A "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: pp 272-276.

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. pp 1079-1080.

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; 1987.

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; 1987.

Picut, G.A.; Lewis, R.M.: Microscopic Features of Canine Dysplasia. Vet. Path. 24:158-163; 1987.

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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

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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 dog.
PMID: 8934429, UI: 97088491
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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

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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

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Acta Vet Hung 1997;45(4):397-408

Ultrasonographic findings of renal dysplasia in cocker spaniels: eight cases.
Felkai C, Voros K, Vrabely T, Vetesi F, Karsai F, Papp L

Department of Internal Medicine, University of Veterinary Science, Budapest, Hungary.

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

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Vet Rec 1990 Dec 15;127(24):596-7

A case of juvenile nephropathy in a Newfoundland dog.
Booth K

Edgewood Veterinary Group, Purleigh, Chelmsford, Essex.

PMID: 2075690, UI: 91165270

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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

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Can Vet J 1977 Jul;18(7):181-9

Familial renal disease in Samoyed dogs.
Bernard MA, Valli VE

PMID: 884645, UI: 77223389

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Zentralbl Veterinarmed [A] 1986 Mar;33(3):193-207

[Pathomorphology of so-called juvenile renal disease in the dog]. [Article in German]
Rosenbruch M

PMID: 3085397, UI: 86210748

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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

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Am J Vet Res 1977 Jul;38(7):941-7

Familial renal disease in Norwegian Elkhound dogs: morphologic examinations.
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

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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

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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 interstitial nephritis.
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

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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

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Vet Rec 1981 Feb 21;108(8):167-8

Familial renal disease in samoyed dogs.
Bloedow AG

PMID: 7210449, UI: 81154850

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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, Urbana 61801.

PMID: 2278134, UI: 91118639

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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

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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

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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, Mitten R

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

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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

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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

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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

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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 arteritis.

PMID: 9097243, UI: 97251561

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J Am Vet Med Assoc 1993 Jan 1;202(1):107-9

Renal failure attributable to atrophic glomerulopathy in four related rottweilers.
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

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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 dysplasia.

PMID: 6493208, UI: 85036221

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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

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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

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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

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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

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Vet Parasitol 1992 Dec;45(1-2):33-47

Pathological changes in kidneys of dogs with natural Leishmania infection.
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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Last edit: March 10, 2005