A to Z Index
"Problem Specific Data Base for Renal Failure in Immature Dogs" is
included in the chapter on renal disease in Veterinary Pediatrics,
Dogs & Cats from Birth to Six Months, 2nd edition, as is a table on
"Medical Management of Chronic Renal Failure". (1)
Kruger, J.M., Osborne, C.A., et al. : Congenital and Hereditary
Disorders of the Kidney. Veterinary Pediatrics Dogs & Cats from
Birth to Six Months., 2nd edition. (J.D. Hoskins, ed.) W.B.Saunders,
Philadelphia, Pa, 1995: pp 401-406.
DiBartola Stephen P. et al: Familial Renal disease in Dogs and Cats.
Textbook of Veterinary Internal Medicine. (S.J. Ettinger, & E.C.
Feldman, ed) W.B. Saunders, Philadelphia, Pa. 1995:pp 1796-1801.
McMaw, D.l; Fleming, E.J.; Mikiciuk, M.G. : Chronic renal failure in
dogs: Managing an irreversible condition. Symposium on Renal
disease. Veterinary Medicine; March 1989; p 297-303.
Polzin, D.J.; Osborne, C.A.: Update - Conservative Medical
Management of Chronic Renal Failure. Current Therapy IX (R.W. Kirk,
ed.) W. B. Saunders, Philadelphia, PA., 1986 pp 1167-1173.
Finco, D.R.: The Role of Phosphorus Restriction in the Management of
Chronic Renal Failure of the Dog and Cat; Proc. 7th Kal Kan Sypm. .
Veterinary Learning Systems, Lawrenceville, NJ 1983; pp 131-133
Willis, Malcolm B: Genetics of the Dog. Howell Book House, New York,
NY, 1989;p 356.
Crawford, M.A.:The Kidneys, Congenital and Inherited
Disorders.Veterinary Pediatrics Dogs & Cats from Birth to Six
Months. (J.D. Hoskins, ed.) W.B. Saunders, Philadelphia, Pa, 1990:
DiBartola S.P., Chew D.J., et al: Juvenile Renal Disease in related
Standard Poodles. JAVMA:183:693-696.
Bovee, K.C.: Overview of the Uremic Syndrome. Current Veterinary
Therapy VII (R.W. Kirk, ed.) W.B. Saunders. Philadelphia, Pa., 1980.
Chew, D.J.; DiBartola, S.P.: Manual of Small Animal Nephrology and
Urology. Churchill Livingston. New York, NY. 1986; pp 1-78.
Krawiec, D.R.: Renal Failure in Immature Dogs. JAAHA 23:101-107;
McMaw, D.l; Fleming, E.J.; Mikiciuk, M.G.. : Selecting the right
diagnostic tests for renal disease. Symposium on Renal disease.
Veterinary Medicine; March 1989; pp 267-272.
McMaw, D.l; Fleming, E.J.; Mikiciuk, M.G. : Interpreting the results
of urinalysis: A key to diagnosing renal disorders. Symposium on
Renal Disease.Veterinary Medicine; March 1989; p 281-286.
Picut, G.A.; Lewis. R.M.: Comparative Pathology of Canine Hereditary
Neuropathies: An Interpretive Review. Vet. Res. Comm. 11:561-581;
Picut, G.A.; Lewis, R.M.: Microscopic Features of Canine Dysplasia.
Vet. Path. 24:158-163; 1987.
J Small Anim Pract 1980 Mar;21(3):169-81
Chronic renal failure in young dogs--possible renal dysplasia.
Lucke VM, Kelly DF, Darke PG, Gaskell CJ
PMID: 7366181, UI: 80163925
J Small Anim Pract 1996 Nov;37(11):552-5
Renal dysplasia in a Rhodesian ridgeback dog.
Lobetti RG, Pearson J, Jimenez M
Department of Medicine, Faculty of Veterinary Science, University of
Pretoria, Onderstepoort, Republic of South Africa.
A six-month-old Rhodesian ridgeback dog was presented for evaluation
of facial swelling. Chronic renal failure was clinically diagnosed
based on urinalysis, biochemical changes and ultrasonography. The
facial swelling was due to fibrousosteodystrophy, which was evident
on survey radiographs of the skull. On post mortem examination,
chronic renal failure as a result of renal dysplasia was confirmed.
This is the first reported case of renal dysplasia in this breed of
PMID: 8934429, UI: 97088491
Vet Pathol 1987 Mar;24(2):156-63
Microscopic features of canine renal dysplasia.
Picut CA, Lewis RM
Forty-five cases of renal dysplasia in dogs are examined.
Microscopic lesions of dysplasia include asynchronous
differentiation of nephrons, persistent mesenchyme, persistent
metanephric ducts, atypical tubular epithelium, and dysontogenic
metaplasia. These may be distinguished from secondary lesions
including compensatory hypertrophy and hyperplasia of the nephron
and a variety of degenerative and inflammatory lesions. Although
morphological features of renal dysplasia in dogs differ somewhat
from those in man, microscopic criteria used in the diagnosis of
human dysplasia may be useful when applied to the dog.
PMID: 3576910, UI: 87207521
J Am Vet Med Assoc 1983 Sep 15;183(6):693-6
Juvenile renal disease in related Standard Poodles.
DiBartola SP, Chew DJ, Boyce JT
Chronic renal failure was diagnosed in 6 young Standard Poodles from
2 related litters. Clinically, the disease was characterized by
polydipsia, polyuria, anorexia, lethargy, vomiting, and bony
deformities suggestive of fibrous osteodystrophy. Laboratory
evaluation revealed azotemia and hypercholesterolemia in all 6 dogs
and nonregenerative anemia in 3 dogs. Two dogs had hyperphosphatemia
and another 2 were hypercalcemic. Isosthenuria and proteinuria were
found in both dogs for which urinalyses were available. The kidneys
were characterized pathologically by interstitial fibrosis, variable
interstitial infiltrates of lymphocytes and plasma cells, tubular
atrophy, tubular dilatation, tubular basement membrane
mineralization, cystic glomerular atrophy, and immaturity of
glomeruli, with inconspicuous capillary lumens.
PMID: 6629980, UI: 84031952 dd
Acta Vet Hung 1997;45(4):397-408
Ultrasonographic findings of renal dysplasia in cocker spaniels:
Felkai C, Voros K, Vrabely T, Vetesi F, Karsai F, Papp L
Department of Internal Medicine, University of Veterinary Science,
A retrospective study of eight young Cocker Spaniels aged 9-24
months was performed to describe the ultrasonographic findings of
histologically confirmed renal dysplasia. Ultrasonography revealed
kidneys of significantly (p < 0.001) reduced volume in all dogs.
During qualitative evaluation, two different types of sonographic
alterations could be seen. In one type of the ultrasound
alterations, corticomedullary demarcation was distinct and the renal
cortex was remarkably thin, which was best seen in the dorsal
(frontal) imaging plane. In the other type of the ultrasound
appearance, overall increased echogenicity with poor
corticomedullary demarcation was noticed, and the kidneys could
hardly be separated from their surroundings. These features were
best recognised in the sagittal (coronal) imaging plane. In one dog
with secondary hypercalcaemia, a hyperechoic corticomedullary area
was also seen. Post-mortem histological diagnosis revealed renal
dysplasia and secondary fibrosis. Based on ultrasound findings
alone, renal dysplasia (renal familial disease) can be suspected
when small kidneys with thin echogenic cortex are present in young
dogs. An ultrasound image, similar to that of fibrotic kidneys
(increased overall echogenicity and reduced corticomedullary
definition) cannot be differentiated from chronic inflammatory
disease and from end-stage kidneys. Therefore, ultrasound-guided
biopsy or post-mortem histology is necessary for the definitive
diagnosis of renal dysplasia. This is the first study reporting on
the ultrasound appearance of renal dysplasia in Cocker Spaniel dogs.
PMID: 9557317, UI: 98218073
Vet Rec 1990 Dec 15;127(24):596-7
A case of juvenile nephropathy in a Newfoundland dog.
Edgewood Veterinary Group, Purleigh, Chelmsford, Essex.
PMID: 2075690, UI: 91165270
Aust Vet J 1979 Apr;55(4):181-3
Renal cortical hypoplasia in a dog.
English PB, Winter H
A case of renal cortical hypoplasia in a Cocker Spaniel bitch is
presented. The dog, under clinical observation between the ages of
15 to 26 months, was found to have advancing chronic renal
insufficiency. Necropsy examination revealed a markedly hypoplastic
renal cortex with a reduced number of glomeruli, some dilated
Bowman's capsules, small glomerular tufts, and early interstitial
nephritis and fibrosis characteristic of renal cortical hypoplasia.
PMID: 464940, UI: 79231316
Can Vet J 1977 Jul;18(7):181-9
Familial renal disease in Samoyed dogs.
Bernard MA, Valli VE
PMID: 884645, UI: 77223389
Zentralbl Veterinarmed [A] 1986 Mar;33(3):193-207
[Pathomorphology of so-called juvenile renal disease in the dog].
[Article in German]
PMID: 3085397, UI: 86210748
J Am Vet Med Assoc 1990 Apr 15;196(8):1279-84
Suspected familial renal disease in chow chows.
Brown CA, Crowell WA, Brown SA, Barsanti JA, Finco DR
Department of Veterinary Pathology, College of Veterinary Medicine,
University of Georgia, Athens 30602.
Renal disease was diagnosed in 6 young Chow Chows. Clinical
abnormalities included vomiting, polyuria, polydipsia, and weight
loss. Common abnormal laboratory findings were azotemia,
hyperphosphatemia, hypocalcemia, nonregenerative anemia, and low
urine specific gravity. All 6 dogs had similar microscopic renal
lesions. characterized by interstitial fibrosis, a population of
small glomeruli, and lack of inflammatory cells. A familial basis
for the renal disease is suggested because of its development in 4
closely related dogs.
PMID: 2332376, UI: 90236807
Am J Vet Res 1977 Jul;38(7):941-7
Familial renal disease in Norwegian Elkhound dogs: morphologic
Finco DR, Duncan JD, Crowell WA, Hulsey ML
Periglomerular and interstitial fibrosis were the earliest renal
lesions in 21 Norwegian Elkhound (NE) dogs with familial renal
disease. Histopathologic study did not reveal the cause of the
disease, and light microscopy did not show renal lesions different
from nonfamilial renal lesions commonly observed in dogs.
Histopathologic evaluation was reliable for detecting disease in NE
dogs prior to onset of isosthenuria and azotemia. Results of
glomerular counts, determining kidney size, and dissection of the
nephron indicated that nephron numbers and size were adequate early
in the disease, but that numbers decreased as the disease
progressed. Electron microscopic and immunofluorescent studies were
not suggestive of an immune basis of the renal disease, nor did
histopathologic or angiographic studies indicate primary vascular
lesions. Nephron dissections revealed sacculations in distal tubules
and collecting ducts of affected NE dogs. Renal disease did not
develop in mongrel pups given injections of an homogenate or renal
tissue from an affected NE dogs.
PMID: 883721, UI: 77240305
Vet Pathol 1995 May;32(3):327-9
Renal dysplasia in golden retrievers.
Kerlin RL, Van Winkle TJ
University of Pennsylvania School of Veterinary Medicine, Laboratory
of Pathology, Philadelphia 19104, USA.
PMID: 7604504, UI: 95328216
Vet Rec 1976 Apr 10;98(15):288-93
Chronic renal failure in dogs: a comparative clinical and
morphological study of chronic glomerulonephritis and chronic
Wright NG, Fisher EW, Morrison WI, Thomson WB, Nash AS
Chronic renal disease is an important clinical problem in dogs.
Until recently, diffuse renal fibrosis with chronic renal failure
has been attributed mainly to chronic interstitial nephritis, itself
considered to be the end stage of acute leptospiral nephritis. A
clinical and morphological analysis of eight cases of chronic
glomerulonephritis is described and a comparison made with eight
dogs suffering from severe chronic interstitial nephritis.
Clinically and biochemically, the two diseases were virtually
indistinguishable, both resulting in uraemia. A possible
distinguishing feature of chronic interstitial nephritis was the
anaemia which was absent from chronic glomerulonephritis cases.
Morphologically, the two diseases appeared to be distinguishable on
three grounds; the pattern and severity of fibrosis, the degree of
fibrin deposition and the immunofluorescence findings.
PMID: 1274139, UI: 76200609
J Am Vet Med Assoc 1996 Aug 15;209(4):792-7
Juvenile renal disease in golden retrievers: 12 cases (1984-1994).
de Morais HS, DiBartola SP, Chew DJ
Department of Veterinary Clinical Sciences, College of Veterinary
Medicine, Ohio State University, Columbus 43210, USA. OBJECTIVE--To
evaluate clinical and pathologic findings in Golden Retrievers with
renal dysplasia. DESIGN--Retrospective study. ANIMALS--12 young
Golden Retrievers with chronic renal disease. PROCEDURE--Medical
records of affected dogs were evaluated on the basis of clinical
findings, laboratory test results, and histologic findings.
RESULTS--Common clinical findings were vomiting, anorexia, weight
loss, polydipsia, and polyuria. Common laboratory findings were
azotemia, hyperphosphatemia, hypercholesterolemia, isosthenuria,
proteinuria, hypercalcemia, and nonregenerative anemia. Many
affected dogs also had urinary tract infections, and some were
hypertensive. Renal lesions consisted of moderate-to-severe
interstitial fibrosis and mild-to-moderate lymphoplasmacytic
interstitial inflammation. Cystic glomerular atrophy and
periglomerular fibrosis were prominent features in most affected
dogs. Fetal lobulation of glomeruli, adenomatoid hyperplasia of
collecting tubule epithelium, and primitive mesenchymal connective
tissue were histologic features suggestive of renal dysplasia.
CLINICAL IMPLICATIONS--Renal dysplasia should be suspected in Golden
Retrievers < 3 years old with clinical findings and laboratory
results indicative of renal disease.
PMID: 8756882, UI: 96328377
Vet Rec 1981 Feb 21;108(8):167-8
Familial renal disease in samoyed dogs.
PMID: 7210449, UI: 81154850
Vet Pathol 1990 Nov;27(6):455-8
Juvenile renal disease in miniature schnauzer dogs.
Morton LD, Sanecki RK, Gordon DE, Sopiarz RL, Bell JS, Sakas PS
Department of Veterinary Pathobiology, University of Illinois,
PMID: 2278134, UI: 91118639
J Nutr 1998 Dec;128(12 Suppl):2765S-2767S
Is there a role for dietary polyunsaturated fatty acid
supplementation in canine renal disease?
Brown SA, Finco DR, Brown CA
Department of Physiology and Pharmacology, College of Veterinary
Medicine, The University of Georgia, Athens, GA 30602, USA.
Dogs with spontaneous renal diseases frequently develop progressive
uremia. After partial nephrectomy, a similar pattern of
progressively declining renal function develops. This pattern may be
attributed in part to the development of glomerular hypertension in
remnant canine nephrons. Changes in the composition of dietary
polyunsaturated fatty acids (PUFA) modify glomerular hemodynamics in
normal rats and affect the chronic course of renal disease in
partially nephrectomized rats. Thus, dietary PUFA supplementation
might alter progressive canine nephropathies. However, the response
of dogs with renal insufficiency to dietary manipulations frequently
differs substantially from that of laboratory rodents, and the
effects of dietary PUFA composition have been poorly characterized
in dogs with chronic renal disease. Here we address the hypothesis
that dietary PUFA supplementation may delay the progression of
chronic renal insufficiency in dogs. In particular, dogs ingesting
diets supplemented with (n-6) PUFA exhibited severe glomerular
hypertension associated with rapidly progressive renal failure. In
contrast, dietary supplementation with (n-3) PUFA prevented
deterioration of the glomerular filtration rate and preserved renal
structure. The results of these model studies demonstrate that
dietary PUFA supplementation may alter renal hemodynamics and the
long-term course of renal injury in dogs. Clinical trials to address
the potential benefits of dietary (n-3) PUFA supplementation in a
variety of spontaneous renal diseases seem warranted.
Publication Types: Review Review, tutorial
PMID: 9868261, UI: 99086592
Vet Q 1998 Oct;20(4):146-8
Renal dysplasia in three young adult Dutch kooiker dogs.
Schulze C, Meyer HP, Blok AL, Schipper K, van den Ingh TS
Department of Pathology, Faculty of Veterinary Medicine, Utrecht
University, Utrecht, The Netherlands.
Chronic renal failure as consequence of renal dysplasia was
diagnosed in three young adult Dutch kooiker dogs (Dutch decoy
dogs). Two animals were anorectic from an early age and were thinner
than healthy dogs of the same breed. All three were presented
because of apathy and weakness. Laboratory examination revealed
anaemia and uraemia. One dog was presented with severe dehydration
and died during emergency treatment. One dog was euthanatised
because of a poor prognosis, and one was given a low-protein diet.
This dog survived for 7 months after the diagnosis of chronic renal
failure. At necropsy all three animals had shrunken, pale, and firm
kidneys that showed microscopical lesions characteristic of canine
renal dysplasia, such as asynchronous differentiation of nephrons,
persistent immature mesenchyme, persistent metanephric ducts, and
adenomatoid proliferation of the tubular epithelium. Secondary
degenerative and inflammatory changes consisted of interstitial
fibrosis and predominantly lymphocytic/plasmacytic inflammation.
This is the first report of renal dysplasia in the Dutch kooiker
dog. The disease should be included in the differential diagnosis in
young Dutch kooiker dogs with signs of chronic renal failure. The
presentation of three cases of this rare disease in this breed,
which is based on a rather small gene pool, suggests that it is a
familial or hereditary nephropathy.
PMID: 9810631, UI: 99028326
Aust Vet J 1989 Jul;66(7):193-5
Chronic renal disease in bull terriers.
Robinson WF, Shaw SE, Stanley B, Huxtable CR, Watson AD, Friend SE,
School of Veterinary Studies, Murdoch University, Western Australia.
Chronic renal failure was diagnosed in 15 Bull terrier dogs. The
dogs ranged in age from one to 8 years. History and clinical
findings typically included lethargy, anorexia, polyuria, polydipsia
and weight loss. Affected dogs were azotaemic, had elevated serum
phosphate and cholesterol, and proteinuria was apparent in all dogs
tested (13/13). The concentration of urine was consistently in the
nil to minimally concentrated range (specific gravities
1.011-1.017). In those dogs necropsied, both kidneys were
approximately two-thirds normal size, tough in consistency, with a
pale cortex and a finely nodular capsular surface. Histologically,
there was marked nephron loss, diffuse interstitial fibrosis and
focal dense radial fibrosis which was especially evident in the
renal medulla. Tubular dilation was widespread with focal
mineralisation of tubular epithelium and adjacent basement
membranes. Glomeruli were often shrunken and segmentally fibrotic.
Some Bowman's spaces were extremely dilated. Many less severely
affected glomeruli had thickened basement membranes.
PMID: 2775060, UI: 89373851
Semin Vet Med Surg (Small Anim) 1992 Aug;7(3):244-50
The influence of dietary protein intake on progression of chronic
renal failure in dogs.
Churchill J, Polzin D, Osborne C, Adams L
Department of Small Animal Clinical Sciences, College of Veterinary
Medicine, University of Minnesota, St. Paul 55108.
Publication Types: Review Review, tutorial
PMID: 1410857, UI: 93029952
Acta Vet Acad Sci Hung 1982;30(4):171-86
Secondary renal amyloidosis and its consequences in the dog.
Dobos-Kovacs M, Deak G, Bartalits L
PMID: 7187810, UI: 84124724
J Am Vet Med Assoc 1983 Mar 1;182(5):481-5
Juvenile renal disease in Doberman Pinscher dogs.
Chew DJ, DiBartola SP, Boyce JT, Hayes HM Jr, Brace JJ
Renal failure was diagnosed in 22 young Doberman Pinscher dogs. The
clinical findings were anorexia, weight loss, vomiting, lethargy,
polydipsia, polyuria, and dehydration. Laboratory findings were
azotemia, hyperphosphatemia, lymphopenia, nonregenerative anemia,
hypercholesterolemia, and proteinuria. The kidneys were
characterized pathologically by glomerular sclerosis, cystic
glomerular atrophy, tubular dilatation, tubular atrophy, mononuclear
interstitial inflammation, interstitial fibrosis, interstitial
mineralization, and hyperplasia of the collecting duct epithelium.
PMID: 6833084, UI: 83160556
J Small Anim Pract 1997 Mar;38(3):115-8
Juvenile nephropathy in a Weimaraner dog.
Roels S, Schoofs S, Ducatelle R
Department of Pathology of Domestic Animals, Faculty of Veterinary,
Medicine, University of Ghent, Merelbeke, Belgium.
A case of juvenile nephropathy in a two-year-old Weimaraner bitch is
reported. Although Juvenile nephropathy has been described in
several breeds of dogs, this is the first report in a Weimaraner.
Clinical aspects, blood analysis, renal pathology and extrarenal
changes are described. The renal changes consisted of tubular as
well as glomerular lesions, similar to those described in the
miniature schnauzer. The main extrarenal lesion was degeneration and
necrosis of subendocardial myocytes in the left atrial wall
associated with an inflammatory reaction and focal necrotising
PMID: 9097243, UI: 97251561
J Am Vet Med Assoc 1993 Jan 1;202(1):107-9
Renal failure attributable to atrophic glomerulopathy in four
Cook SM, Dean DF, Golden DL, Wilkinson JE, Means TL
Department of Pathobiology, College of Veterinary Medicine,
University of Tennessee, Knoxville 37901-1071.
Atrophic glomerulopathy resulting in chronic renal failure was
diagnosed in 4 related Rottweilers, each < 1 year old. All 4 dogs
had severe azotemia and massive protein-losing nephropathy.
Histologically, the glomerular lesion was characterized by mild
dilatation of Bowman's space, with glomerular tufts absent or
markedly atrophied. The lesion is distinct from the congenital
glomerular changes described in Samoyeds or Doberman Pinschers. PMID:
8420894, UI: 93131650
Mod Vet Pract 1984 Aug;65(8):633-5
Primary renal disease in a dog.
Manderino DM, DeVries JG, Tamarkin J
A 7-month-old Lhasa Apso with a history of polydipsia and vomiting
was depressed, thin and dehydrated. Serum chemistry assays revealed
hyperphosphatemia and azotemia, and urinalysis revealed
isosthenuria, suggesting azotemia of renal origin. Antemortem renal
biopsy specimens contained several sclerotic glomeruli, a few
embryonic renal tubules and interstitial fibrosis, indicating renal
PMID: 6493208, UI: 85036221
Aust Vet J 1985 Apr;62(4):109-12
Familial nephropathy in cocker spaniels.
Robinson WF, Huxtable CR, Gooding JP
A clinical diagnosis of chronic renal failure associated with
nephron atrophy and fibrosis was made in 4 blue roan Cocker
Spaniels. The lesion was considered to be the result of a primary
glomerulopathy. All dogs were closely related. The findings were
similar to those previously described for renal cortical hypoplasia.
On the basis of the morphological findings and genetic
characteristics, the use of the more appropriate term, familial
nephropathy is encouraged.
PMID: 4026716, UI: 85279169
J Am Vet Med Assoc 1968 Sep 15;153(6):669-88
Renal amyloidosis in the dog.
Osborne CA, Johnson KH, Perman V, Schall WD
PMID: 5691345, UI: 68367527
J Am Vet Med Assoc 1990 Aug 15;197(4):483-7
Familial renal amyloidosis in Chinese Shar Pei dogs.
DiBartola SP, Tarr MJ, Webb DM, Giger U
Department of Veterinary Clinical Sciences, College of Veterinary
Medicine, Ohio State University, Columbus 43210.
Renal amyloidosis was diagnosed in 14 young Chinese Shar Pei dogs,
all of which were related. Clinical signs were those of renal
failure and included vomiting, anorexia, lethargy, polydipsia,
polyuria, weight loss, and dehydration. Some dogs had a history of
intermittent fever and joint swelling. Laboratory findings also were
compatible with renal failure and included azotemia,
hyperphosphatemia, low total CO2 content in serum, isosthenuria,
proteinuria, and hypercholesterolemia. All dogs had medullary
deposition of amyloid, and 9 of 14 (64%) had glomerular involvement.
The remaining renal lesions were typical of end-stage renal disease.
In some dogs, amyloid deposits were found in other tissues (eg,
liver, spleen, stomach, small intestine, myocardium, lymph node,
prostate gland, thyroid gland, and pancreas). Amyloid deposits were
sensitive to potassium permanganate oxidation, suggesting the
presence of amyloid protein AA.
PMID: 2211293, UI: 91008604
Vet Rec 1986 Jun 28;118(26):735
Chronic renal failure in young bull terriers.
Nash AS, McCandlish IA
Publication Types: Letter
PMID: 3739197, UI: 86291080
Vet Parasitol 1992 Dec;45(1-2):33-47
Pathological changes in kidneys of dogs with natural Leishmania
Nieto CG, Navarrete I, Habela MA, Serrano F, Redondo E
Department of Animal Health and Medicine, Faculty of Veterinary
Sciences, Caceres, Spain.
A study was made of the nephropathy in canine leishmaniasis produced
in ten adult dogs naturally infected with Leishmania infantum. Renal
function analyses were performed (uraemia, creatinaemia, plasma
proteins, biochemistry and urinary sediment), the humoral immune
response (fluorescent antibodies and levels of serum IgG, IgM and
IgA) was assessed and histopathological studies were carried out.
Correlation of the results showed acute renal insufficiency which
was reversible in two animals (endotheliomesangial
glomerulonephritis) and irreversible in four cases corresponding to
glomerulonephritis in its Type I and Type II proliferative forms;
extensive increase in the glomerular basal membrane, proliferation
of mesangial cells and growth of the mesangial matrix were observed,
as was a widespread incidence of immune complex deposits. Two
animals showed chronic renal insufficiency. Lack of renal changes
(minimal-changes glomerulonephritis) in two dogs was accounted for
in one animal by an almost complete absence of symptoms and in the
other by chronic viscerocutaneous symptoms; neither showed more than
a slight immunoglobulin response.
PMID: 1485420, UI: 93134777
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