Distal renal tubular acidosis in a cat with pyelonephritis

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.     

Hyperlipemia and Ketonuria in an Alpaca and a Llama

An alpaca and a llama in late stages of gestation were evaluated for lethargy, anorexia, and recumbency. Both camelids had cloudy, white, turbid serum, elevated serum triglyceride (1564, 5658 mg/dL, respectively) and cholesterol (158, 297 mg/dL, respectively) concentrations, and ketonuria. Signs of fetal stress were evident ultrasonographically in the alpaca, and a live cria was delivered by Cesarean section performed under general anesthesia. The alpaca developed severe metabolic acidosis, hepatic lipidosis, and acute renal failure secondary to renal lipidosis and died 36 hours after admission despite medical therapy. Histopathology revealed renal and hepatic lipidosis and neutrophilic pancreatitis. The cria died 72 hours after birth. The llama responded to IV electrolyte, dextrose, and regular crystalline insulin therapy. The pregnancy was maintained, and the llama was discharged from the hospital 20 days after admission. Two months after discharge, the llama gave birth to a live, 5 kg cria. Findings of hypertriglyceridemia, hypercholesterolemia, elevated sorbitol dehydrogenase activity, metabolic acidosis, azotemia, and ketonuria occurred in these two camelids. Based on this report, camelids appear to be similar to both horses and cattle in their response to severe energy imbalances in late gestation.     

IATROGENIC BILOMA (BILIARY PSEUDOCYST) IN A CAT WITH HEPATIC LIPIDOSIS

An eight-year-old neutered female domestic longhair cat was presented with icterus and a palpable cranial abdominal mass. The cat had undergone an open biopsy of the liver two years previously. Abdominal radiographic findings included a solitary soft tissue mass originating from the right cranial hepatic region. An anechoic cystic structure was identified on ultrasound examination. Surgical exploration revealed the cyst to be filled with bile. The fibrous capsule of the cyst originated in the liver. Severe hepatic lipidosis was also present. It is believed that the bilorna was a complication of the previous hepatic biopsy and not a sequela of hepatic lipidosis.     

Canine distal renal tubular acidosis and urolithiasis

Distal RTA is characterized by decreased distal renal tubular hydrogen ion secretion, decreased ability to acidify urine, hypercalciuria, hyperphosphaturia, hypocitraturia, and metabolic acidosis. Because of the resulting alterations in urine composition and pH, patients with distal RTA are predisposed to urolithiasis and renal calcification. Diagnosis of distal RTA is important because it is a potentially reversible disorder that, left untreated, may cause nephrocalcinosis, recurrent urolith formation, moderate to severe metabolic acidosis, and renal failure.     

Glomerular lipidosis accompanied by renal tubular oxalosis in wild and laboratory-reared Japanese rock ptarmigans (Lagopus mutus japonicus)

Glomerular lipidosis is a disease characterized by lipid accumulation in mesangial cells but that has not been fully investigated in avian species. We examined four wild and two laboratory-reared Japanese rock ptarmigans (Lagopus mutus japonicus)--an endangered avian species--presenting vacuolar deposits in the glomeruli. All cases had vacuolar deposits in the glomeruli. In the wild cases, fewer than 30% of all glomeruli were affected, compared with more than 90% in the laboratory-reared cases. In the wild cases, most deposits were mild and restricted to the mesangial areas of glomeruli. In the laboratory-reared cases, nearly all of the deposits covered entire glomeruli. Electron microscopy of mild deposits revealed vacuoles in the cytoplasm of mesangial cells. These vacuoles were positive for Sudan III, Sudan black B, oil red O, Nile blue, periodic acid-Schiff, Schultz test, and digitonin stain and were negative for performaric acid-Schiff stains. Based on these results, we diagnosed the glomerular lesion as glomerular lipidosis caused by uptake of low-density lipoprotein in mesangial cells. Except for one wild case, all cases exhibited renal tubular oxalosis. The severity of tubular oxalosis tended to be related to the severity of glomerular lipidosis: In cases of mild glomerular lipidosis, tubular oxalosis was also mild or absent. We therefore diagnosed the primary lesion as glomerular lipidosis accompanied by tubular oxalosis. The four wild cases came from different zones and therefore had no opportunities to interbreed and no common relatives. We believe these data support the hypothesis that glomerular lipidosis is a disease of the general population ofJapanese rock ptarmigans. This is the first report of glomerular lipidosis accompanied by renal tubular oxalosis in an avian species.     

Acute Pancreatitis in Cats With Hepatic Lipidosis

The purpose of this study was to characterize the incidence, clinical features, and prognosis of acute pancreatitis in cats with hepatic lipidosis. Of 13 cats histologically diagnosed with hepatic lipidosis between July 1988, and November 1989,5 (38%) were also histologically diagnosed with acute pancreatitis. In cats with hepatic lipidosis alone, the signalment, history, physical examination, and clinicopatho-logic findings were generally indistinguishable from those of cats with concurrent acute pancreatitis except that cats with acute pancreatitis were more likely to be cachectic and to have coagulation abnormalities. Hepatomegaly was seen on abdominal radiographs in both groups. Of the 5 cats with concurrent acute pancreatitis, abdominal ultrasonography detected 1 cat with a hypoechoic pancreas and 5 with peritoneal effusion; those abnormalities were not seen in cats without concurrent acute pancreatitis. Cats with concurrent acute pancreatitis had only a 20% recovery rate, compared with a 50% recovery rate in cats with hepatic lipidosis alone. We conclude that cats with hepatic lipidosis should be rigorously evaluated for concurrent acute pancreatitis because of 1) the rate of disease coincidence, 2) the inability of signalment, history, physical examination, and clinicopathologic findings to adequately distinguish between hepatic lipidosis and acute pancreatitis, 3) the worse prognosis associated with concurrent acute pancreatitis, and 4) the opposing nutritional strategies for hepatic lipidosis and acute pancreatitis. (Journal of Veterinary Internal Medicine 1993; 7:205–209. Copyright © 1993 by the American College of Veterinary Internal Medicine.)     

Gallbladder mucocoele and concurrent hepatic lipidosis in a cat

A 3-year-old Domestic Shorthair cat was presented with weight loss, anorexia and icterus. Feline hepatic lipidosis and gallbladder mucocoele were diagnosed; this is the first report of gallbladder mucocoele in the cat. The case was managed successfully with cholecystojejunostomy, gastrostomy tube placement and tube feeding for 3 months. The cat has survived over the long term with minimal complications.     

Acute response of urine pH following ammonium chloride administration to dogs

To test the acidifying ability of the distal portion of the nephrons in healthy dogs, 0.2 g of NH4Cl/kg of body weight was given PO. Samples for venous blood gas analysis and urine pH were taken hourly for 6 hours. Systemic acidemia developed, as evidenced by a statistically significant (P less than 0.05) decrease in blood pH 1 hour after NH4Cl administration. Four hours after administration, mean urine pH decreased to a low of 5.16 +/- 0.1 and was less than 5.5 3 hours after administration. Changes in urine pH 2 hours after administration were statistically significant (P less than 0.05). In human beings, NH4Cl loading is used to detect patients with distal renal tubular acidosis (defective hydrogen ion secretion by the distal nephrons) and normal acid/base values. Distal renal tubular acidosis is diagnosed if urine pH fails to decrease to less than 5.5 after NH4Cl administration. On the basis of the findings of this study, a similar value would be valid for dogs.     

Spontaneous Occurrence of Hepatic Lipidosis in a Group of Laboratory Cats

Clinical signs consistent with hepatic lipidosis occurred in six obese adult laboratory cats, housed in a group cage, 6 to 7 weeks after changing their diet from a commercial to a purified diet. The affected cats lost 30 to 40% of their body weight in this time period. This rate of weight loss is compatible with little or no food intake. For treatment, 5 cats were tube-fed three or four times daily with a high-fat liquid diet supplemented with L-citrulline and choline. All cats tolerated the diet, which contained 35% protein on an energy basis. Substantial voluntary food intake resumed 12 to 16 days after initiating treatment. The sixth cat was euthanatized. These observations suggest that 6 to 7 weeks of anorexia, associated with 30 to 40% weight loss, can induce hepatic lipidosis in obese but otherwise healthy cats, and confirm that with appropriate management the prognosis for cats with hepatic lipidosis is favorable.     

Necropsy and histopathologic findings in 14 African hedgehogs (Atelerix albiventris): a retrospective study.

From fiscal years 1992 through 1996, 14 African hedgehog (Atelerix albiventris) cases were submitted to the Animal Disease Diagnostic Laboratory at Purdue University. The most common diagnoses were splenic extramedullary hematopoiesis (91%), hepatic lipidosis (50%), renal disease (50%), and neoplastic disease (29%). Other less frequent necropsy findings were myocarditis (21%), colitis (14%), bacterial septicemia (14%), and pneumonia (14%). The data indicate that splenic extramedullary hematopoiesis, hepatic lipidosis, renal disease, and neoplasms are frequent postmortem findings in hedgehogs.     

Relationship of hepatic lipidosis to health and performance in dairy cattle

In a field study of 80 cows in 9 dairy herds, serial liver biopsies were performed over the peripartum period to determine degree of hepatic lipidosis. Cattle were separated into categories of mild, moderate, and severe hepatic lipidosis on the basis of maximal amounts of hepatic triglyceride that accumulated during this period. Number of cattle with mild, moderate, and severe hepatic lipidosis were 52, 16, and 12, respectively. Cattle with severe hepatic lipidosis had greater concentrations of hepatic triglyceride before calving and after parturition, and greater serum nonesterified fatty acid concentrations and body condition loss after parturition than cattle with mild hepatic lipidosis. Rate of disease and culling and death rate because of disease were greater in cattle with severe hepatic lipidosis. Cattle with severe hepatic lipidosis had reproductive performance equal to clinically normal cattle; however, cattle with moderate hepatic lipidosis had increased days to conception, possibly related to greater milk production.     

Potassium depletion in cats: renal and dietary influences

Excessive urinary potassium loss was diagnosed in 7 cats with persistent hypokalemia and high serum creatinine concentrations. Renal tubular acidosis (proximal or distal) was not evident in the affected cats. Plasma aldosterone concentrations and plasma renin activities in affected cats were not significantly different from control values. Potassium depletion and hypokalemia were attributed to the combined effects of decreased dietary potassium intake and excessive urinary potassium losses. It was concluded that increased urinary potassium excretion may represent a basic response to renal dysfunction in cats. Data suggested that dietary potassium supplementation improved renal function in most cats in this study.     

Pancreatitis in Cats

Pancreatitis was considered a rare disease in the cat until a couple of decades ago when several retrospective studies of severe acute pancreatitis were published. It was apparent that few of the diagnostic tests of value in the dog were helpful in cats. With increasing clinical suspicion, availability of abdominal ultrasonography, and introduction of pancreas-specific blood tests of increasing utility, it is now accepted that acute pancreatitis is probably almost as common in cats as it is in dogs, although the etiology(s) remain more obscure. Pancreatitis in cats often co-exists with inflammatory bowel disease, less commonly with cholangitis, and sometimes with both. Additionally, pancreatitis may trigger hepatic lipidosis, while other diseases, such as diabetes mellitus, may be complicated by pancreatitis. Therapy is similar to that used in dogs, with added emphasis on early nutritional support to prevent hepatic lipidosis. Less is known about chronic pancreatitis than the acute form, but chronic pancreatitis is more common in cats than it is in dogs and may respond positively to treatment with corticosteroids.     

Renal tubular acidosis in two horses: diagnostic studies

An 11-year-old Quarter Horse mare and a 2-year-old Quarter Horse colt with clinical diagnoses of renal tubular acidosis (RTA) were donated to the University of California Veterinary Medical Teaching Hospital. A series of diagnostic tests was performed in an attempt to characterize the type and cause of RTA in these horses. Endogenous creatinine clearance and sodium sulfanilate clearance were within reference ranges; thus, no abnormality of glomerular function was detected. To assess renal tubular function in response to acid loading, each horse was given 0.1 g of NH4Cl/kg of body weight via nasogastric tube in 6 L of water. Urine acidification in response to the oral acid load was less than that observed in control horses. The urinary clearance ratio for sodium also was found to be greater for the principals than for the controls. These findings supported a diagnosis of RTA that closely resembled type 1 or distal RTA. In an attempt to determine the cause of RTA, renal ultrasonography, renal biopsy, and a mating study were performed. No abnormalities were identified, and the cause of RTA in these cases remained unknown.     

X‐RAY ATTENUATION OF THE LIVER AND KIDNEY IN CATS CONSIDERED AT VARYING RISK OF HEPATIC LIPIDOSIS

X‐ray attenuation of the liver has been measured using computed tomography (CT) and reported to decrease in cats with experimentally induced hepatic lipidosis. To assess the clinical utility of this technique, medical records and noncontrast CT scans of a series of cats were retrospectively reviewed. A total of 112 cats met inclusion criteria and were stratified into three hepatic lipidosis risk groups. Group 1 cats were considered low‐risk based on no history of inappetence or weight loss, and normal serum chemistry values; Group 2 cats were considered intermediate risk based on weight loss, serum hepatic enzymes above normal limits, or reasonably controlled diabetes mellitus; and Group 3 cats were considered high risk based on poorly controlled diabetes mellitus due to hypersomatotropism. Mean CT attenuation values (Hounsfield units, HU) were measured using regions of interest placed within the liver and cranial pole of the right kidney. Hepatic and renal attenuation were weakly positively correlated with each other (r = 0.2, P = 0.03) and weakly negatively correlated with body weight (r = ?0.21, P = 0.05, and r = ?0.34, P = 0.001, respectively). Mean (SD) hepatic and renal cortical attenuation values were 70.7 (8.7) HU and 49.6 (9.2) HU for Group 1 cats, 71.4 (7.9) HU and 48.6 (9.1) HU for Group 2, and 68.9 (7.6) HU and 47.6 (7.2) HU for Group 3. There were no significant differences in hepatic or renal attenuation among groups. Findings indicated that CT measures of X‐ray attenuation in the liver and kidney may not be accurate predictors of naturally occurring hepatic lipidosis in cats.     

Evaluation of toxicosis of liposome-encapsulated cis-bis-neodecanoato-trans-R,R-1,2-diaminocyclohexane platinum (II) in clinically normal cats

OBJECTIVE: To determine adverse effects of single and multiple doses of liposome-encapsulated cis-bis-neodecanoato-trans-R,R-1,2-diaminocyclohexane platinum (II) (L-NDDP) administered IV to healthy adult cats. ANIMALS: 10 healthy adult cats. PROCEDURE: 8 cats were given a single dose of L-NDDP (at rates of 75, 100, 150, or 200 mg/m2), and 2 cats were given liposomal lipid (1,500 mg/m2). Six of the 10 cats were given doses of L-NDDP at the maximum tolerated dosage (100 mg/m2) or a lower dosage (75 mg of L-NDDP/m2) at 21-day intervals, for a total of 4 treatments. Hematologic and serum biochemical analyses, urinalyses, and physical examinations were used to monitor effects of L-NDDP. RESULTS: All cats had transient pyrexia, lethargy, vomiting (1 to 3 times/24 h), inappetence, and an acute species-specific infusion reaction that was prevented by administration of atropine-diphenhydramine. Dose-limiting toxicosis was evident as a 10-day course of lethargy, intermittent vomiting, and diarrhea. In cats given multiple doses, dose-related thrombocytopenia, cumulative myelosuppression, transient increased hepatic transaminase activity, and mild to moderate hepatic hydropic degeneration and proximal renal tubular lipidosis in excess of lipidosis expected for this species were detected. Bone marrow hypoplasia was detected in some cats that received higher doses (cumulative dosages of 300 or 400 mg of L-NDDP/m2). CONCLUSION: Cats can safely be given L-NDDP at potentially therapeutic dosages without inducing renal or pulmonary toxicoses. CLINICAL RELEVANCE: Because L-NDDP has better tumoricidal activity than cisplatin (in vivo and in vitro) and is not cross resistant, it may be similarly or more efficacious than cisplatin in humans and dogs.     

Comparison of plasma, liver, and skeletal muscle carnitine concentrations in cats with idiopathic hepatic lipidosis and in healthy cats

Concentrations of total, free, and esterified carnitine were determined in plasma, liver, and skeletal muscle from cats with idiopathic hepatic lipidosis and compared with values from healthy cats. The mean concentrations of plasma, liver, and skeletal muscle total carnitine; plasma and skeletal muscle free carnitine; and plasma and liver esterified carnitine were greater (P less than 0.05) in cats with idiopathic hepatic lipidosis than in control cats. The mean for the ratio of free/total carnitine in plasma and liver was lower (P less than 0.05) in cats with idiopathic hepatic lipidosis than in control cats. These data suggest that carnitine deficiency does not contribute to the pathogenesis of feline idiopathic hepatic lipidosis.     

Reduced lymphoid response to skin allotransplants in cows with hepatic lipidosis.

The immune responsiveness of cows with hepatic lipidosis (fatty liver) in comparison to control cows with a normal liver fat content was tested by applying skin allotransplants to the skin of the back of cows on day 3 after parturition. Immunoreactivity was determined by semiquantitative counting of the number of infiltrating lymphocytes in the recipient skin adjacent to the allotransplants during a period of 21 days. There were more invading lymphocytes in samples from control cows than there were in samples from cows with hepatic lipidosis. It was concluded that cows with hepatic lipidosis have a reduced lymphoid response to skin allotransplants.     

Metabolic and hormonal alterations in cats with hepatic lipidosis

Hepatic lipidosis in cats is a commonly diagnosed hepatobiliary disease of unknown cause. The purpose of this prospective study was to characterize the blood hormone and lipid status of cats with hepatic lipidosis, and to compare this status to that of cats with other types of liver disease and to control cats. Twenty-three cats with hepatic disease were assigned to 1 of 2 groups on the basis of cytopathologic or histopathologic examination of the liver: group 1, hepatic lipidosis (n = 18); or group 2, cholangiohepatitis (n = 5). Ten healthy young adult cats were used as controls. Food was withheld from control animals for 24 hours before blood collection. Concentrations of plasma glucagon and serum insulin, cortisol, thyroxine, triglycerides, cholesterol, phospholipids, and nonesterified fatty acids (NEFAs) were determined in all cats, in addition to routine hematologic and serum biochemical testing. Cats with hepatic lipidosis had higher serum NEFA concentrations than cats with cholangiohepatitis or control cats (P < .05). Cats with cholangiohepatitis had higher serum cholesterol and phospholipid concentrations than those of cats with lipidosis or control cats (P < .05); their plasma glucagon concentrations were higher than those of control cats (P < .05), but were not different from those of cats with hepatic lipidosis. Serum insulin concentrations were significantly higher in control cats than in diseased cats (P < .05), but neither serum insulin nor the insulin to glucagon ratio was significantly different among the cats with hepatic disease. The high concentration of NEFAs in cats with hepatic lipidosis suggests that at least 1 factor in the pathogenesis of this syndrome may involve the regulation of hormone-sensitive lipase.