352 2002 ACVIM Abstracts
USE OF HEMODIALYSIS FOR THE MANAGEMENT OF
101 ACUTE RENAL FAILURE IN THE DOG: 124 CASES (1990–
2001). T Francey, LD Cowgill. School of Veterinary Medicine, Uni-
versity of California, Davis, CA.
Hemodialysis (HD) is a standard procedure for the treatment of severe acute
renal failure (SRF) in humans. Its use in dogs with ARF has received only limited
review, thus we reviewed the case records of all dogs that received HD treat-
ments for the management of ARF from January 1990 to February 2001. The
diagnosis of ARF was based on conventional criteria including clinical, labora-
tory, imaging and histopathology. All HD treatments were performed using trans-
cutaneous vascular access, bicarbonate-based dialysate, and Cobe Centrysystem
3 dialysis delivery system. A total of 679 HD treatments were delivered to 124
dogs (6 ⫾ 7.5 treatments per patient, range 1–43). Sex distribution was F ⫽ 15,
FS ⫽ 41, M ⫽ 35, and MC ⫽ 33; age was 6.6 ⫾ 3.4 years (range 0.5–17.2);
and body weight was 27.2 ⫾ 11.7 kg (range 4.6–64). The etiology was cate-
gorized as: toxic (45.2%), infectious (34.7%), hemodynamic/metabolic (7.2%),
inflammatory (3.2%), and undetermined (9.7%). Ethylene glycol toxicosis and
leptospirosis were the leading etiologies at 33.9% and 30.6% of the cases, re-
spectively.
Specifics for all HD treatments are as follows:
Overall survival rate was 41%. Only 18% of the dogs with toxic etiologies
(12% for ethylene glycol poisoning) survived, whereas 70% of those with in-
fectious etiologies (76% of the leptospirosis), and 56% of those with metabolic
and hemodynamic causes survived. These data support the efficacy of HD for
the management of azotemia in severe ARF. Survival was consistent with human
data and was notable considering that these patients had exhausted all possibil-
ities of conventional therapy.
GLOMERULAR PROTEINURIA IS RAPIDLY BUT REVERS-
102 IBLY INCREASED BY SHORT-TERM PREDNISONE ADMIN-
ISTRATION IN HETEROZYGOUS (CARRIER) FEMALE DOGS
WITH X-LINKED HEREDITARY NEPHROPATHY. George E.
Lees, Michael D. Willard, and Joan Dziezyc. Texas A&M Univer-
sity, College Station, TX.
Glucocorticoid excess can cause glomerular lesions and proteinuria in dogs,
but effects of glucocorticoid therapy on proteinuria in dogs with preexisting
glomerular diseases of other causes are not well characterized. Heterozygous
(carrier) female dogs with X-linked hereditary nephropathy (XLHN) have pro-
teinuria attributable to glomerular lesions caused by defective type IV collagen
in their glomerular basement membranes (GBM). The goal of this study was to
determine the effects of short-term prednisone therapy in such dogs.
Six XLHN-carrier females were studied. Results of a CBC, serum chemistry
profile, urinalysis, urine culture and fecal flotation were negative or within nor-
mal limits, except for proteinuria in each dog. Dogs were studied for 12 weeks;
4 weeks for pre-treatment (baseline) observations, 4 weeks of prednisone therapy
(2.2 mg/kg PO q24h), and 4 weeks of post-treatment observations. Each 4-week
treatment period included two 2-week study intervals. Indirect blood pressures
(oscillometric method) were measured weekly. Serum chemistries, including SCr,
were repeated at the end of each 2-week study interval. Urine protein:creatinine
ratio (UPC) was determined for a sample obtained by cystocentesis on each of
the last 3 days of each study interval. The 3-day average UPC value was used
as an index of each dog’s magnitude of proteinuria at the end of each study
interval for data analyses. Observations at the ends of 4-week treatment periods
were compared to assess treatment effects, and data for 2-week study intervals
within treatment periods were used to assess the time-course of responses.
During prednisone treatment, UPC increased significantly (p ⫽ 0.0003) from
1.5 ⫾ 0.87 (mean ⫾ SD) at the end of week 4, to 5.6 ⫾ 2.31 at the end of
week 8, but UPC returned to baseline (1.6 ⫾ 0.46 at the end of week 12) after
prednisone administration ceased. Both onset and offset of treatment effects on
UPC were rapid, with the full effect evident by the end of the initial 2 weeks
of the 4-week treatment period. Prednisone therapy did not have significant ef-
fects on blood pressures or SCr, which were normal throughout the study.
We conclude that short-term prednisone administration rapidly causes a sub-
stantial, reversible increase in the magnitude of proteinuria in carrier female dogs
with XLHN. The mechanisms underlying this phenomenon are unknown, but a
direct effect on the primary defect (i.e., abnormal type IV collagen content of
the GBM) is an unlikely explanation. If the effect of glucocorticoid therapy on
glomerular proteinuria in these dogs is nonspecific, a similar phenomenon should
be expected during prednisone administration to dogs with other types of glo-
merular disease causing proteinuria.
DEVELOPMENT OF MICROALBUMINURIA IN DOGS WITH
103 HEARTWORM DISEASE. GF Grauer,1 EB Oberhauser,2 RJ Bas-
araba,2 MR Lappin,2 DF Simpson,3 and WA Jensen.3 1Kansas State
University, Manhattan, KS; 2Colorado State University, Fort Collins,
CO; and 3Heska Corporation, Fort Collins, CO.
The presence of microalbuminuria (MA) has been shown to be an accurate
predictor of subsequent renal disease in human beings with both systemic hy-
pertension and diabetes mellitus. MA has also been observed in human beings
with systemic diseases that are associated with glomerulopathy. Previous studies
in dogs have shown the prevalence of MA in apparently healthy dogs and soft
coated wheaten terriers genetically predisposed to developing glomerular disease
to be 19% and 76%, respectively. The purpose of this study was to determine
the prevalence of MA in dogs with experimentally infected heartworm disease.
Twelve six-month male beagles were randomly divided into two groups of six.
Group A was fed a diet with a 50:1 n-6: n-3 fatty acid ratio and group B was
fed a diet with a 5:1 n-6: n-3 fatty acid ratio. All of the dogs were infected
subcutaneously with 75 Dirofilaria immitis infective larvae. Urine collections via
urethral catheterization were performed monthly for 14 to 23 months post in-
fection. Urine albumin concentrations were measured using an antigen capture
ELISA. To account for varying urine concentrations, results were normalized to
a specific gravity of 1.010. MA was defined as urinary excretion of albumin
greater than 1.0 mg/dl but less than 30.0 mg/dl.
All dogs developed MA; the initial month of detection of MA was different
between groups as measured by ANOVA (Group A 7.5⫾1.9 vs Group B
9.7⫾1.0, P ⫽ 0.032). After the initial episode of MA, 67/82 (82%) of samples
from Group A dogs had MA and 4/82 (5%) samples had overt proteinuria (⬎
30 mg/dl). The average concentration of urine protein in these 82 samples was
7.7⫾11 mg/dl. In comparison, after the initial episode of MA, Group B dogs
had 45/68 (66%) samples with MA and 7/68 (10%) samples with overt protein-
uria. The average concentration of urine protein in these 68 samples was 8.3⫾14
mg/dl. In both groups MA increased over time and MA preceded overt protein-
uria when it occurred. The overall number of proteinuric urine samples (⬎ 1.0
mg/dl) in both groups after the initial onset was 123/150 (82%) with 75% of the
samples having MA and 7% having overt proteinuria. Eleven of these 12 dogs
had histologic evidence of glomerular lesions on light microscopic and/or im-
munocytochemical evaluation.
This study shows that the prevalence of MA in dogs with experimentally
infected heartworm disease is higher than that observed in apparently healthy
dogs and similar to that observed in soft coated wheaten terriers. Further study
is necessary to determine if all heartworm-infected dogs with MA will progress
to develop overt proteinuria.
INHERITANCE OF PROTEIN-LOSING ENTEROPATHY AND
104 NEPROPHATHY OF SOFT COATED WHEATEN TERRIERS. S
Vaden,1 U Giger,2 K Spaulding,1 R Sellon,3 M Littman,2 T Harris,1
M Afrouzian,4 J Jennette,4 D Williams,5 S VanCamp.1 1North Car-
olina State Univ, Raleigh, NC; 2Univ of Pennsylvania, Philadelphia,
PA; 3Washington State Univ, Pullman, WA; 4Univ of North Caro-
lina, Chapel Hill, NC; 5Texas A&M Univ, College Station, TX.
A common syndrome of protein-losing enteropathy (PLE) and/or protein-los-
ing nephropathy (PLN) has been documented in male and female soft-coated
wheaten terriers (SCWT). PLE is associated with eosinophilic or lymphocytic/
plasmacytic inflammatory bowel disease and is usually diagnosed at an earlier
age (mean 4.5 years) than PLN (mean 6 yrs), which is the result of focal mes-
angioproliferative and sclerosing glomerulonephritis. Although analysis of ped-
igrees from SCWT at large revealed a common male ancestor, the exact mode
of inheritance could not be determined.
The purpose of this study was to further characterize the mode of inheritance
of PLE and PLN in SCWT by three types of breedings: Group 1 consists of a
litter of 6 SCWT (3 M, 3 F) born to an affected female ⫻ affected male SCWT.
Group 2 represents a litter of 4 SCWT (1 M, 3 F) born to a brother ⫻ sister
mating of Group 1 dogs. Group 3 involves an outcross of an affected male
SCWT from Group 1 to a healthy Beagle and resulted in 8 (4 M, 4 F) offspring.
These dogs were maintained at the North Carolina State University, fed a stan-
dard diet, and were serially evaluated through serum biochemical profiles, CBCs,
urinalyses, urine protein:creatinine ratios (normal ⬍1) and fecal ␣1 proteinase
inhibitor (␣1-PI; normal ⬍5.67 ␮g/g) every 3 months, small intestinal biopsy
and renal ultrasound every 6 months and renal biopsy every 12 months. In order
to make a diagnosis of PLE and/or PLN, dogs needed to have both laboratory
and histopathologic abnormalities that were consistent with the diseases.
In Group 1 SCWT, 6 of 6 developed PLE (n ⫽ 1), PLN (3) or both (2); the
present age of 2 survivors (PLE/PLN, 1; PLN, 1) is 7 yrs. Both of the parents
of Group 2 but none of the 4 dogs in Group 2, developed PLN at 4.5 yrs of
age, however, 3 of them have PLE (1 dog appears to have no evidence of disease,
but has just reached the mean age to develop PLE). Of the 8 outcross dogs in
group 3 (present age 5.5 yrs), 1 has PLE/PLN and 1 has PLN.
Although the breeding of affected to affected SCWT in Group 1 and 2 pro-
ducing primarily affected SCWT is consistent with an autosomal recessive mode
of inheritance, the development of PLE and PLN in the SCWT ⫻ Beagle out-
cross suggests an autosomal dominant trait. The risk for SCWT to develop PLE
and PLN is clearly inherited, however, further breeding and clinical follow up
is needed to reach a definitive conclusion.