Int Urol Nephrol (2007) 39:587–593

DOI 10.1007/s11255-006-9035-3

ORIGINAL PAPER

Management of extreme azotemia from urinary tract

obstruction without dialysis. Clinical correlates and kinetic
modeling of the recovery of renal function
Richard Wang Æ Antonios H. Tzamaloukas Æ
Emmanuel I. Agaba Æ Karen S. Servilla Æ
Dorothy J. VanderJagt Æ Laurence J. Gibel Æ
Michael F. Hartshorne Æ Betty Chang

Received: 13 March 2006 / Accepted: 5 May 2006 / Published online: 21 February 2007

Springer Science+Business Media B.V. 2007

Abstract The recovery of renal function fol-
lowing release of urinary tract obstruction with
advanced azotemia determines both the need for
emergency dialysis in the early post-obstructive
period and the long-term planning for chronic
kidney disease management. A man with pros-
R. Wang Æ A. H. Tzamaloukas (&) Æ
K. S. Servilla Æ B. Chang
Departments of Medicine, Renal Section (111C),
New Mexico Veterans Affairs Health Care System
and University of New Mexico School of Medicine,
1501 San Pedro, SE, Albuquerque, New Mexico, USA
e-mail: Antonios.Tzamaloukas@med.va.gov
E. I. Agaba
Department of Medicine, Jos University Hospital,
Jos University, Jos, Plateau State, Nigeria
D. J. VanderJagt
Department of Biochemistry and Molecular Biology,
University of New Mexico School of Medicine,
Albuquerque, New Mexico, USA
L. J. Gibel
Department of Surgery, New Mexico Veterans
Affairs Health Care System and University of
New Mexico School of Medicine, Albuquerque,
New Mexico, USA
tatic cancer who presented with 16 days of anuria
and a serum creatinine (Scr) of 42.7 mg/dl but had
evidence suggesting residual renal function was
managed conservatively and reached a steady-
state Scr of 1.6 mg/dl within 84 h of urinary
bladder catheterization. Modeling of the decrease
in Scr taking into account the decline in the body
creatinine pool that existed prior to the release of
the obstruction and the accumulation in body
fluids of creatinine produced after the release of
the obstruction suggested that recovery of the
value of glomerular filtration rate corresponding
to the steady-state Scr occurred at the release of
the urinary obstruction. The case illustrates both
the clinical factors that may lead to the decision
to postpone dialysis in a patient presenting with
extreme obstructive azotemia and a novel method
of modeling the recovery of renal function after
release of the obstruction.
Keywords Obstructive uropathy Æ Azotemia Æ
Acute dialysis Æ Creatinine clearance Æ
Creatinine kinetics
Introduction

M. F. Hartshorne Emergency renal replacement therapies are

Department of Radiology, New Mexico Veterans
Affairs Health Care System and University of
New Mexico School of Medicine, Albuquerque,
New Mexico, USA
expensive, personnel-intensive, and associated
with certain risks including those generated by
the placement of large catheters in central veins

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and the risks of the renal replacement procedure
itself. Therefore, the decision to dialyze at pre-
sentation or to manage conservatively a patient
with newly diagnosed potentially reversible azo-
temia is important and depends on the presence
of clinical indications for dialysis, including frank
uremic manifestations, hypervolemia, hyperkal-
emia and severe metabolic acidosis [1] and on the
potential for rapid recovery of renal function.
Azotemia secondary to lower urinary tract
obstruction can be managed conservatively when
there is early evidence of rapid recovery of renal
function after release of the obstruction. We
present a patient with extreme obstructive azo-
temia managed without dialysis because both
clinical findings at presentation and the early
course of recovery of renal function after release
of the obstruction suggested preservation of the
renal function. Kinetic analysis of the changes in
serum creatinine (Scr) in this patient suggested
recovery of the baseline renal function at the
moment of release of the urinary obstruction.
Case report
A 63-year-old man with history of hypertension
was admitted with inability to pass urine. Four
years prior to this presentation, Scr was 1.3 mg/dl
and prostate specific antigen (PSA) 10.2 ng/ml
(normal range 0–2.0 ng/ml). Around 16 days
prior to admission, during an Emergency
Department visit with a complaint of constipa-
tion, urinalysis was normal while Scr was not
measured. Ingestion of magnesium citrate was
followed by several loose stools. However, he
passed no urine in the ensuing 16 days and no-
ticed the development of progressive abdominal
distention, fatigue and anorexia followed by
nausea, vomiting and hiccups.
Abnormal physical findings on admission in-
cluded elevated blood pressure (180/110 mmHg),
Kussmaul respiration, a visible, large, smooth,
round mid-line lower abdominal mass with its
upper end at the umbilicus, modest bilateral leg
edema and a greatly enlarged prostate gland.
Neurological and cardiac signs of uremia and
signs of bleeding tendency were absent. Chest
X-ray showed small bilateral pleural effusions
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Int Urol Nephrol (2007) 39:587–593
and a small nodule in the right lower lobe, but no
cardiomegaly or pulmonary congestion. Abdom-
inal computed tomography confirmed the pres-
ence of a large urinary bladder with preservation
of the renal parenchyma.
An indwelling urinary bladder catheter pro-
duced urine with a specific gravity of 1.010, trace
protein and many red blood cells. Urine output
was 9 l in the first 8 h and another 7 l in the next
24 h of hospitalization. He received an intrave-
nous infusion of several liters of normal saline. In
the first 4 h, insulin with glucose, sodium bicar-
bonate, and calcium gluconate were added to the
infusion. The abnormal clinical symptoms and
signs disappeared within 24 h with the exception
of the prostatic enlargement.
Table 1 shows the admission and resolution
values of the laboratory measurements, which
were repeated during hospitalization. Serum
potassium concentration was 5.9 mmol/l 2 h after
placement of the bladder catheter and was nor-
malized within 8 h, total serum carbon dioxide
content (TCO2) was normalized within 18 h and
anion gap was normalized within 26 h. Scr
reached steady state (1.6 mg/dl) 84 h after
admission. Admission serum measurements that
were normal included albumin (4.1 g/dl), creati-
nine phosphokinase (127 U/l) and lactate
(0.9 mmol/l), while admission arterial blood gases
at room air were: pH 7.25; pO2 41 mmHg; pCO2
24 mmHg; and bicarbonate 12.4 mmol/l. The
electrocardiogram on admission had no features
of hyperkalemia. Serum PSA was 33.9 ng/ml. He
was discharged with a chronic indwelling bladder
catheter. A needle biopsy of the prostate ob-
tained in an outpatient setting revealed adeno-
carcinoma. Scr over the next 3 months remained
in the range of 1.4–1.7 mg/dl. Nine weeks after
release of the obstruction, a 24-h urine collection
contained 1618 mg of creatinine with a calculated
creatinine clearance (Ccr) of 62.4 ml/min (Scr
1.7 mg/dl).
Modeling of the recovery of renal function
This modeling is based on established pharma-
cokinetic principles. The decline in Scr after a
sudden rise in Ccr secondary to the release of
Int Urol Nephrol (2007) 39:587–593 589

Table 1 Blood cell

Variable Admission Resolution Time, hoursa
counts and serum
concentrations at Blood
admission and at White cell count, k/mm3 7.3 9.0 84
resolution Hemoglobin, g/dl 14.0 15.1 84
Hematocrit, % 41.8 44.4 84
Platelets, k/mm3 268 295 84
Serum
Glucose, mg/dl 58 83 84
Urea nitrogen, mg/dl 165 21 60
a
Creatinine, mg/dl 42.7 1.6 84
Time between the Sodium, mmol/l 136 141 84
admission value and the Potassium, mmol/l 7.4 4.7 8
value at which the first TCO2, mmol/l 13 22 18
normal value or the Anion gap, mEq/l 25 11 26
closest to normal value Calcium, mg/dl 9.2 9.6 84
(resolution value) was Phosphorus, mg/dl 12.7 3.5 35
obtained. TCO2, total Magnesium, mg/dl 4.1 1.7 60
carbon dioxide content

urinary obstruction follows the mathematical

principles of the change in the serum levels of a 40

drug infused at a continuous rate after a sudden Serum creatinine (mg/dl) 35

change in the clearance of this drug [2–4], and is 30

the result of two processes occurring after the
release of the urinary obstruction, the decline in
the pool of creatinine that had accumulated in the
body during the period of anuria and the contin-
uous addition of new creatinine to the same pool.
We used this kinetic modeling to examine the
hypothesis that the recovery of renal function
(renal creatinine clearance—Ccr) to the level
corresponding to the steady-state Scr of 1.6 mg/dl
occurred at the moment of release of the urinary
obstruction. The hypothesis was tested by com-
paring Scr levels predicted by the model at dif-
ferent times after the release of the obstruction to
the Scr levels obtained by actual measurements at
the same times. Figure 1 shows this comparison.
Predicted and measured levels were close. This
finding supports the hypothesis that recovery of
baseline creatinine clearance occurred at the
moment of the release of the urinary obstruction.
The Appendix contains the details of the
kinetic model.
Discussion
The clinical point illustrated by this report is the
set of conditions that allow conservative early
management of a patient presenting with extreme
25
20
15
10
5
0
0 10 20 30 40 50 60 70 80 90
Time (hrs)
Fig. 1 Modeling of the decline in serum creatinine
concentration (exponentially declining intermittent curve)
and measured serum creatinine concentration (closed
circles)
azotemia. The decision not to perform immedi-
ately dialysis in such a patient must be supported
by important clinical findings. These findings in
the patient of the present report included the
following: (1) The cause of azotemia was extra-
renal, and therefore its correction could poten-
tially lead to rapid recovery of the renal function.
Comparable azotemia and clinical manifestations
resulting from renal parenchymal disease should
be managed by emergency dialysis, because
recovery of renal function, even if it does happen,
is usually relatively slow in this setting. (2) There
was radiographic evidence of preservation of the
renal parenchyma. (3) Neurological, cardiac and
hematological signs of uremia were absent. (4)
There was no acute catabolic illness, particularly

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rhabdomyolysis. (5) The history and laboratory
indices, particularly the normal hemogram, were
not consistent with chronic renal failure. (6)
Profound diuresis started with the release of the
urinary obstruction and hypokalemia recovered
rapidly. This last clinical finding was the most
important factor in the decision to treat the pa-
tient conservatively.
The recovery of renal function after release of
urinary obstruction has been studied in both
experimental animals and humans. In humans,
there is a rough correlation between renal dys-
function after relief of the obstruction and duration
of complete urinary obstruction [5, 6]. However,
the number of patients studied is small [7, 8] and
many reports analyzed ureteral obstruction, not
lower urinary tract obstruction in which the pres-
ence of the distensible urinary bladder between the
obstruction and the kidneys modifies the impact of
obstruction on renal function. In addition, several
human studies focused on changes in tubular ra-
ther than glomerular function.
The recovery of glomerular function after re-
lease of complete urinary obstruction has been
studied in humans with either formal clearance
studies [9–14] or decrease in the serum levels of
azotemic parameters without formal modeling [15,
16]. Rapid recovery (few days) has been reported
in some patients [12, 13, 15], slow recovery
(months, year) in others [9, 11, 14], while one study
reported a biphasic recovery, with one increase in
glomerular filtration documented 2 days after re-
lease of the obstruction and a second increase a few
months later [17]. Predictors of recovery of renal
function include long duration of the symptoms,
absence of urinary tract infection, large residual
urine volume, and preservation of the normal
radiographic characteristics of the kidneys [16].
The use of formal clearances to evaluate
recovery of renal function after release of lower
urinary tract obstruction can provide precise
information, but has certain limitations. Endoge-
nous Ccr is traditionally used after Scr has
reached a steady state, while clearances of exog-
enous indices of glomerular filtration, which can
be used immediately after release of the
obstruction, are costly. Comparison between lev-
els of Scr predicted by kinetic modeling and ac-
tual Scr levels allows testing of the hypothesis that
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Int Urol Nephrol (2007) 39:587–593
the recovery of the early steady-state glomerular
function takes place immediately after release of
the obstruction.
The patient of the present report had complete
lower urinary tract obstruction for 16 days. Partial
obstruction was, probably, much longer accounting
for the degree of bladder dilatation at presenta-
tion. Despite this, the decrease in Scr after place-
ment of the bladder catheter followed a pattern
suggesting that Ccr corresponding to the early
steady-state Scr was achieved immediately after
release of the obstruction (Fig. 1). A visually sim-
ilar pattern of decrease in serum urea nitrogen
after release of bladder outlet obstruction has been
reported in another study [15]. More observations
using a similar kinetic analysis will be needed to
determine the percent of patients with obstructive
azotemia who achieve recovery of the baseline
glomerular function soon after release of the
obstruction and to study the effects of factors, such
as volume depletion, sepsis etc., that can confound
the recovery of renal function. The accuracy of the
kinetic analysis can be influenced adversely by the
fact that both body water and creatinine produc-
tion are obtained from indirect methods.
The decision to hold dialysis in a patient pre-
senting with extreme azotemia cannot be based on
kinetic analysis or measured clearances, because
these methods require measurements after the
release of the obstruction. This decision should be
based on clinical indicators and must be coupled
with close monitoring of both the renal function
and the presence of indications for acute dialysis.
Modeling of the decline in Scr after release of
urinary obstruction can be useful in establishing
the pattern of recovery of renal function.
Acknowledgement This work was supported by the New
Mexico VA Health Care System.
Appendix
Modeling of the decline in serum creatinine
after release of the urinary obstruction
The general model
The information needed to calculate the model is
the serum creatinine (Scr) levels prior to and
Int Urol Nephrol (2007) 39:587–593
following the release of the urinary obstruction,
including the level just prior to the release of the
obstruction plus the steady-state Scr post release
of the obstruction, the times after the release of
the obstruction that the Scr levels were measured,
an estimate of the creatinine clearance (Ccr)
corresponding to the steady-state Scr after release
of the obstruction, and gender, age, weight and
height of the patient.
Scr at time t after release of the urinary
obstruction (Scrt) is the result of two processes,
the decline in the creatinine pool because of the
sudden, at the moment of release of the obstruc-
tion, rise in Ccr which results in a Scr value Scrt1
and the constant generation of new creatinine
which results in a Scr value Scrt2. Therefore:
Scrt ¼ Scrt1 þ Scrt2 ð1Þ
If Scr0 is the initial (at the release of the
obstruction) Scr, the values Scrt1 and Scrt2 are
determined by the following equations:
Scrt1 ¼ Scr0
eðCcr=VÞ
t ð2Þ
Scrt2 ¼ Scrss
ð1  efCcr=Vg
t Þ ð3Þ
where Ccr is the value after the release of the
urinary obstruction, Scrss is the steady-state Scr at
Ccr, V is the volume of distribution of creatinine,
and the term Ccr/V, as a pharmacokinetic func-
tion, is the ‘‘elimination constant’’ [2] for creati-
nine.
The time at which Scr level is halved (T1/2) is
calculated by pharmacokinetic principles [2] as:
T1=2 ¼ 0:693
V=Ccr ð4Þ
Modeling Scr changes in the patient of the present
report
To test the hypothesis that renal Ccr reached the
baseline level at the placement of the bladder
catheter, we used first as baseline Ccr the level of
55.6 ml/min, calculated by the Cockroft–Gault
formula [18] in the patient of this report for a
steady state Scr of 1.6 mg/dl. Note that the
Modification of Diet in Renal Disease (MDRD)
formula [19] calculated a glomerular filtration
591
rate (not a Ccr) of 47 ml/min for a Scr of 1.6 mg/
dl in the same patient. We also assumed that the
patient’s volume of distribution of creatinine (V),
which is considered equal to body water, re-
mained throughout the hospitalization constant at
the value of 43.8 l calculated from the Watson
formula [20] for the discharge body weight of
83.2 kg and a height of 180.3 cm. This last
assumption is not strictly correct because the rate
of urine production was higher than the rate of
intravenous fluid infusion. Between admission
and discharge, blood hemoglobin increased by
7.9% and hematocrit by 6.2% (Table 1). This
suggests that extracellular volume decreased by
about 7% and body water by approximately 3.5%
(1.5 l) during hospitalization.
We used Eqs. 2 and 3 to calculate levels of Scr
at hourly intervals. For example, 1 h after release
of the urinary obstruction, and using 42.7 mg/dl as
Scr0, 3.336 l/h (60 · 55.6/1000) as Ccr, 43.8 l as V
and 1.6 mg/dl as Scrss, Scrt1 (Eq. 2) would be
39.569 mg/dl, Scrt2 (Eq. 3) would be 0.117 mg/dl
and Scrt (Eq. 1) would be 39.686 mg/dl. The value
of 39.686 mg/dl represented the Scr0 value at the
beginning of the second hour and the same pro-
cess was repeated for 90 h. Appendix Table A
shows the sequence of the calculations. The
interrupted exponential curve in Fig. 1 shows the
decline in Scr calculated by this model.
Using different time intervals between the
different steps of the calculations could poten-
tially affect the precision of the model shown in
Fig. 1. We tested this hypothesis in two ways:
First, we calculated the model, as stated, using
hourly intervals. For the first hour, we repeated
the calculations using intervals of 1 min. Ccr is
then 0.0556 l/min instead of 3.336 l/h, but all
other input values are the same. This series of
calculations resulted in a Scr of 39.702 mg/dl 1 h
after release of the obstruction. This value differs
from the value of 39.686 mg/dl obtained by the
hourly calculations by only 0.04%.
Second, we calculated the time at which Scr
was halved by Eq. 4 and by the successive steps of
the model. Using a Ccr of 3.336 l/h in Eq. 4, the
time to reduce Scr by half would be 9.1 h. The
predicted time of halving of Scr by the model
shown in Fig. 1 was also 9.1 h after release of the
urinary obstruction. Note: The calculations for
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Table A Calculation of the predicted Scr at hourly
intervals after release of the obstruction
Hour Scr0, mg/dl Scrt1, mg/dla Scrt2, mg/dlb Scrt, mg/dlc
0 42.700 – –
1 42.700 39.565 0.117
2 39.682 36.660 0.117
3 39.777 34.077 0.117
89 1.600 1.483 0.117
90 1.600 1.483 0.117
a
At each step, Scrt1 = Scr0 · e–(3.346/43.8) (t = 1 h)
b
At each step, Scrt2 = 1.6 · (1 – e–{3.346/43.8}) (t = 1 h)
c
At each hourly step, Scrt = Scrt1 + Scrt2
Fig. 1 assumed zero extrarenal Ccr. If a value of
0.036 l/(kg 24-h) [21] for extrarenal Ccr is added
to a renal Ccr of 3.336 l/h, Eq. 4 calculates a T1/2
for Scr equal to 8.8 h.
Testing of the hypothesis that recovery of the
steady-state baseline Ccr occurred at the release
of the obstruction
To test this hypothesis, we compared the mea-
sured Scr levels and the levels predicted by the
model in the same two ways as the testing of the
precision of the model: First, the eight measured
Scr levels following the initial value differed by
11.9 ± 13.2% from the Scr levels of the model at
the corresponding times. However, the first three
measured levels after the initial level differed
from the corresponding model levels by only
4 ± 4%. These first three Scr levels were critical
for the determination of the actual time of halving
of Scr and, therefore, for testing the assumption
that the patient recovered the baseline Ccr at the
release of the obstruction. Second, the measured
Scr was 21.1 mg/dl 10.4 h after initiation of
bladder drainage. Thus the actual time of halving
of Scr was approximately 10 h (9% difference
from the value calculated from the model).
Finally, we calculated the duration of anuria
that would be needed to raise Scr from 1.6 mg/dl
to 42.7 mg/dl first by estimating creatinine pro-
duction (Pcr) as follows [18]:
Pcr ¼ W
ð28  0:20
AÞ
where Pcr is in mg/24-h, weight (W) is in kg and
age (A) is in years. Equation 5 calculated a
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Int Urol Nephrol (2007) 39:587–593
creatinine production of 1281.3 mg/24-h for the
patient in this report. If extrarenal Ccr is zero,
Scr would rise by 2.9 mg/dl (1281.3/43.8) daily
and it would take 14.2 days ({42.7 – 1.6}/2.9) of
42.700
39.682
anuria to reach a value of 42.7 mg/dl. We ob-
36.777 tained a second estimate of the time of anuria
34.194 that would be needed for Scr to reach a value of
1.600 42.7 mg/dl through the use an extrarenal Ccr of
1.600
2.995 l/24-h for this patient [21, 22]. At this Ccr,
it would take 10.1 days to reach a Scr one-half
the value of the steady-state Scr (Eq. 5) and the
new steady-state Scr, which would be reached
after 40.4 days, would be, at 42.8 mg/dl (1281.3/
2.995), almost identical to the admission value of
42.7 mg/dl.
All calculations were repeated using the
measured Ccr of 62.4 ml/min estimated from
the 24-h urine collection 9 weeks after release
of the obstruction. The time of halving of Scr
would then be 8.1 h (approximately 20%
shorter than the observed time), while the pre-
dicted from this model Scr values differed from
the measured values by 11.1 ± 2.5% for all
measurements and by 11.6 ± 0.7% for the first
three measurements. The calculated time of
anuria that would be needed to reach a Scr of
42.8 mg/dl would be 11.1 days if total Ccr were
zero and again 40.4 days to reach a steady-state
Scr value of 54.0 mg/dl if extrarenal Ccr were
2.995 l/h.
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