : a multicenter study. Transplan-
tation 1998; 66: 1718–1726.
842. de Geest S, Borgermans L, Gemoets H, Abraham I, Vlaminck H,
Evers G et al. Incidence, determinants, and consequences of sub-
clinical noncompliance with immunosuppressive therapy in renal
transplant recipients. Transplantation 1995; 59: 340–347.
843. Hilbrands LB, Hoitsma AJ, Koene RA. Medication compliance after
renal transplantation. Transplantation 1995; 60: 914–920.
844. Butkus DE, Meydrech EF, Raju SS. Racial differences in the survival
of cadaveric renal allografts. Overriding effects of HLA matching and
socioeconomic factors. N Engl J Med 1992; 327: 840–845.
2001; Suppl. 1: Vol. 2: 5–95
 The Evaluation of Renal Transplant Candidates: Clinical Practice Guidelines
845. Kalil RS, Heim-Duthoy KL, Kasiske BL. Patients with a low income
have reduced renal allograft survival. Am J Kidney Dis 1992; 20: 63–
69.
846. Agular LJ. Role of the transplant financial coordinator and its effect
on recipient compliance. Transplant Proc 1979; 55S-57S.
847. Washington AW. Cross-cultural issues in transplant compliance.
Transplant Proc 1999; 31: 27S-28S.
848. Kabler RL, Cerny JC. Pre-transplant urologic investigation and treat-
ment of end stage renal disease. J Urol 1983; 129: 475–478.
849. Shandera K, Sago A, Angstadt J, Peretsman S, Jaffers G. An assess-
ment of the need for the voiding cystourethrogram for urologic
screening prior to renal transplantation. Clin Sci 1993; 7: 299–301.
850. Shandera KC, Rozanski TA, Jaffers G. The necessity of voiding cys-
tourethrogram in the pretransplant urologic evaluation. Urology
1996; 47: 198–200.
851. Glazier DB, Whang MI, Geffner SR, Lyman NW, Friedman GS, Viscu-
so R et al. Evaluation of voiding cystourethrography prior to renal
transplantation. Transplantation 1996; 62: 1762–1765.
852. Yang CC, Rohr MC, Assimos DG. Pretransplant urologic evaluation.
Urology 1994; 43: 169–173.
853. Jefferson RH, Burns JR. Urological evaluation of adult renal trans-
plant recipients. J Urol 1995; 153: 615–618.
854. Martin X, Aboutaieb R, Soliman S, el Essawy A, Dawahra M, LeFran-
cois N. The use of long-term defunctionalized bladder in renal trans-
plantation: is it safe? Eur Urol 1999; 36: 450–453.
855. Nguyen DH, Reinberg Y, Gonzalez R, Fryd D, Najarian JS. Outcome
of renal transplantation after urinary diversion and enterocystoplasty:
a retrospective, controlled study. J Urol 1990; 144: 1349–1351.
856. Serrano DP, Flechner SMMCS, Wyner LM, Novick AC. transplan-
tation into the long-term defunctionalized bladder. J Urol 1996; 156:
885–888.
857. Gill IS, Hayes JM, Hodge EE, Novick AC. Clean intermittent cath-
eterization and urinary diversion in the management of renal trans-
plant recipients with lower urinary tract dysfunction. J Urol 1992;
148: 1397–1400.
858. Flechner SM, Conley SB, Brewer ED, Benson GS. Intermittent clean
catheterization: an alternative to diversion in continent transplant recipi-
ents with lower urinary tract dysfunction. J Urol 1983; 130: 878–881.
859. Shneidman RJ, Pulliam JP, Barry JM. Clean, intermittent self-cath-
eterization in renal transplant recipients. Transplantation 1984; 38:
312–314.
860. Barnett M, Bruskewitz R, Glass N, Sollinger H, Uehling D, Belzer FO.
Long-term clean intermittent self-catheterization in renal transplant
recipients. J Urol 1985; 134: 654–657.
861. Stanley OH, Chambers TL, Pentlow BD. Renal transplantation in
children with occult neurogenic bladders drained by intermittent self
catheterisation. Br Med J Clin Res Ed. 1983; 286: 1775–1776.
862. Mohler JL, Cowen DL, Flanigan RC. Suppression and treatment of
urinary tract infection in patients with an intermittently catheterized
neurogenic bladder. J Urol 1987; 138: 336–340.
863. McInerney PD, Picramenos D, Koffman CG, Mundy AR. Is cystoplas-
ty a safe alternative to urinary diversion in patients requiring renal
transplantation? Eur Urol 1995; 27: 117–120.
864. Yamazaki Y, Tanabe K, Ota T, Ito K, Toma H. Renal transplantation
into augmented bladders. Int J Urol 1998; 5: 423–427.
865. Fontaine E, Gagnadoux MF, Niaudet P, Broyer M, Beurton D. Renal
transplantation in children with augmentation cystoplasty: long- term
results. J Urol 1998; 159: 2110–2113.
866. Abusin K, Rix D, Mohammed M, Bawa SM, Talbot D, Manas D et al.
Long-term adult renal graft outcome after ureteric drainage into an
augmented bladder or ileal conduit. Transplant Int 1998; 11 Suppl
1: S147-S149.
867. Cornejo F, Arango O, Talbot-Wright R, Carretero P, Gil-Vernet JM.
Ileal conduit and orthotopic renal transplantation. An alternative in
2001; Suppl. 1: Vol. 2: 5–95
pathology of the nonviable lower urinary tract. Eur Urol 1988; 14:
77–79.
868. Purohit RS, Bretan PN, Jr. Successful long-term outcome using
existing native cutaneous ureterostomy for renal transplant drainage.
J Urol 2000; 163: 446–449.
869. Garrison RN, Bentley FR, Amin M. Terminal loop cutaneous ureteros-
tomy in cadaveric kidney transplantation. Arch Surg 1989; 124:
467–469.
870. Ahlering TE, Weinberg AC, Razor B. A comparative study of the ileal
conduit, Kock pouch and modified Indiana pouch. Acta Urol Belg
1991; 59: 303–313.
871. Hatch DA, Belitsky P, Barry JM, Novick AC, Taylor RJ, Jordan ML et
al. Fate of renal allografts transplanted in patients with urinary diver-
sion. Transplantation 1993; 56: 838–842.
872. Griffin PJ, Stephenson TP, Brough S, Salaman JR. Transplanting pa-
tients with abnormal lower urinary tracts. Transplant Int 1994; 7:
288–291.
873. Crowe A, Cairns HS, Wood S, Rudge CJ, Woodhouse CR, Neild GH.
Renal transplantation following renal failure due to urological dis-
orders. Nephrol Dial Transplant 1998; 13: 2065–69.
875. Akoh JA, Choon TC, Akyol MA, Kyle K, Briggs JD. Outcome of renal
transplantation in patients with lower urinary tract abnormality. J R
Coll Surg Edinb 1999; 44: 78–81.
876. Warholm C, Berglund J, Andersson J, Tydén G. Renal transplantation
in patients with urinary diversion: a case- control study. Nephrol Dial
Transplant 1999; 14: 2937–2940.
876. Riedmiller H, Gerharz EW, Kohl U, Weingartner K. Continent urinary
diversion in preparation for renal transplantation: a staged approach.
Transplantation 2000; 70: 1713–1717.
877. Spechtenhauser B, Hochleitner BW, Ellemunter H, Simma B, Horm-
ann C, Konigsrainer A et al. Bilateral nephrectomy, peritoneal dialysis
and subsequent cadaveric renal transplantation for treatment of renal
failure due to polycystic kidney disease requiring continuous venti-
lation. Pediatr Transplant 1999; 3: 246–248.
878. Brazda E, Ofner D, Riedmann B, Spechtenhauser B, Margreiter R.
The effect of nephrectomy on the outcome of renal transplantation
in patients with polycystic kidney disease. Ann Transplant 1996; 1:
15–18.
879. Glassman DT, Nipkow L, Bartlett ST, Jacobs SC. Bilateral nephrec-
tomy with concomitant renal graft transplantation for autosomal
dominant polycystic kidney disease. J Urol 2000; 164: 661–664.
880. Knispel HH, Klan R, Offermann G, Miller K. Transplantation in auto-
somal dominant polycystic kidney disease without nephrectomy.
Urol Int 1996; 56: 75–78.
881. Darby CR, Cranston D, Raine AE, Morris PJ. Bilateral nephrectomy
before transplantation: indications, surgical approach, morbidity and
mortality. Br J Surg 1991; 78: 305–307.
882. Erturk E, Burzon DT, Orloff M, Rabinowitz R. Outcome of patients
with vesicoureteral reflux after renal transplantation: the effect of pre-
transplantation surgery on posttransplant urinary tract infections.
Urology 1998; 51: 27–30.
883. Kliem V, Kolditz M, Behrend M, Ehlerding G, Pichlmayr R, Koch KM
et al. Risk of renal cell carcinoma after kidney transplantation. Clin
Sci 1997; 11: 255–258.
884. Slaughenhoupt BL, Lohrasbi FF, Harrison HL, Van Savage JG. Uro-
logic management of congenital nephrotic syndrome of the Finnish
type. Urology 1998; 51: 492–494.
885. Mailloux LU, Levey AS. Hypertension in patients with chronic renal
disease. Am J Kidney Dis 1998; 32: S120-S141.
886. U.S.Renal Data System. USRDS 2000 Annual Data Report. Beth-
esda, MD: National Institutes of Health, National Institute of Dia-
betes, Digestive and Kidney Diseases; 2001.
887. First M, Neylan J, Rocher L, Tejani A. Hypertension after renal trans-
plantation. J Am Soc Nephrol 1994; 4: S30-S36.
89
Kasiske et al.
888. Guidi E, Menghetti D, Milani S, Montagnino G, Palazzi P, Bianchi G.
Hypertension may be transplanted with the kidney in humans: a
long-term historical prospective follow-up of recipients grafted with
kidneys coming from donors with or without hypertension in their
families. J Am Soc Nephrol 1996; 7: 1131–1138.
889. Perez Fontan M, Rodriguez-Carmona A, Garcia Falcon T, Fernandez
Rivera C, Valdes F. Early immunologic and nonimmunologic predic-
tors of arterial hypertension after renal transplantation. Am J Kidney
Dis 1999; 33: 21–28.
890. Frei U, Schindler R, Wieters D, Grouven U, Brunkhorst R, Koch K.
Pre-transplant hypertension: a major risk factor for chronic progress-
ive renal allograft dysfunction? Nephrol Dial Transplant 1995; 10:
1206–1211.
891. Cosio FG, Falkenhain ME, Pesavento T, Henry M, Elkhammas EA,
Davies EA et al. Relationships between arterial hypertension and re-
nal allograft survival in African-American patients. Am J Kidney Dis
1997; 29: 419–427.
892. Cosio FG, Dillon JJ, Falkenhain ME, Tesi RJ, Henry M, Elkhammas EA
et al. Racial differences in renal allograft survival: the role of systemic
hypertension. Kidney Int 1995; 47: 1136–1141.
893. Curtis JJ, Luke RG, Dustan HP, Kashgarian M, Whelchel JD, Jones
P et al. Remission of essential hypertension after renal transplan-
tation. N Engl J Med 1983; 309: 1009–1015.
894. Kasiske BL. Possible causes and consequences of hypertension in
stable renal transplant patients. Transplantation 1987; 44: 639–643.
895. Curtis JJ, Luke RG, Diethelm AG, Whelchel JD, Jones P. Benefits of
removal of native kidneys in hypertension after renal transplantation.
Lancet 1985; 2: 739–742.
896. Curtis JJ, Lucas BA, Kotchen TA, Luke RG. Surgical therapy for per-
sistent hypertension after renal transplantation. Transplantation 1981;
31: 125–128.
897. Midtvedt K, Hartmann A, Bentdal O, Brekke IB, Fauchald P. Bilateral
nephrectomy simultaneously with renal allografting does not allevi-
ate hypertension 3 months following living-donor transplantation.
Nephrol Dial Transplant 1996; 11: 2045–2049.
898. Fornara P, Doehn C, Fricke L, Durek C, Thyssen G, Jocham D. Laparo-
scopic bilateral nephrectomy: results in 11 renal transplant patients.
J Urol 1997; 157: 445–449.
899. Fricke L, Doehn C, Steinhoff J, Sack K, Jocham D, Fornara P. Treat-
ment of posttransplant hypertension by laparoscopic bilateral neph-
rectomy? Transplantation 1998; 65: 1182–1187.
900. Curtis JJ. Management of hypertension after transplantation. Kidney
Int 1993; 44 Suppl 43: 45–49.
901. Kim MS, Stablein D, Harmon WE. Renal transplantation in children
with congenital nephrotic syndrome: a report of the North American
Pediatric Renal Transplant Cooperative Study NAPRTCS. Pediatr
Transplant 1998; 2: 305–308.
902. Holmberg C, Antikainen M, Ronnholm K, Ala HM, Jalanko H. Man-
agement of congenital nephrotic syndrome of the Finnish type. Pedi-
atr Nephrol 1995; 9: 87–93.
903. Olivero JJ, Frommer JP, Gonzalez JM. Medical nephrectomy: the
last resort for intractable complications of the nephrotic syndrome.
Am J Kidney Dis 1993; 21: 260–263.
904. NHLBI Obesity Education Initiative Expert Panel on the Identification,
Evaluation and Treatment of Overweight and Obesity in Adults. Clin-
ical guidelines on the identification, evaluation, and treatment of
overweight and obesity in adults, 1998. Bethesda, MD: National In-
stitutes of Health, National Heart, Lung and Blood Institute; 1998.
905. Calle EA, Thun MJ, Petrelli J, Rodriguez C, Heath Jr C. Body-mass
index and mortality in a prospective cohort of U.S. adults. N Engl J
Med 1999; 341: 1097–1105.
906. Leavey SF, Strawderman R, Jones C, Port F, Held P. Simple nutritional
indicators as independent predictors of mortality in hemodialysis pa-
tients. Am J Kidney Dis 1998; 31: 997–1006.
90
907. Holley J, Monaghan J, Byer B, Bronsther O. An examination of the
renal transplant evaluation process focusing on cost and the reasons
for patient exclusion. Am J Kidney Dis 1998; 32: 567–574.
908. Halme L, Eklund B, Kyllonen L, Salmela K. Is obesity still a risk factor
in renal transplantation? Transplant Int 1997; 10: 284–288.
909. Modlin C, Flechner S, Goormastic M, Goldfarb D, Papajcik D, Mastro-
ianni B et al. Should obese patients lose weight before receiving a
kidney transplant? Transplantation 1997; 64: 599–604.
910. Pirsch JD, Armbrust MJ, Knechtle SJ, D’Alessandro AM, Sollinger
HW, Heisey DM et al. Obesity as a risk factor following renal trans-
plantation. Transplantation 1995; 59: 631–647.
911. Drafts HH, Anjum M, Wynn JJ, Mulloy L, Bowley JN, Humphries A.
The impact of pre-transplant obesity on renal transplant outcomes.
Clin Transplant 1997; 11: 493–496.
912. Holley JL, Shapiro R, Lopatin WB, Tzakis AG, Hakala TR, Starzl TE.
Obesity as a risk factor following cadaveric renal transplantation.
Transplantation 1990; 49: 387–389.
913. Blümke M, Keller E, Eble F, Nausner M, Kirste G. Obesity in kidney
transplant patients as a risk factor. Transplant Proc 1993; 25: 2618.
914. Gill IS, Hodge EE, Novick AC, Steinmuller DR, Garred D. Impact of
obesity on renal transplantation. Transplant Proc 1993; 25: 1047–
1048.
915. Meier-Kriesche HU, Vaghela M, Thambuganipalle R, Friedman G,
Jacobs M, Kaplan B. The effect of body mass index on long-term
renal allograft survival. Transplantation 1999; 68: 1294–1297.
916. Bumgardner GL, Henry M, Elkhammas E, Wilson G, Tso P, Davies E
et al. Obesity as a risk factor after combined pancreas/kidney trans-
plantation. Transplantation 1995; 60: 1426–1430.
917. Friedman E. Management choices in diabetic end-stage renal dis-
ease. Nephrol Dial Transplant 1995; 10: 61–69.
918. Port F, Wolfe RA, Mauger EA, Berling D, Jiang K. Comparison of
survival probabilities for dialysis patients vs cadaveric renal transplant
recipients. JAMA 1993; 270: 1339–1343.
919. Sutherland D. Pancreas and pancreas-kidney transplantation. Curr
Opin Nephrol Hypertens 1998; 7: 317–325.
920. American Diabetes Association. Pancreas transplantation for patients
with type 1 diabetes. Diabetes Care 2000; 23: 117.
921. Kiebert GM, van Oosterhout EC, van Bronswijk H, Lemkes HH,
Gooszen HG. Quality of life after combined kidney-pancreas or kid-
ney transplantation in diabetic patients with end-stage renal disease.
Clin Transplant 1994; 8: 239–245.
922. Gross CR, Limwattananon C, Matthees B, Zehrer JL, Savik K. Impact
of transplantation on quality of life in patients with diabetes and renal
dysfunction. Transplantation 2000; 70: 1736–1746.
923. The Diabetes Control and Complications Trial Research Group. The
effect of intensive treatment of diabetes on the development and
progression of long-term complications in insulin-dependent dia-
betes mellitus. N Engl J Med 1993; 329: 977–986.
924. Gruessner AC, Sutherland DER. Analysis of United States US. and
non-US pancreas transplants as reported to the International Pan-
creas Transplant Registry IPTR. and to the United Network for Organ
Sharing UNOS. In: Cecka JM, Terasaki PI, eds. Clinical transplants
1998. Los Angeles, CA: UCLA Tissue Typing Laboratory, 1998: 53–
71.
925. Smets YF, Westendorp RG, van der Pijl JW, de Charro FT, Ringers J,
de Fijter JW et al. Effect of simultaneous pancreas-kidney transplan-
tation on mortality of patients with type-1 diabetes mellitus and end-
stage renal failure. Lancet 1999; 353: 1915–1919.
926. Becker BN, Brazy PC, Becker YT, Odorico JS, Pintar TJ, Collins BH
et al. Simultaneous pancreas-kidney transplantation reduces excess
mortality in type 1 diabetic patients with end-stage renal disease.
Kidney Int 2000; 57: 2129–2135.
927. Ojo AO, Meier-Kriesche HU, Hanson JA, Leichtman A, Magee JC,
Cibrik D et al. The impact of simultaneous pancreas-kidney trans-
2001; Suppl. 1: Vol. 2: 5–95
 The Evaluation of Renal Transplant Candidates: Clinical Practice Guidelines
plantation on long-term patient survival. Transplantation 2001; 71:
82–90.
928. Barbosa J, Steffes M, Sutherland D, Connett J, Rao K, Mauer SM.
Effect of glycemic control on early diabetic renal lesions: a 5-year
randomized controlled clinical trial of insulin-dependent diabetic kid-
ney transplant recipients. JAMA 1994; 272: 600–606.
929. Fioretto P, Steffes M, Sutherland D, Goetz F, Mauer M. Reversal of
lesions of diabetic nephropathy after pancreas transplantation. N
Engl J Med 1998; 339: 69–75.
930. Mauer SM, Steffes MW, Connett J, Najarian JS, Sutherland DE, Bar-
bosa J. The development of lesions in the glomerular basement
membrane and mesangium after transplantation of normal kidneys
to diabetic patients. Diabetes 1983; 32: 948–952.
931. Hariharan S, Smith R, Viero R, First M. Diabetic nephropathy after
renal transplantation. Clinical and pathologic features. Transplan-
tation 1996; 62: 632–635.
932. Mauer SM, Barbosa J, Vernier RL, Kjellstrand CM, Buselmeier TJ,
Simmons RL et al. Development of diabetic vascular lesions in nor-
mal kidneys transplanted into patients with diabetes mellitus. N Engl
J Med 1976; 295: 916–920.
933. Lundgren G, Wilczek H, Bohman SO, Jaremko G, Groth CG. Develop-
ment of diabetic nephropathy in renal allografts of diabetic patients.
Transplant Proc 1985; 17: 18–20.
934. Najarian JS, Kaufman DB, Fryd DS, McHugh L, Mauer SM, Ramsay
RC et al. Long-term survival following kidney transplantation in 100
type I diabetic patients. Transplantation 1989; 47: 106–113.
935. Bilous RW, Mauer SM, Sutherland DER, Najarian JS, Goetz FC, Steff-
es MW. The effect of pancreas transplantation on the glomerular
structure of renal allografts in patients with insulin-dependent dia-
betes. N Engl J Med 1989; 321: 80–85.
936. Wilczek H, Jaremko C, Tydén G, Groth C. Evolution of diabetic neph-
ropathy in kidney grafts: evidence that a simultaneously transplanted
pancreas exerts a protective effect. Transplantation 1995; 59: 51–
57.
937. Ramsey RC, Goetz FC, Sutherland DER, Mauer SM, Robison LL, Can-
trill HL et al. Progression of diabetic retinopathy after pancreas trans-
plantation for insulin-dependent diabetes mellitus. N Engl J Med
1988; 318: 208–214.
938. Wang Q, Klein R, Moss S, Klein B, Hoyer C, Burke K et al. The influ-
ence of combined kidney-pancreas transplantation on the pro-
gression of diabetic retinopathy. A case series. Ophthalmology 1994;
101: 1071–1076.
939. Pearce IA, Ilango B, Sells RA, Wong D. Stabilisation of diabetic retino-
pathy following simultaneous pancreas and kidney transplant . Br J
Ophthalmol 2000; 84: 736–740.
940. Cheung ATW, Perez R, Chen P. Improvements in diabetic microangi-
opathy after successful simultaneous pancreas-kidney transplan-
tation: a computer-assisted intravital microscopy study on the con-
junctival microcirculation. Transplantation 1999; 68: 927–932.
941. Landgraf R, Nusser J, Müller W, Landgraf-Leurs MC, Thurau S, Ulbig
M et al. Fate of late complications in type I diabetic patients after
successful pancreas-kidney transplantation. Diabetes 1989; 38
Suppl 1: 33–37.
942. Kennedy WR, Navarro X, Goetz FC, Sutherland DER, Najarian JS.
Effects of pancreatic transplantation on diabetic neuropathy. N Engl
J Med 1990; 322: 1031–1037.
943. Allen R, Al-Harbi I, Morris J, Clouston PD, O’Connell P, Chapman JR
et al. Diabetic neuropathy after pancreas transplantation: determi-
nants of recovery. Transplantation 1997; 63: 830–838.
944. Navarro X, Sutherland D, Kennedy W. Long-term effects of pancre-
atic transplantation on diabetic neuropathy. Ann Neur 1997; 42:
727–736.
945. Solders G, Wilczek H, Gunnarsson R, Tydén G, Persson A, Groth C-G.
Effects of combined pancreatic and renal transplantation on diabetic
2001; Suppl. 1: Vol. 2: 5–95
neuropathy: a two-year follow-up study. Lancet 1987; 2: 1232–
1235.
946. Morrissey P, Shaffer D, Monaco A, Conway P, Madras PN. Peripheral
vascular disease after kidney-pancreas transplantation in diabetic
patients with end-stage renal disease. Arch Surg 1997; 132: 358–
361.
947. Biesenbach G, Margreiter R, Konigsrainer A, Bosmuller C, Janko O,
Brucke P et al. Comparison of progression of macrovascular diseases
after kidney or pancreas and kidney transplantation in diabetic pa-
tients with end-stage renal disease. Diabetologia 2000; 43: 231–
234.
948. Schaapherder AF, de Roos A, Shaw PC, van der Woude FJ, Lemkes
HH, Gooszen HG. The role of early baseline computed tomography
in the interpretation of morphological changes after kidney-pancreas
transplantation. Transplant Int 1993; 6: 270–276.
949. Remuzzi G, Ruggenenti P, Mauer SM. Pancreas and kidney/pancreas
transplants: experimental medicine or renal improvement? Lancet
1994; 343: 27–31.
950. Rosen C, Frohnert P, Velosa JA, Engen DE, Sterioff S. Morbidity of
pancreas transplantation during cadaveric renal transplantation.
Transplantation 1991; 51: 123–127.
951. Gruessner RW, Sutherland DE, Troppman C, Benedetti E, Hakim N,
Dunn DL et al. The surgical risk of pancreas transplantation in the
cyclosporine era: an overview. J Am Coll Surg 1997; 185: 128–144.
952. Cheung AHS, Sutherland DER, Gullingham KJ, McHugh LE, Moudry-
Munns KC, Dunn DL et al. Simultaneous pancreas-kidney transplant
versus kidney transplant alone in diabetic patients. Kidney Int 1992;
41: 924–29.
953. Douzdjian V, Abecassis MM, Corry RJ, Hunsicker LG. Simultaneous
pancreas-kidney versus kidney-alone transplants in diabetics: in-
creased risk of early cardiac death and acute rejection following pan-
creas transplants. Clin Sci 1994; 8: 246–251.
954. Hricik DE, Phinney MS, Weigel KA, Knauss TC, Schulak JA. Long-
term renal function in type I diabetics after kidney or kidney-pan-
creas transplantation: influence of number, timing, and treatment of
acute rejection episodes. Transplantation 1997; 64: 1283–1288.
955. Rayhill SC, D’Alessandro AM, Odorico JS, Knechtle SJ, Pirsch JD,
Heisey DM et al. Simultaneous pancreas-kidney transplantation and
living related donor renal transplantation in patients with diabetes: is
there a difference in survival? Ann Surg 2000; 231: 417–423.
956. Cantarovich D, Karam G, Giral-Classe M, Hourmant M, Dantal J,
Blancho G et al. Randomized comparison of triple therapy and anti-
thymocyte globulin induction treatment after simultaneous pan-
creas-kidney transplantation. Kidney Int 1998; 54: 1351–1356.
957. Peddi VR, Kamath S, Munda R, Demmy AM, Alexander JW. First MR.
Use of tacrolimus eliminates acute rejection as a major complication
following simultaneous kidney and pancreas transplantation. Clin
Transplant 1998; 12: 401–405.
958. Adang E, Engel GL, van Hooff J, Kootstra G. Comparison before and
after transplantation of pancreas-kidney and pancreas-kidney with
loss of pancreas: a prospective controlled quality of life study. Trans-
plantation 1996; 62: 754–758.
959. Sakhaee K, Gonzalez G. Update on renal osteodystrophy: patho-
genesis and clinical management. Am J Med 1999; 317: 251–260.
960. Massari P. Disorders of bone and mineral metabolism after renal
transplantation. Kidney Int 1997; 52: 1412–1421.
961. Dumoulin G, Hory B, Nguyen N, Bresson C, Fournier V, Bouhaddi M
et al. No trend toward a spontaneous improvement of hyperpara-
thyroidism and high bone turnover in normocalcemic long-term renal
transplant recipients. Am J Kidney Dis 1997; 29: 746–753.
962. Torres A, Rodriguez AP, Concepcion MT, Garcia S, Rufino M, Martin
B et al. Parathyroid function in long-term renal transplant patients:
importance of pre-transplant PTH concentrations. Nephrol Dial
Transplant 1998; 13 Suppl 3: 94–97.
91
Kasiske et al.
963. Tajima A, Ishikawa N, Ohta N, Suzuki K, Kawabe K, Aso Y. Parathyroid
function after kidney allografting. Transplant Proc 1996; 28: 1629–
1630.
964. Garvin P, Castaneda M, Linderer R, Dickhans M. Management of
hypercalcemic hyperparathyroidism after renal transplantation. Arch
Surg 1985; 120: 578–583.
965. Nogueira PC, Rey N, Said MH, Cochat P. Evolution of hyperpara-
thyroidism after renal transplantation in children–effect of pre-
emptive transplantation and duration of dialysis. Nephrol Dial Trans-
plant 1997; 12: 984–987.
966. Cundy T, Kanis J, Heynen G, Morris P, Oliver D. Calcium metabolism
and hyperparathyroidism after renal transplantation. Q J Med 1983;
52: 67–78.
967. D’Alessandro AM, Sollinger H, Kalayoglu M, Vernon W, Belzer F,
Starling J. Tertiary hyperparathyroidism after renal transplantation:
operative indications. Surgery 1989; 106: 1049–1056.
968. Wenzel Seifert K, Harwig S, Keller F. Fulminant calcinosis in two pa-
tients after kidney transplantation. Am J Nephrol 1991; 11: 497–
500.
969. Rault R, Carpenter B. Pseudoclubbing in chronic renal failure. Q J
Med 1989; 73: 1063–1069.
970. Beleva B, Filev A, Donovski L, Kumanov Kh, Todorov T. [A case of
tertiary hyperparathyroidism following kidney transplantation compli-
cated by lithiasis]. Khirurgiia 1990; 43: 100–102.
971. Vlcek J, Binswanger U, Keusch G, Záruba J. Hyperparathyroidism
after kidney transplantation: a retrospective case controlled study.
Klin Wochenschr 1991; 69: 669–673.
972. Zeidan B, Shabtai M, Waltzer WC, Wadhwa NK, Siddarth P, Rapaport
FT. Improvement in renal transplant function after subtotal parathyro-
idectomy in a hypercalcemic kidney allograft recipient. Transplant
Proc 1991; 23: 2285–2286.
973. Dotzenrath C, Goretzki PE, Roher HD. Operative Therapie des se-
kundären Hyperparathyreoidismus nach Nierentransplantation. Lan-
genbecks Arch Chir 1993; 378: 121–124.
974. Cruzado JM, Gonzalez MT, Gil-Vernet S, Seron D, Castelao AM,
Andres E et al. Secondary hyperparathyroidism and acute ischemic
posttransplant renal failure. Transplant Proc 1995; 27: 2264–2265.
975. Rostaing L, Moreau-Gaudry X, Baron E, Cisterne JM, Bernadet-Mon-
rozies P, Durand D. Changes in blood pressure and renal function
after subtotal parathyroidectomy in renal transplant patients present-
ing persistent hypercalcemic hyperparathyroidism. Transplant Proc
1997; 29: 204–6.
976. Dahl E, Nordal KP, Halse J, Flatmark A. Pretransplant parathyroidec-
tomy in renal failure: effects on bone histology and aluminum de-
posits during dialysis and after kidney transplantation. Scand J Urol
Nephrol 1992; 26: 283–288.
977. Ittel T, Schmitt H, Sieberth H-G. Hyperparathyroidism and bone loss
in renal graft recipients. Kidney Blood Press Res 1997; 20: 157–162.
978. Koonsman M, Hughes K, Dickerman R, Brinker K, Dunn E. Parathyro-
idectomy in chronic renal failure. Am J Surg 1994; 168: 631–635.
979. Punch J, Thompson NW, Merion R. Subtotal parathyroidectomy in
dialysis-dependent and post-renal transplant patients. Arch Surg
1995; 130: 538–543.
980. Kilgo M, Pirsch J, Warner T, Starling J. Tertiary hyperparathyroidism
after renal transplantation: surgical strategy. Surgery 1998; 124:
677–684.
981. Stracke S, Jehle P, Sturm D, Schoenberg M, Widmaier U, Beger H
et al. Clinical course after total parathyroidectomy without autotrans-
plantation in patients with end-stage renal failure. Am J Kidney Dis
1999; 33: 304–311.
982. Tominaga Y, Uchida K, Sato K, Numano M, Tanaka Y, Takagi H. Para-
thyroidectomy before and after renal transplantation. Transplant Proc
1992; 24: 1861–1862.
983. Higgins RM, Richardson AJ, Ratcliffe PJ, Woods CG, Oliver DO, Mor-
92
ris PJ. Total parathyroidectomy alone or with autograft for renal
hyperparathyroidism? Q J Med 1991; 79: 323–332.
984. Penny MJ, Nankivell BJ, Disney AP, Byth K, Chapman JR. Renal
graft thrombosis. A survey of 134 consecutive cases. Transplan-
tation 1994; 58: 565–569.
985. Harmon WE, Stablein D, Alexander SR, Tejani A. Graft thrombosis
in pediatric renal transplant recipients. A report of the North Ameri-
canPediatric Renal Transplant Cooperative Study. Transplantation
1991; 51: 406–412.
986. Singh A, Stablein D, Tejani A. Risk factors for vascular thrombosis
in pediatric renal transplantation: a special report of the North
American Pediatric Renal Transplant Cooperative Study. Transplan-
tation 1997; 63: 1263–1267.
987. Ismail H, Kalicinski P, Drewniak T, Smirska E, Kaminski A, Prokurat
A et al. Primary vascular thrombosis after renal transplantation in
children. Pediatr Transplant 1997; 1: 43–47.
988. van der Vliet JA, Barendregt WB, Hoitsma AJ, Buskens FG. In-
creased incidence of renal allograft thrombosis after continuous
ambulatory peritoneal dialysis. Clin Transplant 1996; 10: 51–54.
989. Bakir N, Sluiter WJ, Ploeg RJ, van Son WJ, Tegzess AM. Primary
renal graft thrombosis. Nephrol Dial Transplant 1996; 11: 140–147.
990. van Lieburg AF, de Jong MC, Hoitsma AJ, Buskens FG, Schroder
CH, Monnens LA. Renal transplant thrombosis in children. J Pediatr
Surg 1995; 30: 615–619.
991. Wagenknecht DR, Becker DG, LeFor WM, McIntyre JA. Antiphos-
pholipid antibodies are a risk factor for early renal allograft failure.
Transplantation 1999; 68: 241–246.
992. Stone JH, Amend WJ, Criswell LA. Antiphospholipid antibody syn-
drome in renal transplantation: occurrence of clinical events in 96
consecutive patients with systemic lupus erythematosus. Am J Kid-
ney Dis 1999; 34: 1040–1047.
993. Radhakrishnan J, Williams GS, Appel GB, Cohen DJ. Renal trans-
plantation in anticardiolipin antibody-positive lupus erythematosus
patients. Am J Kidney Dis 1994; 23: 286–289.
994. Ducloux D, Pellet E, Fournier V, Rebibou JM, Bresson-Vautrin C,
Racadot E et al. Prevalence and clinical significance of antiphos-
pholipid antibodies in renal transplant recipients. Transplantation
1999; 67: 90–93.
995. Baid S. Renal thrombotic microangiopathy associated with anti-
cardiolipin antibodies in hepatitis C-positive renal allograft recipi-
ents. J Am Soc Nephrol 1999; 10: 146–153.
996. Knight RJ, Schanzer H, Rand JH, Burrows L. Renal allograft throm-
bosis associated with the antiphospholipid antibody syndrome.
Transplantation 1995; 60: 614–615.
997. Vaidya S, Wang CC, Gugliuzza C, Fish JC. Relative risk of post-
transplant renal thrombosis in patients with antiphospholipid anti-
bodies. Clin Transplant 1998; 12: 439–444.
998. Vaidya S, Sellers R, Kimball P, Shanahan T, Gitomer J, Gugliuzza K
et al. Frequency, potential risk and therapeutic intervention in end-
stage renal disease patients with antiphospholipid antibody syn-
drome: a multicenter study. Transplantation 2000; 69: 1348–1352.
999. Irish AB, Green FR, Gray DW, Morris PJ. The factor V Leiden R506Q.
mutation and risk of thrombosis in renal transplant recipients.
Transplantation 1997; 64: 604–607.
1000. Guirguis N, Budisavljevic MN, Self S, Rajagopalan PR, Lazarchick J.
Acute renal artery and vein thrombosis after renal transplant, as-
sociated with a short partial thromboplastin time and factor V Leid-
en mutation. Ann Clin Lab Sci 2000; 30: 75–78.
1001. Oh J, Schaefer F, Veldmann A, Nowak G, Nowak-Gottl U, Tonshoff B
et al. Heterozygous prothrombin gene mutation: a new risk factor for
early renal allograft thrombosis. Transplantation 1999; 68: 575–78.
1002. Koester BH, Koveker GB, Potsch B, Becker HD. [Hereditary throm-
bophilia as a cause of recurrent transplant thromboses]. Chirurg
1993; 64: 809–812.
2001; Suppl. 1: Vol. 2: 5–95
 The Evaluation of Renal Transplant Candidates: Clinical Practice Guidelines
1003. Higgins RM, Gray DW, Morris PJ. Association of thrombosis after
renal transplantation with elevation of the platelet count. Transplan-
tation 1995; 59: 1353–1355.
1004. Fischereder M, Gohring P, Schneeberger H, Lohse P, Von Appen K,
Samtleben W et al. Early loss of renal transplants in patients with
thrombophilia. Transplantation 1998; 65: 936–939.
1005. Jones CL, Andrew M, Eddy A, O’Neil M, Shalom NI, Balfe JW.
Coagulation abnormalities in chronic peritoneal dialysis. Pediatr
Nephrol 1990; 4: 152–155.
1006. Ray JG. Meta-analysis of hyperhomocysteinemia as a risk factor
for venous thromboembolic disease. Arch Intern Med 1998; 158:
2101–2106.
1007. den Heijer M, Rosendaal FR, Blom HJ, Gerrits WB, Bos GM. Hyper-
homocysteinemia and venous thrombosis: a meta-analysis.
Thromb Haemost 1998; 80: 874–877.
1008. Langman LJ, Ray JG, Evrovski J, Yeo E, Cole DE. Hyperhomocys-
teinemia and the increased risk of venous thromboembolism: more
evidence from a case-control study. Arch Intern Med 2000; 160:
961–964.
1009. Gemmati D, Serino ML, Trivellato C, Fiorini S, Scapoli GL. C677T
substitution in the methylenetetrahydrofolate reductase gene as a
risk factor for venous thrombosis and arterial disease in selected
patients. Haematologica 1999; 84: 824–828.
1010. Koch HG, Nabel P, Junker R, Auberger K, Schobess R, Homberger
A et al. The 677T genotype of the common MTHFR thermolabile
variant and fasting homocysteine in childhood venous thrombosis.
Eur J Pediatr 1999; 158 Suppl 3: S113–S116.
1011. Fujimura H, Kawasaki T, Sakata T, Ariyoshi H, Kato H, Monden M et
al. Common C677T polymorphism in the methylenetetrahydrofolate
reductase gene increases the risk for deep vein thrombosis in pa-
tients with predisposition of thrombophilia. Thromb Res 2000; 98:
1–8.
1012. Schroder CH, de Boer AW, Giesen AM, Monnens LA, Blom H.
Treatment of hyperhomocysteinemia in children on dialysis by folic
acid. Pediatr Nephrol 1999; 13: 583–585.
1013. Jungers P, Joly D, Massy Z, Chauveau P, Nguyen AT, Aupetit J et
al. Sustained reduction of hyperhomocysteinaemia with folic acid
supplementation in predialysis patients. Nephrol Dial Transplant
1999; 14: 2903–2906.
1014. Touam M, Zingraff J, Jungers P, Chadefaux-Vekemans B, Drueke T,
Massy ZA. Effective correction of hyperhomocysteinemia in hemo-
dialysis patients by intravenous folinic acid and pyridoxine therapy.
Kidney Int 1999; 56: 2292–2296.
1015. Luke RG, Beck LH. Gerontologizing nephrology. J Am Soc Nephrol
1999; 10: 1824–1827.
1016. 1998 Annual Report of the U.S. Scientific Registry for Transplant
Recipients and the Organ Procurement and Transplantation Net-
work: Transplant Data: 1988–1997. U.S. Department of Health and
Human Services, Health Resources and Services Administration,
Office of Special Programs, Division of Transplantation, Rockville,
MD, UNOS, Richmond, VA; 1998.
1017. Schaubel D, Desmeules M, Mao Y, Jeffery J, Fenton S. Survival
experience among elderly end-stage renal disease patients: a con-
trolled comparison of transplantation and dialysis. Transplantation
1995; 60: 1389–1394.
1018. Johnson DW, Herzig K, Purdie D, Brown A, Rigby R, Nicol D et al.
A comparison of the effects of dialysis and renal transplantation on
the survival of older uremic patients. Transplantation 2000; 69:
794–799.
1019. Roodnat J, Mulder P, Rischen-Vos J, van Gelder T, IJzermans J,
Weimar W. The vanishing importance of age in renal transplan-
tation. Transplantation 1999; 67: 576–580.
1020. Tesi RJ, Elkhammas EA, Davies EA, Henry M, Ferguson R. Renal
transplantation in older people. Lancet 1994; 343: 461–464.
2001; Suppl. 1: Vol. 2: 5–95
1021. Ismail N, Hakim RM, Helderman JH. Renal replacement therapies
in the elderly: Part II. Renal transplantation. Am J Kidney Dis 1994;
23: 1–15.
1022. Berthou F, Jones E, Mehls O, Valderrabano F. Transplantation Re-
port 1: renal transplantation in recipients aged 60 years or older at
time of grafting. Nephrol Dial Transplant 1996; 11: 37–40.
1023. Meier-Kriesche HU, Ojo A, Hanson J, Cibrik D, Lake K, Agodoa
LY et al. Increased immunosuppressive vulnerability in elderly renal
transplant recipients. Transplantation 2000; 69: 885–889.
1024. Benedetti E, Matas AJ, Hakim N, Fasola C, Gillingham K, McHugh
L et al. Renal transplantation for patients 60 years of age or
older: a single-institution experience. Ann Surg 1994; 220: 445–
460.
1025. Xenos EX, Ciancio G, Burke GW, Roth D, Miller J. The use of tacrol-
imus as induction and maintenance immunosuppression in renal
cadaveric transplant recipients over the age of 60. Clin Transplant
1997; 11: 497–499.
1026. Lake K, Canafax DM. Important interactions of drugs with immuno-
suppressive agents used in transplant recipients. J Antimicrob
Chemother 1995; 36: 11–22.
1027. Yasumura T, Oka T, Aikawa I, Arakawa K, Ohmori Y, Nakane Y.
Beneficial effect of bilateral native nephrectomy on long-term sur-
vival of living related kidney allografts. Transplant Proc 1989; 21:
1967–1969.
1028. Wadhwa NK, Schroeder TJ, Pesce AJ, Myre SA, Clardy CW, First
MR. Cyclosporine drug interactions: a review. Ther Drug Monit
1987; 9: 399–406.
1029. Cockburn ITR, Krupp P. An appraisal of drug interactions with Sand-
immun. Transplant Proc 1989; 21: 3845–3850.
1030. Lake KD. Management of drug interactions with cyclosporine.
Pharmacotherapy 1991; 11: 110S–8S.
1031. Mignat C. Clinically significant drug interactions with new immuno-
suppressive agents. Drug Safety 1997; 16: 267–278.
1032. Chocair P, Duley J, Simmonds HA, Cameron JS, Ianhez L, Arap S et
al. Low-dose allopurinol plus azathioprine/cyclosporin/prednisolone,
a novel immunosuppressive regimen. Lancet 1993; 342: 83–84.
1033. Venkat Raman G, Sharman VL, Lee HA. Azathioprine and allopurin-
ol: a potentially dangerous combination. J Intern Med 1990; 228:
69–71.
1034. Nelson PW, Landreneau MD, Luger AM, Pierce GE, Ross G, Shield
CF, III et al. Ten-year experience in transplantation of A2 kidneys
into B and O recipients. Transplantation 1998; 65: 256–260.
1035. Osorio AV, Sullivan EK, Alexander SR, Bryan CF, Shield CF, Warady
BA. ABO-mismatched renal transplantation in children: a report of
the North American Pediatric Renal Transplant Cooperative Study
NAPRTCS. and the Midwest Organ Bank MOB. Pediatr Transplant
1998; 2: 26–29.
1036. Alkhunaizi AM, de Mattos AM, Barry JM, Bennett WM, Norman
DJ. Renal transplantation across the ABO barrier using A2 kidneys.
Transplantation 1999; 67: 1319–24.
1037. Yamazaki Y, Kawaguchi H, Ito K, Takahashi K, Toma H, Ota K. ABO
incompatible kidney transplantation in children. J Urol 1995; 154:
914–916.
1038. Tanabe K, Takahashi K, Sonda K, Tokumoto T, Ishikawa N, Kawai T
et al. Long-term results of ABO-incompatible living kidney trans-
plantation: a single-center experience. Transplantation 1998; 65:
224–228.
1039. Ishikawa A, Itoh M, Ushlyama T, Suzuki K, Fujita K. Experience of
ABO-incompatible living kidney transplantation after double fil-
tration plasmapheresis. Clin Sci 1998; 12: 80–83.
1040. Tamaki T, Tanaka M, Katori M, Osanai M, Yasuhara M, Meguro J
et al. Cryofiltration apheresis for major ABO-incompatible kidney
transplantation. Ther Apher 1998; 2: 308–310.
1041. Ohta T, Kawaguchi H, Hattori M, Takahashi K, Nagafuchi H, Akioka
93
Kasiske et al.
Y et al. ABO-incompatible pediatric kidney transplantation in a
single-center trial. Pediatr Nephrol 2000; 14: 1–5.
1042. Ishida H, Koyama I, Sawada T, Utsumi K, Murakami T, Sannomiya
A et al. Anti-AB titer changes in patients with ABO incompatibility
after living-related kidney transplantations: survey of 101 cases to
determine whether splenectomies are necessary for successful
transplantation. Transplantation 2000; 70: 681–685.
1043. Opelz G, Mytilineos J, Scherer S, Dunckley H, Trejaut J, Chapman
J et al. Analysis of HLA-DR matching in DNA-typed cadaver kidney
transplants. Transplantation 1993; 55: 782–785.
1044. Mytilineos J, Scherer S, Dunckley H, Trejaut J, Chapman J, Fischer
G et al. DNA HLA-DR typing results of 4000 kidney transplants.
Transplantation 1993; 55: 778–781.
1045. Ting A, Welsh K. HLA Matching and Crossmatching in Renal trans-
plantation. In: Morris PJ, ed. Kidney transplantation: Principles and
Practice. 4th edn. Philadelphia: W.B. Saunders Company; 1994. p.
109–126.
1046. Edwards EB, Bennett LE, Cecka JM. Effect of HLA matching on
the relative risk of mortality for kidney recipients: a comparison of
the mortality risk after transplant to the mortality risk of remaining
on the waiting list. Transplantation 1997; 64: 1274–1277.
1047. Opelz G. Impact of HLA compatibility on survival of kidney trans-
plants from unrelated live donors. Transplantation 1997; 64: 1473–
1475.
1048. McKenna RM, Lee KR, Gough JC, Jeffery JR, Grimm PC, Rush DN
et al. Matching for private or public HLA epitopes reduces acute
rejection episodes and improves two-year renal allograft function.
Transplantation 1998; 66: 38–43.
1049. Reisaeter AV, Leivestad T, Vartdal F, Spurkland A, Fauchald P, Brek-
ke IB et al. A strong impact of matching for a limited number of
HLA-DR antigens on graft survival and rejection episodes: a single-
center study of first cadaveric kidneys to nonsensitized recipients.
Transplantation 1998; 66: 523–528.
1050. Cecka JM. The UNOS Scientific Renal Transplant Registry. Clin
Transplant 1998; 1–16.
1051. Morris PJ, Johnson RJ, Fuggle SV, Belger MA, Briggs JD. Analysis
of factors that affect outcome of primary cadaveric renal transplan-
tation in the UK. HLA Task Force of the Kidney Advisory Group of
the United Kingdom Transplant Support Service Authority UKTSSA.
Lancet 1999; 354: 1147–1152.
1052. Schnitzler MA, Hollenbeak CS, Cohen DS, Woodward RS, Lowell
JA, Singer GG et al. The economic implications of HLA matching
in cadaveric renal transplantation. N Engl J Med 1999; 341: 1440–
1446.
1053. Sijpkens YW, Doxiadis II, de Fijter JW, Mallat MJ, van Es LA, de
Lange P et al. Sharing cross-reactive groups of MHC class I im-
proves long-term graft survival. Kidney Int 1999; 56: 1920–1927.
1054. Milford EL. HLA molecular typing. Curr Opin Nephrol Hypertens
1993; 2: 892–897.
1055. Mytilineos J, Christ U, Lempert M, Opelz G. Comparison of typing
results by serology and polymerase chain reaction with sequence-
specific primers for HLA-Cw in 650 individuals. Tissue Antigens
1997; 50: 395–400.
1056. Mytilineos J, Lempert M, Scherer S, Schwarz V, Opelz G. Compari-
son of serological and DNA PCR-SSP typing results for HLA-A and
HLA-B in 421 Black individuals: a Collaborative Transplant Study
report. Hum Immunol 1998; 59: 512–517.
1057. Sanfilippo F, Vaughn WK, Bollinger RR, Spees EK. Comparative ef-
fects of pregnancy, transfusion and prior graft rejection on sensit-
ization and renal transplant results. Transplantation 1982; 34: 360–
364.
1058. Barger BO, Shroyer TW, Hudson SL, Deierhoi MH, Barber WH,
Curtis JJ et al. Early graft loss in cyclosporine A-treated cadaveric
renal allograft recipients receiving retransplants against previous
94
mismatched HLA-A, -B, -DR donor antigens. Transplant Proc 1988;
20: 170–172.
1059. Kerman RH, van Buren CT, Lewis RM, DeVera V, Baghdahsarian V,
Gerolami K et al. Improved graft survival for flow cytometry and
antihuman globulin crossmatch-negative retransplant recipients.
Transplantation 1990; 49: 52–56.
1060. Povlsen JV, Madsen M, Birkeland SA, Lokkegaard H, Pedersen EB,
Svejgaard A et al. The impact of repeated HLA mismatches on the
outcome of renal allograft retransplantation. Transplant Proc 1992;
24: 307–308.
1061. Gaston RS, Shroyer TW, Hudson SW, Deierhoi MH, Laskow DA,
Barber WH et al. Renal retransplantation: the role of race, quadru-
ple immunosuppression, and the flow cytometry crossmatch.
Transplantation 1994; 57: 47–54.
1062. Cecka JM, Terasaki PI. Repeating HLA antigen mismatches in renal
retransplants – a second class mistake? Transplantation 1994; 57:
515–519.
1063. Thompson J, Thacker L, Takemoto S. CREG matching for first kid-
ney transplants performed by SEOPF Centers between October
1987 and September 1995: an analysis of outcome and prospec-
tive benefit. Southeastern Procurement Foundation. Transplant Proc
1997; 29: 1435–1438.
1064. Takemoto SK, Cecka JM, Terasaki PI. Benefits of HLA-CREG
matching for sensitized recipients as illustrated in kidney regrafts.
Transplant Proc 1997; 29: 1417.
1065. Stobbe I, Meer-Prins EM, de Lange P, Oudshoorn M, De Meester
J, Doxiadis II et al. Cross-reactive group matching does not lead to
a better allocation and survival of donor kidneys. Transplantation
2000; 70: 157–161.
1066. Sumitran-Karuppan S, Tydén G, Reinholt F, Berg U, Moller E.
Hyperacute rejections of two consecutive renal allografts and early
loss of the third transplant caused by non-HLA antibodies specific
for endothelial cells. Transplant Immunol 1997; 5: 321–327.
1067. Halloran PF, Lui SL, Miller LW. Review of transplantation-1996. In:
Cecka JM, Terasaki PI, eds. Clinical transplants 1996. Los Angeles:
UCLA Tissue Typing Laboratory, 1997: 291–319.
1068. Terasaki PI, Thrasher DL, Hauber TH. Serotyping for homotrans-
plantation: XIII. Immediate kidney rejection and associated pre-
formed antibodies. In: Dausset J, Hamburger J, Mathe G, eds.
Advances in transplantation. Copenhagen: Munksgaard, 1968:
225–229.
1069. Amos DB, Bashir H, Boyle W, MacQueen M, Tiilikainen A. A simple
microcytotoxicity test. Transplantation 1969; 7: 220–223.
1070. Johnson AH, Rossen RD, Butler WT. Detection of alloantibodies
using a sensitive antiglobulin microcytotoxicity test: identification
of low levels of pre-formed antibodies in accelerated allograft rejec-
tion. Tissue Antigens 1972; 2: 215–26.
1071. Cross DE, Greiner R, Whittier FC. Importance of the autocontrol
crossmatch in human renal transplantation. Transplantation 1976;
21: 307–311.
1072. Ting A, Morris PJ. Successful transplantation with a positive T and
B cell crossmatch due to autoreactive antibodies. Tissue Antigens
1983; 21: 219–226.
1073. McCalmon RTJr, Tardiff GN, Sheehan MA, Fitting K, Kortz W, Kam
I. IgM antibodies in renal transplantation. Clin Transplant 1997; 11:
558–564.
1074. Kerman RH. The major histocompatibility complex in human trans-
plantation. In: Tejani A, Fine R, eds. Pediatric Renal transplantation.
New York: John Wiley-Lis, Inc, 1994: 51–67.
1075. Clinical Immunogenetics: Understanding Pretransplant Cross-
matches. In: Norman DJ, Suki WN, eds. Primer of transplantation.
1st edn. Throrofare, N.J.: The American Society of Transplantation
Physicians, 1998: 61–68.
1076. Lazda VA. Identification of patients at risk for inferior renal allograft
2001; Suppl. 1: Vol. 2: 5–95
 The Evaluation of Renal Transplant Candidates: Clinical Practice Guidelines
outcome by a strongly positive B cell flow cytometry crossmatch.
Transplantation 1994; 57: 964–969.
1077. Ghasemian SR, Light JA, Currier CB, Sasaki T, Aquino A, Rees J
et al. The significance of the IgG anti-B-cell crossmatch on renal
transplant outcome. Clin Transplant 1997; 11: 485–487.
1078. Bittencourt MC, Rebibou JM, Saint-Hillier Y, Chabod J, Dupont I,
Chalopin JM et al. Impaired renal graft survival after a positive B-
cell flow-cytometry crossmatch. Nephrol Dial Transplant 1998; 13:
2059–2064.
1079. Kotb M, Russell WC, Hathaway DK, Gaber LW, Gaber AO. The use
of positive B cell flow cytometry crossmatch in predicting rejection
among renal transplant recipients. Clin Transplant 1999; 13: 83–
89.
1080. Garovoy MR, Rheinschmidt MA, Bigos M, Perkins H, Colombe B,
Feduska N et al. Flow cytometry analysis: a high technology cross-
match technique facilitating transplantation. Transplant Proc 1983;
15: 1939–1944.
1081. Cook DJ, Fettouh HI, Gjertson DW, Cecka JM. Flow cytometry
crossmatching FCXM. in the UNOS kidney transplant registry. In:
Cecka JM, Terasaki PI, eds. Clinical transplants 1998. Los Angeles,
CA: UCLA Tissue Typing Laboratory; 1999. p. 413–419.
1082. Lazda VA, Pollak R, Mozes MF, Jonasson O. The relationship be-
tween flow cytometer crossmatch results and subsequent rejection
episodes in cadevar renal allograft recipients. Transplantation 1988;
45: 562–565.
1083. Braun WE. Laboratory and clinical management of the highly sensi-
tized organ transplant recipient. Hum Immunol 1989; 26: 245–
260.
1084. Mahoney RJ, Ault KA, Given SR, Adams RJ, Breggia AC, Paris PA
et al. The flow cytometric crossmatch and early renal transplant
loss. Transplantation 1990; 49: 527–535.
1085. Bertell AJ, Daniel V, Mohring K, Staehler G, Opelz G. Association of
kidney graft failure with a positive flow cytometric crossmatch. Clin
Sci 1992; 6: 31–34.
1086. Nelson PW, Eschliman P, Shield CF, Aeder MI, Luger AM, Pierce
GE et al. Improved graft survival in cadaveric renal retransplantation
by flow crossmatching. Arch Surg 1996; 131: 599–603.
1087. Utzig MJ, Blumke M, Wolff-Vorbeck G, Lang H, Kirste G. Flow cyto-
metry cross-match: a method for predicting graft rejection. Trans-
plantation 1997; 63: 551–554.
1088. O’Rourke RW, Osorio RW, Freise CE, Lou CD, Garovoy MR, Bacch-
etti P et al. Flow cytometry crossmatching as a predictor of acute
rejection in sensitized recipients of cadaveric renal transplants. Clin
Transplant 2000; 14: 167–173.
1089. Stratta RJ, Mason B, Lorentzen DF, Sollinger HW, D’Alessandro AM,
Pirsch JD et al. Cadaveric renal transplantation with quadruple im-
munosuppression in patients with a positive antiglobulin cross-
match. Transplantation 1989; 47: 282–286.
1090. Ogura K, Terasaki PI, Johnson C, Mendez R, Rosenthal JT, Ettenger
R et al. The significance of a postive flow cytometry crossmatch
test in primary kidney transplantation. Transplantation 1993; 56:
294–298.
1091. Bryan CF, Baier KA, Nelson PW, Luger AM, Martinez J, Pierce GE
et al. Long-term graft survival is improved in cadaveric renal re-
transplantation by flow cytometric crossmatching. Transplantation
1998; 66: 1827–1832.
1092. Kerman RH, Susskind B, Ruth J, Katz S, van Buren CT, Kahan BD.
Can an immunologically, nonreactive potential allograft recipient
undergo transplantation without a donor-specific crossmatch?
Transplantation 1998; 66: 1833–1834.
1093. Gebel HM, Bray RA. Sensitization and sensitivity: defining the un-
sensitized patient. Transplantation 2000; 69: 1370–1374.
1094. Regan J, Monteiro F, Speiser D, Kalil J, Pouletty P, Buelow R. Pre-
2001; Suppl. 1: Vol. 2: 5–95
transplant rejection risk assessment through enzyme-linked immu-
nosorbent assay analysis of anti-HLA class I antibodies. Am J Kid-
ney Dis 1996; 28: 92–98.
1095. Kerman RH, Susskind B, Buelow R, Regan J, Pouletty P, Williams J
et al. Correlation of ELISA-detected IgG and IgA anti-HLA anti-
bodies in pretransplantsera with renal allograft rejection. Transplan-
tation 1996; 62: 201–205.
1096. Alarabi A, Backman U, Wikstrom B, Sjoberg O, Tufveson G. Plasma-
pheresis in HLA-immunosensitized patients prior to kidney trans-
plantation. Int J Artif Organs 1997; 20: 51–56.
1097. Monteiro F, Buelow R, Mineiro C, Rodrigues H, Kalil J. Identification
of patients at high risk of graft loss by pre- and posttransplant
monitoring of anti-HLA class I IgG antibodies by enzyme-linked
immunosorbent assay. Transplantation 1997; 63: 542–546.
1098. Harmer AW, Heads AJ, Vaughn RW. Detection of HLA class I- and
class II-specific antibodies by flow cytometry and PRA-STAT
screening in renal transplant recipients. Transplantation 1997; 63:
1828–1832.
1099. Worthington JE, Thomas AA, Dyer PA, Martin S. Detection of HLA-
specific antibodies by PRA-STAT and their association with trans-
plant outcome. Transplantation 1998; 65: 121–125.
1100. Gebel HM, Bray RA, Ruth JA, Zibari GB, McDonald JC, Kahan BD
et al. Flow PRA to detect clinically relevant HLA antibodies. Trans-
plant Proc 2001; [In press].
1101. Katznelson S, Bhaduri S, Cecka JM. Clinical aspects of sensitiza-
tion. In: Cecka JM, Terasaki PI, eds. Clinical transplants 1997. Los
Angeles: UCL Tissue Typing Laboratory, 1998: 285–296.
1102. Scornik JC, Ireland JE, Howard RJ, Pfaff WW. Assessment of the
risk for broad sensitization by blood transfusions. Transplantation
1984; 37: 249–253.
1103. Scornik JC, Ireland JE, Salomon DR, Howard RJ, Fennell RS, Pfaff
WW. Pretransplant blood transfusions in patients with previous
pregnancies. Transplantation 1987; 43: 449–450.
1104. Ettenger RB, Marik J, Grimm P. The impact of recombinant human
erythropoietin therapy on renal transplantation. Am J Kidney Dis
1991; 18: 57–61.
1105. Deierhoi MH, Barger BO, Hudson SL, Shroyer TW, Diethelm AG.
The effect of erythropoietin and blood transfusions on highly sensi-
tized patients on a single cadaver renal allograft waiting list. Trans-
plantation 1992; 53: 363–368.
1106. Palmer A, Welsh K, Gjorstrup P, Taube D, Bewick M, Thick M. Re-
moval of anti-HLA antibodies by extracorporeal immunoadsorption
to enable renal transplantation. Lancet 1989; 1: 10–12.
1107. Taube D, Palmer A, Welsh K, Bewick M, Snowden S, Thick M. Re-
moval of anti-HLA antibodies prior to transplantation: an effective
and successful strategy for highly sensitised renal allograft recipi-
ents. Transplant Proc 1989; 21: 694–695.
1108. Taube D. Immunoadsorption in the sensitized transplant recipient.
Kidney Int 1990; 38: 350–358.
1109. Kupin WL, Venkat KK, Hayashi H, Mozes MF, Oh HK, Watt R. Re-
moval of lymphocytotoxic antibodies by pretransplant immunoad-
sorption therapy in highly sensitized renal transplant recipients.
Transplantation 1991; 51: 324–329.
1110. Glotz D, Haymann JP, Sansonetti N, Francois A, Menoyo-Calonge
V, Bariety J et al. Suppression of HLA-specific alloantibodies by
high-dose intravenous immunoglobulins IVIg. A potential tool for
transplantation of immunized patients. Transplantation 1993; 56:
335–337.
1111. Tyan DB, Li VA, Czer L, Trento A, Jordan SC. Intravenous immuno-
globulin suppression of HLA alloantibody in highly sensitized trans-
plant candidates and Transplantation with a histoincompatible or-
gan. Transplantation 1994; 57: 553–562.
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