Amyloidosis, PKD, Diabetes 


Amyloidosis is rare but a diagnose that is overrepresented in the Abyssinian and Siamese breed. There is no DNA test for Amyloidosis presently, and it is difficult to diagnose. PKD is common in Persians and is a automal dominant hereditary disease.


Since there is a DNA test for Polycystic Kidney Disease, PKD, its possible to detect Persians and cats of related breeds that will be affected already as kittens. Since cats only need one gene copy to be affected, there are no carriers of the mutation, all cats with a mutation will die a very painful death of the disease. Of course no cats with this mutation should be used in breeding. If the remaining population of cats is to small, you simply have to make outcrosses with other breeds.

Read about the test and which breeds the DNA test is valid for at VGL at UC Davis.


Maroti-Agots, A., A. Marko and L. Zoldag (2008). "Modified molecular genetic diagnosis of feline polycystic kidney disease". Magy. Allatorv. Lapja FIELD Full Journal Title:Magyar Allatorvosok Lapja 130(4): 205-211.

                Polycystic kidney disease (PKD) is one of the most common inherited feline diseases nowadays, affecting 38% of Persian and Persian-related cats worldwide, including the British Shorthair, Maine Coon, Exotic Shorthair, Himalayan, and Siamese. The way of inheritance of PKD is proven to be autosomal dominant. During the pathogenesis of the disease, fluid-filled cysts evolve in the kidney and sometimes in other organs, such as the liver, uterus, or the pancreas. The cysts cause the atrophy of the kidney followed by chronic renal failure. The aim here was to det. the value of mol. diagnosis of feline PKD, from both new and fixed histol. samples. Total genomic DNA was extd. and purified, the mutated sequences (PKD1 gene, exon 29) were amplified, sequenced, and digested by restriction endonuclease (RFLP), finally sepd. by electrophoresis. The developed allele specific PCR reaction was successfully applied for diagnosis in a special 3 primer contg. PCR reaction. Mol. examn. of PKD is well-suited for practical application and can be used for routine early diagnosis, screening, and reducing the incidence of warranty cases. [on SciFinder (R)]


Terio, K. A., T. O'Brien, N. Lamberski, T. R. Famula and L. Munson (2008). "Amyloidosis in black-footed cats (Felis nigripes)". Vet Pathol 45(3): 393-400.

                A high prevalence of systemic amyloidosis was documented in the black-footed cat (Felis nigripes) based on a retrospective review of necropsy tissues (n = 38) submitted as part of ongoing disease surveillance. Some degree of amyloid deposition was present in 33 of 38 (87%) of the examined cats, and amyloidosis was the most common cause of death (26/38, 68%). Amyloid deposition was most severe in the renal medullary interstitium (30/33, 91%) and glomeruli (21/33, 63%). Other common sites included the splenic follicular germinal centers (26/31, 84%), gastric lamina propria (9/23, 39%), and intestinal lamina propria (3/23, 13%). Amyloid in all sites stained with Congo red, and in 13 of 15 (87%) cats, deposits had strong immunoreactivity for canine AA protein by immunohistochemistry. There was no association with concurrent chronic inflammatory conditions (P = .51), suggesting that amyloidosis was not secondary to inflammation. Adrenal cortical hyperplasia, a morphologic indicator of stress that can predispose to amyloid deposition, was similarly not associated (P = .09) with amyloidosis. However, adrenals were not available from the majority of cats without amyloidosis; therefore, further analysis of this risk factor is warranted. Heritability estimation suggested that amyloidosis might be familial in this species. Additionally, tissues from a single free-ranging black-footed cat had small amounts of amyloid deposition, suggesting that there could be a predilection for amyloidosis in this species. Research to identify the protein sequence of serum amyloid A (SAA) in the black-footed cat is needed to further investigate the possibility of an amyloidogenic SAA in this species. [on SciFinder (R)]


White Joanna, D., M. Norris Jacqueline, L. Bosward Katrina, R. Fleay, C. Lauer and R. Malik (2008). "Persistent haematuria and proteinuria due to glomerular disease in related Abyssinian cats". J Feline Med Surg 10(3): 219-29.

                Eight cases of glomerular disease in young, related Abyssinian cats are described. Haematuria was the most consistent feature. Six cats developed the nephrotic syndrome. The short-term prognosis was good for cats with haematuria and fair for cats with the nephrotic syndrome as oedema resolved in three of the six cats. Light microscopic examination of renal biopsies from three cats was considered normal or revealed only mild abnormalities. In the three cases subjected to necropsy, histological abnormalities included mild mesangial hypercellularity and adhesions between the glomerular tuft and Bowman's capsule consistent with a focal proliferative glomerulopathy. Further investigation into this glomerulopathy will require ultrastructural and immunohistochemical studies to characterise the glomerular abnormality and genetic analyses to investigate its potential to be an inherited disease. Glomerular disease, potentially a familial one, should be considered in the investigation of persistent haematuria or proteinuria in Abyssinian and related cats. [on SciFinder (R)]


Williams, J. H., E. Van Wilpe and M. Momberg (2005). Renal medullary AA amyloidosis, hepatocyte dissociation and multinucleated hepatocytes in a 14-year-old free-ranging lioness (Panthera leo). South Africa, Department of Paraclinical Sciences, Section of Pathology, Faculty of Veterinary Science, University of Pretoria, Onderstepoort, 0110, South Africa.: 90-8.


                A 14-year-old lioness, originating from Etosha in Namibia, and a member of a pride in Pilanesberg National Park since translocation in 1994, was euthanased due to fight-related vertebral fracture and spinal injury, incurred approximately 6-8 weeks previously. Blood specimens collected at the time of death showed mild anaemia and a leukogram reflecting stress and chronic infection. Necropsy conducted within 2 hours of death was on a dehydrated, emaciated animal with hindquarter wasting and chronic traumatic friction injuries from dragging her hindlegs. There was cellulitis in the region of bite-wounds adjacent to the thoraco-lumbar vertebral fracture, at which site there was spinal cord compression, and there was marked intestinal helminthiasis. The outer renal medullae appeared pale and waxy and the liver was macroscopically unremarkable. Histopathology and electron microscopy of the kidneys revealed multifocal to coalescing deposits of proximal medullary interstitial amyloid, which fluoresced strongly with thioflavine T, and was sensitive to potassium permanganate treatment prior to Congo Red staining, thus indicating inflammatory (AA) origin. There was diffuse hepatocyte dissociation, as well as numerous binucleated and scattered multinucleated (up to 8 nuclei/cell) hepatocytes, with swollen hepatocyte mitochondria, in liver examined light microscopically. Ultrastructurally, the mono-, bi- and multinucleated hepatocytes contained multifocal irregular membrane-bound accumulations of finely-granular, amorphous material both intra-cytoplasmically and intra-nuclearly, as well as evidence of irreversible mitochondrial injury. The incidence and relevance in cats and other species of amyloidosis, particularly with renal medullary distribution, as well as of hepatocyte dissociation and multinucleation, as reported in selected literature, is briefly overviewed and their occurrence in this lioness is discussed. [on SciFinder (R)]


Lyons, L. A., D. S. Biller, C. A. Erdman, M. J. Lipinski, A. E. Young, B. A. Roe, B. Qin and R. A. Grahn (2004). "Feline polycystic kidney disease mutation identified in PKD1". J. Am. Soc. Nephrol. FIELD Full Journal Title:Journal of the American Society of Nephrology 15(10): 2548-2555.

                Autosomal dominant polycystic kidney disease (ADPKD) is a commonly inherited disorder in humans that causes the formation of fluid-filled renal cysts, often leading to renal failure. PKD1 mutations cause 85% of ADPKD. Feline PKD is autosomal dominant and has clin. presentations similar to humans. PKD affects .apprx.38% of Persian cats worldwide, which is .apprx.6% of cats, making it the most prominent inherited feline disease. Previous analyses have shown significant linkage between the PKD phenotype and microsatellite markers linked to the feline homolog for PKD1. In this report, the feline PKD1 gene was scanned for causative mutations and a C>A transversion was identified at c.10063 (human ref NM_000296) in exon 29, resulting in a stop mutation at position 3284, which suggests a loss of .apprx.25% of the C-terminus of the protein. The same mutation has not been identified in humans, although similar regions of the protein are truncated. The C>A transversion has been identified in the heterozygous state in 48 affected cats examd., including 41 Persians, a Siamese, and several other breeds that have been known to outcross with Persians. In addn., the mutation is segregating concordantly in all available PKD families. No unaffected cats have been identified with the mutation. No homozygous cats have been identified, supporting the suggestion that the mutation is embryonic lethal. These data suggest that the stop mutation causes feline PKD, providing a test to identify cats that will develop PKD and demonstrating that the domestic cat is an ideal model for human PKD. [on SciFinder (R)]


Plechner, A. J. (2003). "An effective veterinary model may offer therapeutic promise for human conditions: roles of cortisol and thyroid hormones". Med. Hypotheses FIELD Full Journal Title:Medical Hypotheses 60(3): 309-314.

                For nearly three decades, the author has treated multiple serious diseases of cats and dogs by correcting an unrecognized endocrine-immune imbalance originating with a deficiency or defect of cortisol. The cortisol abnormality creates a domino effect on feedback loops involving the hypothalamus-pituitary-adrenal axis. In this scenario estrogen becomes elevated, thyroid hormone becomes bound, and B and T cells become deregulated. Diseases with this aberration as a primary etiol. component range from allergies and strange behavior to severe cases of autoimmunity and cancer. Successful treatment and control, even in crit. cases, have been consistently achieved with a long-term physiol. (not pharmacol.) replacement with cortisone along with thyroid hormone (in dogs). The treatment represents a major healing modality for many seemingly unrelated chronic diseases of animals. In humans, this endocrine-immune dysfunction appears to exist and, as in veterinary medicine, has been overlooked by researchers and clinicians. Testing and treatment patterned after the animal model may offer significant clin. benefits for challenging human afflictions. [on SciFinder (R)]


Greco, D. S. (2001). "Congenital and inherited renal disease of small animals". Vet Clin North Am Small Anim Pract FIELD Full Journal Title:The Veterinary clinics of North America. Small animal practice 31(2): 393-9, viii.

                Congenital renal diseases are present at birth and may be determined genetically; familial renal disorders occur in related animals with a higher frequency than would be expected by chance, and frequently are inherited. The most common familial disorders in cats and dogs include renal amyloidosis, renal dysplasia, polycystic kidneys, basement membrane disorders, and tubular dysfunction (Fanconi's syndrome). This article alerts the veterinarian to commonly observed congenital and hereditary conditions of the kidneys in small animals. [on SciFinder (R)]


Hege, R., C. Zimmer and C. Reusch (2001). Polycystic kidney disease in a Persian cat. Switzerland, Klinik fur Kleintiermedizin, Universitat Zurich: 203-7.

                This case report is about a 9-year-old male castrated Persian cat with chronic renal failure. After physical examination and ultrasonography polycystic kidney disease (PKD) was diagnosed. Various aspects of etiology, pathophysiology and diagnosis of PKD are discussed. [on SciFinder (R)]


Nelson, R. W., S. M. Griffey, E. C. Feldman and S. L. Ford (1999). "Transient clinical diabetes mellitus in cats: 10 cases (1989-1991)". J Vet Intern Med 13(1): 28-35.

                Medical records of 10 cats with transient clinical diabetes mellitus were reviewed. At the time diabetes was diagnosed, clinical signs included polyuria and polydipsia (10 cats), weight loss (8 cats), polyphagia (3 cats), lethargy (2 cats), and inappetence (1 cat). Mean (+/- SD) fasting blood glucose concentration was 454 +/- 121 mg/dL, mean blood glucose concentration during an 8-hour period (MBG/8 hours) was 378 +/- 72 mg/dL, and glycosuria and trace ketonuria were identified in 10 and 5 cats, respectively. Baseline serum insulin concentration was undetectable (6 cats) or within the reference range (4 cats) and serum insulin concentration did not increase after i.v. glucagon administration in any cat. Insulin-antagonistic drugs were being administered to 5 cats and concurrent disorders were identified in all cats. Management of diabetes included administration of glipizide (6 cats), insulin (3 cats), or both (1 cat), discontinuation of insulin-antagonistic drugs, and treatment of concurrent disorders. Insulin and glipizide treatment was discontinued 4-16 weeks (mean, 7 weeks) after the initial diagnosis of diabetes was confirmed. At the time treatment for diabetes was discontinued, clinical signs had resolved, mean fasting blood glucose concentration was 102 +/- 48 mg/dL, MBG/ 8 hours was 96 +/- 32 mg/dL, glycosuria and ketonuria were not identified in any cat, and concurrent disorders (except mild renal insufficiency in 1 cat) had resolved. Significant (P < .05) increases occurred in postglucagon serum insulin concentrations, insulin peak response, and total insulin secretion, compared with values obtained when clinical diabetes was diagnosed. Histologic abnormalities were identified in pancreatic islets of 5 cats in which pancreatic biopsies were obtained and included decreased number of islets (4 cats), islet amyloidosis (3 cats), and vacuolar degeneration of islet cells (3 cats). Mean beta cell density was significantly (P < .001) decreased in diabetic cats compared with control cats (1.4 +/- 0.7 versus 2.6 +/- 0.5%, respectively). Cells within islets stained positive for insulin, however, the number of insulin-staining cells per islet and the intensity of insulin staining were decreased in 5 and 2 cats, respectively. Clinical diabetes had not recurred in 1 cat after 6 years, in 4 cats lost to follow-up after 1.5, 1.5, 2.0, and 2.5 years, and in 2 cats that died 6 months and 5.5 years after clinical diabetes resolved. Clinical diabetes recurred in 3 cats after 6 months, 14 months, and 3.4 years, respectively. These findings suggest that cats with transient clinical diabetes have pancreatic islet pathology, including decreased beta cell density, and that treatment of diabetes and concurrent disorders results in improved beta cell function, reestablishment of euglycemia, and a transition from a clinical to subclinical diabetic state. [on SciFinder (R)]


Godfrey, D. R. and M. J. Day (1998). Generalised amyloidosis in two Siamese cats: spontaneous liver haemorrhage and chronic renal failure. ENGLAND: United Kingdom, Nine Lives Veterinary Practice for Cats, West Midlands: 442-7.

                Two cases are reported, illustrating the antemortem diagnosis of systemic amyloidosis in Siamese cats. A cat presenting with inappetence and depression was diagnosed as having systemic amyloidosis with spontaneous haemorrhage from the liver. In another cat from the same breeding cattery, chronic renal failure due to systemic amyloidosis was an incidental finding. Little treatment was possible in either case and both were later euthanased. The two cats had similar renal and hepatic pathology but different signs of disease. [on SciFinder (R)]


Takebayashi, S. (1995). "Histopathology of the biopsied kidney and its related glomerular deterioration". Nippon Jinzo Gakkai Shi 37(5): 263-70.

                This paper presents the incidence of glomerulonephritis (-pathy: GN) from a large number of more than 10,000 serial renal biopsies examined in one laboratory using the same criteria over the past 25 yrs. in Japan. Each incidence is as follows: IgA nephropathy (IgAN), 33%; thin glomerular basement membrane disease (TBMD), 17.8; athletic pausal urinary abnormality (APUA), 8.2; primary membranous glomerulonephritis (memb GN), 6.5; while all others were less than 5% each. Out of 3,300 IgAN cases, 51% consisted of a minimal change IgAN (MCIgAN), while the IgAN cases with moderate to severe glomerular damage comprised 20% of all cases. In addition, the survival curves of the IgAN cases coincided with those of FGS and benign nephrosclerosis (BNS) with a similar extent of glomerular damages. On the other hand, glomerular damage mostly occurred due to intra- and intercapillary cell infiltration; poststreptococcal GN (AGN), lupus N, Cat. III a IV a and IV b, and MCIgAN all had a favorable outcome (follow-up mean: 12.4 +/- 6.7 yrs). More than 50% of the dialized patients came from both IgAN, focal type with hypertension, and IgAN with more than moderate glomerular damage regardless hypertension. The incidences of AGN, MPGN, HBvN have all decreased at the present time, while renal amyloidosis and crescentic glomerulonephritis (Cres. GN) have increased in number and this is reflected by the increased number of renal biopsies in elderly men. Glomerular deterioration is thus considered to be caused more by non-immunologic and hemodynamic injuries than by immune-derived, repeated inflammation, in human chronic glomerulonephritis(-pathy). [on SciFinder (R)]


Gregory, C. R., H. J. Olander, E. J. Kochin, I. M. Gourley, D. Cousyn and J. Levy (1993). "Oxalate nephrosis and renal sclerosis after renal transplantation in a cat". Vet Surg FIELD Full Journal Title:Veterinary surgery : VS : the official journal of the American College of Veterinary Surgeons 22(3): 221-4.

                A 10-year-old castrated domestic shorthair cat received two renal allografts, 14 days apart, for the treatment of chronic renal failure. Oxalate nephrosis developed in both allografts, and they became nonfunctional. During the transplantation period, the cat was not exposed to exogenous sources of oxalate, and there was no evidence of primary type 2 hyperoxaluria before surgery. Urologic surgery, in particular renal transplantation, has been identified as a factor that can precipitate renal failure in human patients with decompensated renal function and hyperoxaluria. If hyperoxaluria was present before surgery in this cat, it was most likely caused by increased absorption or decreased metabolism of dietary oxalate. [on SciFinder (R)]


Podell, M., S. P. DiBartola and T. J. Rosol (1992). Polycystic kidney disease and renal lymphoma in a cat. United States, Department of Veterinary Clinical Sciences, College of Veterinary Medicine, Ohio State University, Columbus 43210: 906-9.

                A 2-year-old castrated domestic shorthair cat was determined to have polycystic kidney disease (PKD) and renal lymphoma. History and examination findings consisted of progressive lethargy, asymmetric renomegaly, thick segments of small intestine, and anisocoria. Initial diagnostic tests revealed nonregenerative anemia, mild azotemia, and multiple, round anechoic cysts in both kidneys. Renal cystic fluid contained many mature lymphocytes, and results of biochemical analysis indicated that the fluid was consistent with proximal tubular fluid. Stage-3 lymphoma was diagnosed on the basis of histologic evidence of unresectable lymphoma in multiple abdominal organs. Chemotherapy with vincristine sulfate, cytarabine, cyclophosphamide, and prednisone was unsuccessful. Morphologic association between PKD and lymphoma could not be identified after histologic evaluation of the kidneys. [on SciFinder (R)]


DiBartola, S. P., H. C. Rutgers, P. M. Zack and M. J. Tarr (1987). "Clinicopathologic findings associated with chronic renal disease in cats: 74 cases (1973-1984)". J Am Vet Med Assoc 190(9): 1196-202.

                The historic, physical, laboratory, and histologic findings for 74 cats with chronic renal disease were reviewed. Most cats were older, and no breed or sex predilection was detected. This most common clinical signs detected by owners were lethargy, anorexia, and weight loss. Dehydration and emaciation were common physical examination findings. Common laboratory findings were nonregenerative anemia, lymphopenia, azotemia, hypercholesterolemia, metabolic acidosis, hyperphosphatemia, and isosthenuria. The most common morphologic diagnosis was chronic tubulointerstitial nephritis of unknown cause. The other pathologic diagnoses were renal lymphosarcoma, renal amyloidosis, chronic pyelonephritis, chronic glomerulonephritis, polycystic renal disease, and pyogranulomatous nephritis secondary to feline infectious peritonitis. [on SciFinder (R)]


DiBartola, S. P., M. J. Tarr and M. D. Benson (1986). "Tissue distribution of amyloid deposits in Abyssinian cats with familial amyloidosis". J Comp Pathol FIELD Full Journal Title:Journal of comparative pathology 96(4): 387-98.

                The tissue distribution of amyloid deposits was studied in 15 related Abyssinian cats with familial amyloidosis. There was interstitial medullary amyloidosis in the kidneys of all 15 cats but only 11 had detectable glomerular involvement. The thyroid glands, stomach and colon were affected in all cats examined. Most of the cats also had amyloid deposits in the small intestine, spleen, heart, adrenals, pancreas, liver, lymph nodes and bladder. In 50 per cent or fewer of the cats examined, there was involvement of the parathyroids, lung and gonads. The central nervous system was not involved in any of the 3 cats evaluated. In 8 of the cats, no concurrent inflammatory disease could be detected. The tissue distribution of amyloid deposits resembled that found in other breeds of domestic cats with systemic amyloidosis. Despite the wide tissue distribution of amyloid deposits, clinical signs were related to renal amyloidosis. Familial amyloidosis in the Abyssinian cat may represent a valuable spontaneous animal model for the study of Familial Mediterranean Fever in man and the pathogenesis of reactive amyloidosis in general. [on SciFinder (R)]


Watson, A. D., J. A. Culvenor, D. J. Middleton and T. L. Rothwell (1986). Distal renal tubular acidosis in a cat with pyelonephritis. ENGLAND: United Kingdom: 65-8.

                A four-year-old castrated male domestic shorthair cat with recent onset of lethargy and depression was found to have hypokalaemia, low plasma bicarbonate concentration and a urine pH of 7. Subsequent findings of hyperchloraemic metabolic acidosis with failure to produce acid urine led to a diagnosis of distal renal tubular acidosis. Pyelonephritis associated with Escherichia coli infection of the urinary tract was also diagnosed. The urinary tract infection was eliminated by antibiotic treatment. For two years subsequently, the clinical effects of distal renal tubular acidosis have been controlled by oral administration of potassium bicarbonate, although some biochemical abnormalities have persisted. [on SciFinder (R)]


DiBartola, S. P., M. D. Benson, F. E. Dwulet and J. B. Cornacoff (1985). "Isolation and characterization of amyloid protein AA in the Abyssinian cat". Lab. Invest. FIELD Full Journal Title:Laboratory Investigation 52(5): 485-9.

                Amyloid fibrils were isolated from the kidneys of an Abyssinian cat with familial renal amyloidosis. The primary structure of the amyloid fibril subunit protein showed strong homol. with amyloid protein AA found in man and animals with spontaneous and exptl. induced reactive systemic amyloidosis. This study confirms the reactive nature of familial renal amyloidosis in the Abyssinian cat and suggests that this disease may be a valuable spontaneous animal model for the study of familial Mediterranean fever in man. [on SciFinder (R)]


August, J. R. and M. S. Leib (1984). "Primary renal diseases of the cat". Vet Clin North Am Small Anim Pract 14(6): 1247-60.

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Boyce, J. T., S. P. DiBartola, D. J. Chew and P. W. Gasper (1984). "Familial renal amyloidosis in Abyssinian cats". Vet Pathol FIELD Full Journal Title:Veterinary pathology 21(1): 33-8.

                Medullary and glomerular amyloidosis, papillary necrosis, and secondary interstitial disease were diagnosed in eight related adult Abyssinian cats from two catteries. The lesions were similar to those in two unrelated mongrel cats with renal amyloidosis. Ultrastructurally, the patterns of amyloid deposition were as described in other species, although medullary deposition predominated. Potassium permanganate oxidation blocked Congo red staining of the deposits suggesting that they contained amyloid A protein (secondary amyloid). The disease may be a model of familial secondary amyloidosis and offers an opportunity to study the pathogenesis of both amyloid deposition and papillary necrosis. The histochemical characteristics of feline renal amyloid require careful attention to technique. Section thickness affects Congo red affinity and both dichroism as well as birefringence should be considered when interpreting staining reactions. Thioflavine-T may be the preferred stain for identification of small deposits of amyloid. Variation in section thickness markedly affected the degree of potassium permanganate oxidation. [on SciFinder (R)]


Chew, D. J., S. P. DiBartola, J. T. Boyce and P. W. Gasper (1982). Renal amyloidosis in related Abyssinian cats. United States: 139-42.

                Renal amyloidosis was diagnosed in 8 related Abyssinian cats. The kidneys were characterized pathologically by medullary interstitial and glomerular amyloid deposition, interstitial fibrosis, and papillary necrosis. Amyloid deposits were birefringent under polarized light after Congo red staining, were thioflavine-T positive, and lost Congo red staining after permanganate oxidation. Four of the cats were evaluated clinically. Two of these cats were terminally uremic, with nonregenerative anemia, azotemia, hyperphosphatemia, metabolic acidosis, mild hyperglycemia, isosthenuria, proteinuria, cylindruria, and mild hematuria. The remaining 2 cats were only moderately azotemic. Three of the cats had severe gingivitis and all 4 cats had hyperproteinemia due to hyperglobulinemia. [on SciFinder (R)]


Saegusa, S., F. Shimizu, M. Nagase and A. Kasegawa (1979). "Concurrent feline immune-complex nephritis. Tubular antigen-positive and renal amyloidosis". Arch Pathol Lab Med 103(9): 475-8.

                We describe tubular antigen-positive immune-complex nephritis in a case of feline renal amyloidosis. Amyloid deposition was observed in mesangial area, and thickening of capillary walls was shown in the majority of the glomeruli. This case was also characterized with typical fluorescent granular depositions of cat IgG and C3 along the glomerular capillary walls as seen in human membranous glomerulonephritis. The fluorescent pattern of tubular antigen was identical with that of IgG and C3. Electron micrograph showed the thickening and irregularity of glomerular basement membranes, fusion of foot processes, and deposits of electron-dense or sometimes translucent materials, mostly in the intramembranous location. The causal sequence of the coincidental deposition of amyloid and immune complexes is discussed. [on SciFinder (R)]


Giddens, W. E., Jr., R. F. Labbe, L. J. Swango and G. A. Padgett (1975). "Feline congenital erythropoietic porphyria associated with severe anemia and renal disease. Clinical, morphologic, and biochemical studies". Am. J. Pathol. FIELD Full Journal Title:American Journal of Pathology 80(3): 367-86.

                A feline erythropoietic porphyria was studied in an affected female Siamese cat and 2 male offspring. The principal elevated porphyrins were Type I isomers of uroporphyrin and coproporphyrin; the porphyrin precursors, porphobilinogen and d-aminolevulinic acid, were also detected. Porphyrins were present in the blood and in all the viscera, teeth, bones, and excreta. There was severe macrocytic hypochromic anemia, hepatomegaly, splenomegaly, and uremia assocd. with a renal disease characterized by mesangial hypercellularity and proliferation (resulting in narrowing of glomerular capillaries) and ischemic tubular injury. There was thickening of tubular basement membranes and tubular epithelial lipidosis, degeneration, and necrosis, electron microscopic studies of bone marrow and kidney revealed the presence of membrane-enclosed lamellar bodies 150-1000 nm in diam. in cytoplasmic and extracellular locations. [on SciFinder (R)]


Crowell, W. A., R. T. Goldston, W. D. Schall and D. R. Finco (1972). "Generalized amyloidosis in a cat". J Am Vet Med Assoc 161(10): 1127-33.

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Osborne, C. A., D. G. Low and K. H. Johnson (1971). "Renal disease". Vet Clin North Am 1(2): 323-53.

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Clark, L. and A. A. Seawright (1969). "Generalised amyloidosis in seven cats". Pathol Vet 6(2): 117-34.

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Godfrey, D. R. and M. J. Day "Generalised amyloidosis in two Siamese cats: spontaneous liver haemorrhage and chronic renal failure". J Small Anim Pract FIELD Full Journal Title:The Journal of small animal practice FIELD Publication Date:1998 39(9): 442-7. FIELD Reference Number: FIELD Journal Code:0165053 FIELD Call Number:.

                Two cases are reported, illustrating the antemortem diagnosis of systemic amyloidosis in Siamese cats. A cat presenting with inappetence and depression was diagnosed as having systemic amyloidosis with spontaneous haemorrhage from the liver. In another cat from the same breeding cattery, chronic renal failure due to systemic amyloidosis was an incidental finding. Little treatment was possible in either case and both were later euthanased. The two cats had similar renal and hepatic pathology but different signs of disease. [on SciFinder (R)] FIELD Check Tags:Female


Harkin Kenneth, R., S. Biller David and L. Balentine Heather "Glomerulocystic kidney disease in a kitten". J Am Vet Med Assoc FIELD Full Journal Title:Journal of the American Veterinary Medical Association FIELD Publication Date:2003 223(12): 1780-2, 1778. FIELD Reference Number: FIELD Journal Code:7503067 FIELD Call Number:.

                A 4-month-old 1-kg female Siamese-Manx cross kitten was evaluated because of renomegaly and renal failure. Ultrasonography and cytologic examination of a renal aspirate failed to provide an antemortem diagnosis. Histologic lesions included diffuse cystic dilatation of all tubules and Bowman's spaces in the renal cortex and occasional small glomerular tufts; the lesions were similar to those of glomerulocystic kidney disease of humans. Glomerulocystic kidney disease is a rare cause of early-onset renal failure, but should be considered when renomegaly is detected, cysts are not detected in the kidney by ultrasonography, and cytologic examination of a renal aspirate is nondiagnostic. [on SciFinder (R)] FIELD Check Tags:Female




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