Selected Diseases of the Feline Kidney
World Small Animal Veterinary Association World Congress Proceedings, 2001
Stephen DiBartola
United States


The clinical significance of polycystic renal disease depends on whether it is unilateral or bilateral and the amount of associated renal parenchymal damage. Congenital polycystic renal disease has been reported in related long-haired kittens of both sexes. Acquired polycystic renal disease has been described in male and female cats three to eight years of age. It is inherited as an autosomal dominant trait in the Persian cat. Renal cysts can be detected by ultrasonography as early as six to eight weeks of age, but renal failure does not occur until later in life. If chronic renal failure is present, compatible clinical signs are observed, including polyuria, polydipsia, anorexia, weight loss, and lethargy. On physical examination, enlarged irregular kidneys may be palpated, often accompanied by dehydration, pallor of mucous membranes, and emaciation. Laboratory findings include azotemia, hyperphosphatemia, isosthenuria, nonregenerative anemia, and metabolic acidosis if chronic renal failure is present. Ultrasonography shows multiple, anechoic spherical lesions with distal acoustic enhancement. On pathologic examination, there are multiple cysts of varying size in the renal cortex and medulla. With bilateral involvement, treatment is limited to medical management for chronic renal failure.


Pyelonephritis refers to interstitial inflammation, often most severe in the renal pelvis and adjacent medullary tissue, associated with bacterial infection of the kidney. Bacterial urinary tract infection is less common in the cat than in the dog and the importance of ascending infection and obstructive nephropathy in the pathogenesis of pyelonephritis in the cat is not clear. Pyelonephritis in cats may result in fever, anorexia, lethargy, dehydration, and weight loss. Such clinical signs are not expected in all affected animals and may be present for a very short period, making recognition of the disease difficult. Depending on the extent of renal parenchymal involvement, azotemia, hyperphosphatemia, nonregenerative anemia, and metabolic acidosis also may be found. Unfortunately, urinalysis findings often are nonspecific and urine cultures may be negative in chronic pyelonephritis. Excretory urography may show dilatation of the renal pelvis and diverticula or decreased renal size. Treatment consists of bactericidal antibiotics (for four to eight weeks) to eradicate the infection, definitive therapy to remove any predisposing factors (e.g., calculi, obstruction), and fluid therapy to restore and maintain hydration. The prognosis is good if predisposing factors can be eliminated and if treatment is instituted before the development of endstage renal disease.


In most reports of GN in the cat, no predisposing factors have been found and the disease has been classified as idiopathic. Young adult male cats typically are affected and there is no breed predisposition. The clinical presentation falls into two categories: classical nephrotic syndrome characterized by subcutaneous edema, ascites, proteinuria, hypercholesterolemia, and hypoalbuminemia without marked azotemia, and chronic renal failure with azotemia. Laboratory abnormalities in cats with GN include proteinuria, hypoalbuminemia, hypercholesterolemia, and nonregenerative anemia. The presence of azotemia and hyperphosphatemia is variable. Histologically, the lesions are those of membranous nephropathy with IgG and complement deposition. An attempt should be made to diagnose and treat any underlying disease process that might have resulted in the development of GN. Cats with edema and ascites but without azotemia may be treated with furosemide (2–4 mg/kg q24h) and prednisolone (2–4 mg/kg q24h). These cats also should be fed a high protein, low sodium diet. Cats with azotemia and endstage renal disease due to GN should be treated for chronic renal failure. The prognosis for cats with GN is variable. The disease is slowly progressive although remissions have been described. Cats with endstage renal disease secondary to GN have the shortest survival times (a few weeks to a few months). Non-azotemic cats presented with the nephrotic syndrome do better and survive several months to several years.


Spontaneous systemic amyloidosis is uncommon in the domestic cat but occurs as a familial disease in the Abyssinian cat. Affected Abyssinian cats usually are presented between one and five years of age. Amyloid deposits first appear in the kidneys of affected Abyssinian cats between 9 and 24 months of age. In some of these cats, amyloid deposition is rapid and severe and renal failure develops within one year of diagnosis. In others, amyloid deposition in the kidney is mild and affected cats may live to an advanced age without detection of their amyloid deposits. Affected Abyssinian cats usually are presented for poor haircoat, weight loss, polydipsia, polyuria, lethargy, and anorexia. Physical examination findings include dehydration; pallor of mucous membranes, gingivitis and oral ulceration; and kidneys that are small, firm, and irregular on palpation. Laboratory evaluation reveals evidence of chronic renal failure including azotemia, hyperphosphatemia, metabolic acidosis, nonregenerative anemia, and isosthenuria. Proteinuria is a variable finding and reflects the severity of glomerular involvement. The diagnosis of amyloidosis requires proper pathologic evaluation of an adequate renal biopsy specimen. A wedge of kidney containing both cortical and medullary tissue obtained at laparotomy is more likely to yield a definitive diagnosis than a percutaneous needle biopsy specimen, because of the prominent medullary distribution of renal amyloidosis in the cat. Treatment of amyloidosis is largely limited to symptomatic therapy of chronic renal failure. Underlying inflammatory disease is uncommonly detected but any concomitant infections should be treated appropriately. Systemic reactive amyloidosis also has been observed in Siamese and Oriental shorthaired cats. Severe liver involvement in these breeds can lead to liver rupture and acute abdominal hemorrhage.


Chronic interstitial nephritis is a common morphologic diagnosis and may represent the end result of several different renal diseases including chronic glomerulonephritis and chronic pyelonephritis. In most patients, however, the inciting cause cannot be determined. The most common historical findings in cats with endstage renal disease are weight loss, anorexia, and lethargy. Polyuria, polydipsia, and vomiting are detected less commonly by owners. Physical examination may show poor hair coat, emaciation, pallor of mucous membranes, and dehydration. The kidneys are small, firm, and irregular on abdominal palpation. Laboratory findings include nonregenerative anemia, azotemia, hyperphosphatemia, metabolic acidosis, hypokalemia, and isosthenuria. Except for urine specific gravity, urinalysis findings in cats with endstage renal disease generally are unremarkable. Renal biopsy will allow identification of a specific disease process or confirmation of the diagnosis of chronic interstitial nephritis of unknown cause.

Initial treatment requires rehydration over 24–72 hours. Renal function should be evaluated after rehydration before judgment is made about the ultimate disposition of the cat. Long term medical management is begun after the cat has been rehydrated and stabilized. This therapy includes dietary restriction of protein (3.5-4.0 g/kg q24) and phosphorus; supplementation with vitamins, taurine, and potassium; endocrine replacement therapy including calcitriol and erythropoietin; management of hypertension; and subcutaneous administration of fluids at home by the owner. Protein restriction should be considered when moderate azotemia persists in the well-hydrated state. Effective use of a low protein diet is indicated by reduction in BUN, stable body weight, and stable serum albumin concentration on serial measurements. Fresh water should be provided ad libitum and consumption of liquids should be encouraged. Phosphorus restriction is accomplished by dietary restriction and phosphorus-binding agents if necessary (aluminium hydroxide, aluminium carbonate, calcium carbonate, or calcium acetate) at a dosage of 60–100 mg/kg/day and administered with meals. Hypokalemia occurs in 20% to 30% of cats with chronic renal failure and may be treated using oral potassium gluconate (2–4 mEq q24h). Anabolic steroids have a low margin of safety in cats (risk of hepatotoxicity) and therefore are not routinely recommended for cats with chronic renal failure. Vomiting and uremic gastroenteritis are less common in cats with chronic renal failure than in dogs and may be managed with famotidine (5 mg orally once per day). Recently, an extremely low dosage of calcitriol (2–4 ng/kg q24h) has been used in cats with stable chronic renal failure to blunt renal secondary hyperparathyroidism. Calcitriol should not be administered until hyperphosphatemia has been controlled. Recombinant human erythropoietin (100 U/kg SQ three times per week) has been used to correct nonregenerative anemia in cats with chronic renal failure. There is a substantial risk of antibody formation in cats treated with human erythropoietin, and the drug has not been approved for use in animals. Hypertension usually is treated with amlodipine (0.625 mg orally once per day) or enalapril (0.5 mg/kg orally once or twice per day) in cats with glomerulonephritis that are not azotemic. The prognosis for cats with chronic renal failure is variable, and the disease appears to progress at different rates in different patients. Affected cats may live several months to years with conservative medical management.


The non-effusive form of the coronaviral disease, feline infectious peritonitis (FIP), often affects the kidneys, liver, mesenteric lymph nodes, central nervous system, and eyes. There is renal involvement in many of these cats and they may be presented for evaluation of enlarged, irregular kidneys. Cats with non-effusive FIP and renal involvement may be presented for vague signs of systemic illness such as fever, lethargy, anorexia, and weight loss. With extensive renal involvement, however, signs referable to renal insufficiency (e.g., polydipsia, polyuria) also may occur. Physical examination reveals irregular, enlarged, firm kidneys. Other findings suggestive of FIP may be present, for example, uveitis, chorioretinitis, enlarged mesenteric lymph nodes, and neurologic abnormalities. Cats with FIP may have proteinuria, and, if there has been sufficient destruction of renal parenchyma, may develop azotemia. Presumptive diagnosis of renal FIP can be made by a fine needle aspirate of the enlarged kidney and the observation of pyogranulomatous inflammation consisting of a mixture of neutrophils, macrophages, lymphocytes, and plasma cells. The treatment of FIP consists of immunosuppressive drugs (e.g., prednisolone, cyclophosphamide).


Lymphosarcoma is the most common renal neoplasm of the cat. It is bilateral and often associated with the alimentary form of the disease. Frequently, clinical signs result primarily from gastrointestinal involvement and the extent of renal involvement is insufficient to cause signs of renal failure. Occasionally, however, renal involvement may be extensive enough to cause renal failure. Cats with renal lymphosarcoma may be presented for anorexia, lethargy, weight loss, polydipsia, polyuria, dehydration, pallor of the mucous membranes, and bilateral renomegaly. Azotemia, hyperphosphatemia, proteinuria, isosthenuria, and nonregenerative anemia may be observed on laboratory evaluation. Approximately 50% of cats with renal lymphosarcoma are FeLV-positive. The diagnosis of renal lymphosarcoma can be made by cytologic examination of a fine needle aspirate of the kidney demonstrating a monomorphic population of immature lymphocytes. Treatment can be attempted using conventional chemotherapy, but the prognosis is poor.


Laboratory evaluation of cats with chronic renal failure and presumed potassium depletion shows moderate to severe hypokalemia (usually < 3.1 mEq/L), increased creatine kinase concentration, azotemia, hyperchloremic metabolic acidosis, variable hyperphosphatemia, and isosthenuria. Histopathologic findings observed in the kidneys of cats with chronic renal failure and presumed potassium depletion, include interstitial fibrosis, lymphoplasmacytic interstitial inflammation, tubular dilation, tubular atrophy, and variable glomerular sclerosis. Acute treatment requires diligent potassium supplementation by both oral and intravenous routes. Potassium should not be infused intravenously at a rate greater than 0.5 mEq/kg body weight per hour. Infusion of potassium-containing crystalloid fluids initially may be associated with a decrease in serum potassium concentration as a result of dilution, increased tubular fluid flow in the distal renal tubules, and cellular uptake of potassium. This effect may be minimized by selecting a fluid that does not contain glucose, administering fluids at an appropriate rate, and beginning oral potassium gluconate (4 to 8 mEq q24h) as soon as possible. Clinical improvement usually is observed within one to three days. Chronic treatment involves oral administration of potassium gluconate (2 to 4 mEq q24h). Treatment results in resolution of muscle weakness, hypokalemia, and anemia. Renal function stabilizes or improves in most instances.


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Stephen DiBartola
United States

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