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Objective: To determine whether underfilling blood collection tubes leads to in vitro reduction in serum measured total CO2 concentration ([TCO2]m) in canine and feline blood samples sufficient to create the impression of metabolic acidosis (pseudometabolic acidosis) or high anion gap., Sample Population: Blood samples from healthy client-owned animals (16 dogs, 17 cats)., Procedure: Venous blood samples were collected in random order for determination of serum [TCO2] and blood gas tensions. Blood gas analysis was performed on iced, capped blood samples. In dogs, serum [TCO2] was measured in 1-, 3-, and 10-ml samples in 10-ml type-B tubes and in a 3-ml sample in 3-ml type-A tubes. In cats, serum [TCO2] was determined in 1-, 2-, and 3-ml samples in 3-ml type-A tubes and in a 3-ml sample in 10-ml type-B tubes., Results: For dogs, serum [TCO2] in full-tube, 10-ml samples was a mean +/- SD, 2.0 +/- 1.1 mmol/L greater than that in 3-ml samples and 3.7 +/- 1.3 mmol/L greater than the value in 1-ml samples; both differences were significant at P < 0.0001. The serum [TCO2] in full 3-ml samples was lower by 0.4 +/- 0.6 mmol/L than the value in full-tube 10-ml samples (P = 0.019). For cats, serum [TCO2] in full-tube, 3-ml samples was 0.5 +/- 0.6 mmol/L greater than that in 2-ml samples (P = 0.004) and was 1.5 +/- 0.8 mmol/L greater than the value in 1-ml samples (P < 0.0001). Serum [TCO2] in 3-ml samples of feline blood in 10-ml tubes was 0.8 +/- 0.8 mmol/L lower than that in samples from full 3-ml tubes (P = 0.0007). In dogs and cats, [TCO2] in fully filled collection tubes was approximately 6 mmol/L higher when calculated from blood gas analysis data than when chemically determined in serum., Conclusions and Clinical Relevance: Underfilling blood collection tubes results in a false decrease in serum [TCO2], which can contribute in part to descrepancies between blood gas and chemical analyses as estimates of plasma bicarbonate concentration. This, and other in vitro effects of sample handling and collection, may result in a false assessment of metabolic acidosis in dogs and cats.

Objective: To determine the potential clinical usefulness of duplex Doppler estimation of arcuate artery resistive index (a measure of intrarenal blood flow impedance) for diagnosis of aminoglycoside-induced nephrotoxicosis., Animals: 30 adult, female, mixed-breed dogs, allotted to 3 groups of 10 dogs each as: toxic dosage of gentamicin, therapeutic dosage of gentamicin, and saline solution sham equivalent in volume to that of the toxic dosage of gentamicin., Procedure: After baseline screening to establish normalcy (serum biochemical analysis, endogenous creatinine clearance determination, urinalysis, urine protein-to-creatinine ratio, urine culture, gray-scale sonography, and percutaneous ultrasound-guided renal biopsy), results of arcuate artery resistive index determination were compared with serum creatinine and urine specific gravity values on a Monday-Wednesday-Friday data collection schedule for 10 days. Endogenous creatinine clearance determination, ultrasound-guided renal biopsy, and urine culture were repeated at the end of data collection in all 3 groups., Results: Significant differences in resistive index measurements were not observed, despite clinicopathologic and renal biopsy results compatible with severe acute tubular necrosis in dogs of the toxic dosage group., Conclusions: Duplex Doppler sonography of arcuate artery blood flow impedance, expressed as the resistive index, appears to have poor clinical usefulness as a diagnostic tool in this disorder., Clinical Relevance: Normal arcuate artery resistive index values obtained in dogs for which aminoglycoside-induced nephrotoxicosis is suspected do not exclude the disorder. If abnormal arcuate artery resistive index values are obtained for such dogs, further evaluation for nephropathies other than aminoglycoside-induced nephrotoxicosis may be considered.

To determine the effects of long-term dietary protein restriction in cats with chronic renal failure (CRF), 4 healthy adult cats and 7 cats with surgically induced CRF were fed a high-protein (HP, 51.7% protein) diet and 4 healthy adult cats and 7 cats with surgically induced CRF were fed a low-protein (LP, 27.6% protein) diet for 1 year. Cats with induced CRF that were fed the LP diet had reduced serum urea nitrogen concentrations, despite lower glomerular filtration rates, compared with cats with CRF fed the HP diet. Despite five-sixths reduction in renal mass, reduced glomerular filtration rate, and azotemia, 13 of the 14 cats with induced CRF retained the ability to concentrate urine and produced urine with a specific gravity > 1.035. Cats fed the HP diet consumed significantly more calories than did cats fed the LP diet, presumably because the HP diet was more palatable. As a result of the lower caloric intake in cats fed the LP diet, these cats were protein and calorie restricted, compared with cats fed the HP diet. Cats fed the HP diet weighed significantly more than did cats fed the LP diet. Mean hematocrit and mean serum albumin concentration were significantly lower in control cats and in cats with CRF fed the LP diet, compared with control cats and cats with CRF fed the HP diet. Hypokalemia developed in 4 of 7 cats with CRF fed the HP diet (containing 0.3% potassium); hypokalemia did not develop in control cats fed the same diet or in cats with CRF fed the LP diet containing 0.4% potassium. Excessive kaliuresis, hypomagnesemia, and metabolic acidosis did not appear to contribute to the hypokalemia. Subsequent supplementation of the HP diet with potassium gluconate prevented hypokalemia in cats with CRF.

Twenty-four-hour excretion of urine metabolites was determined in 33 clinically normal Beagles during periods of consumption of a standard diet and when food was withheld. The goal was to determine normal canine values for urine analytes incriminated in the genesis of calcium oxalate uroliths. During periods when dogs consumed food, dairy urinary excretion of calcium, uric acid, sodium, potassium, magnesium, ammonium, and hydrogen ions were significantly (P = 0.0004, 0.0038, 0.001, 0.0001, 0.0004, 0.0001, and 0.024, respectively) higher than when food was withheld. Urinary excretion of phosphorus, oxalate, and citrate were not significantly different between samples obtained during periods of food consumption and when food was withheld. Male dogs excreted significantly higher quantities of urine oxalate than females during fed (P = 0.003) and nonfed (P = 0.003) conditions. When food was withheld, urinary uric acid excretion was significantly higher in males than females (P = 0.01). Females excreted significantly more urine calcium than males when food was withheld (P = 0.003). Our results indicated that dietary conditions influence the quantity of sodium, potassium, calcium, magnesium, and uric acid excreted in the urine of clinically normal dogs; therefore, dietary conditions should be considered when measuring the concentration of these analytes in urine.

To evaluate underlying causes of calcium oxalate urolithiasis, 24-hour excretion of urine metabolites was measured in 6 Miniature Schnauzers that formed calcium oxalate (CaOx) uroliths during periods when they were fed a standard diet and during periods when food was withheld. Serum concentrations of parathyroid hormone and 1,25-dihydroxyvitamin D also were evaluated. Serum calcium concentrations were normal in all 6 affected Miniature Schnauzers; however, during diet consumption, mean 24-hour urinary excretion of calcium was significantly (P = 0.025) higher than calcium excretion when food was withheld. In 1 dog, urinary calcium excretion was lower during the period of food consumption, compared with the period when food was withheld. Compared with clinically normal Beagles, Miniature Schnauzers that formed CaOx uroliths excreted significantly greater quantities of calcium when food was consumed (P = 0.0004) and when food was withheld (P = 0.001). Miniature Schnauzers that formed CaOx uroliths excreted significantly less oxalate than clinically normal Beagles during fed (P = 0.028) and nonfed (P = 0.004) conditions. Affected Miniature Schnauzers also excreted abnormally high quantities of uric acid. Excretion of citrate was not different between Miniature Schnauzers with CaOx urolithiasis and clinically normal Beagles. In 5 of 6 Miniature Schnauzers with CaOx urolithiasis, concentrations of serum parathyroid hormone were similar to values from age- and gender-matched Miniature Schnauzers without uroliths. The concentration of serum parathyroid hormone in 1 dog was greater than 4 times the mean concentration of clinically normal Miniature Schnauzers. Mean serum concentrations of 1,25-dihydroxyvitamin D in Miniature Schnauzers with calcium oxalate urolithiasis were similar to concentrations of clinically normal Miniature Schnauzers.

The influence of induced chronic renal failure on 24-hour urinary excretion and fractional excretion of sodium and potassium was studied in cats. Induction of chronic renal failure significantly increased fractional excretion of potassium (P less than 0.0001) and sodium (P less than 0.05); however, 24-hour urinary excretion of sodium and potassium decreased slightly following induction of chronic renal failure. Fractional excretion and 24-hour urinary excretion of sodium and potassium were compared by linear regression in clinically normal cats, cats with chronic renal failure, and clinically normal and affected cats combined. In clinically normal cats, linear regression revealed only moderate correlation between fractional excretion and 24-hour urinary excretion for sodium and potassium. Linear regression of these same relationships in cats with chronic renal failure, and in clinically normal cats and cats with chronic renal failure combined, indicated low correlation. Fractional excretions of sodium and potassium were not reliable indicators of 24-hour urinary excretion of these electrolytes in cats with chronic renal failure or unknown glomerular filtration rate. Fractional excretion of potassium and sodium correlated only moderately with 24-hour urinary excretion in clinically normal cats.

The efficacy of a diet designed to facilitate dissolution of feline magnesium ammonium phosphate (struvite) uroliths was evaluated in 30 cases of urolithiasis, sterile struvite uroliths dissolved in a mean of 36 days after initiation of dietary treatment. In 5 cases of urolithiasis, struvite urocystoliths associated with urease-negative bacterial urinary tract infection dissolved in a mean of 23 days after initiation of dietary and antimicrobial treatment. In 3 cases of urolithiasis, struvite urocystoliths associated with urease-positive staphylococcal urinary tract infection dissolved in a mean of 79 days after initiation of dietary and antimicrobial treatment. Dissolution of uroliths in cats fed the treatment diet was associated with concomitant remission of dysuria, hematuria, and pyuria, and reduction in urine pH and struvite crystalluria. In one case, a urocystolith composed of 100% ammonium urate, and in another case, a urolith composed of 60% calcium phosphate, 20% calcium oxalate, and 20% magnesium ammonium phosphate did not dissolve.

The influence of a canine maintenance diet containing 44.4% protein (dry weight) and 2 reduced-protein renal-failure diets containing 8.2% or 17.2% protein (dry weight) on the nutritional status of dogs with induced chronic renal failure was evaluated for 40 weeks. Nutritional status was assessed by changes in serially determined body weights, hindlimb circumferences, serum protein concentrations, complete blood cell counts, serum cholesterol concentrations, glucose tolerance tests, and blood glucose concentrations. Evidence of suboptimum nutritional status was observed in dogs fed the 8.2% or 44.4% protein diets, but not in dogs fed the 17.2% protein diet. Only a small reduction in hindlimb circumference developed in dogs fed the 17.2% protein diet. Reduced body weight and hindlimb circumference and normocytic normochromic anemia developed in dogs fed the 44.4% protein diet. Reduced body weight and hindlimb circumference, hypoalbuminemia, hypoproteinemia, hypercholesterolemia, and normocytic normochromic anemia developed in dogs fed the 8.2% protein diet. A beneficial effect of moderate dietary protein restriction (17.2% protein) on the nutritional status of the dogs was observed. In contrast, excessive intake or restriction of dietary protein was associated with detrimental effects.

A maintenance diet containing 44.4% dry weight protein and 2 reduced protein diets containing 17.2% and 8.2% dry weight protein were studied in dogs with induced chronic renal failure to determine effects on their (1) clinical status, (2) renal function, (3) electrolyte and acid-base balance, (4) divalent ion balance, (5) nutritional status, (6) hematologic status, and (7) hemostasis. A cross-over design of feeding was utilized so that the effect of diet could be studied in each dog at a known state of renal dysfunction and so that reversibility of effects could be determined. The inulin clearance rate was higher when the 44.4% protein diet was fed than when the 8.2% or 17.2% protein diets were fed. However, consumption of lower protein diets was associated with greater physical activity and reduction in serum urea nitrogen concentrations, compared with consumption of the 44.4% protein maintenance diet. Varying degrees of hyperchloremic metabolic acidosis developed in dogs fed the 8.2% and 17.2% protein diets. Reduced total serum protein and albumin concentrations, and hypercholesterolemia developed in dogs fed the 8.2% protein diet. All effects were reversible after diets were changed. It was concluded that diet-induced alterations in renal function associated with moderate dietary protein restriction did not adversely effect clinical and biochemical status of dogs with renal failure. It was unclear whether the clinical and biochemical changes observed with more severe protein restriction resulted from diet-induced changes in renal function.

Mebendazole was administered to 7 adult Dachshunds and 2 adult Doberman Pinschers at 6-month intervals for routine parasite control. Two weeks after the 1st treatment, a 3-year-old Dachshund died of acute hepatic failure. Approximately 2 weeks following the 2nd treatment, two 5-year-old Dachshunds and one 3-year-old Dachshund had evidence of acute hepatic necrosis; 1 of these dogs died of fulminant hepatic failure. Typical clinical signs in affected dogs included anorexia, depression, vomiting, icterus, and hemorrhagic diarrhea. Two additional Dachshunds had biochemical evidence of hepatic dysfunction, ie. high serum alanine aminotransferase and serum alkaline phosphatase activities. One Dachshund and 2 Doberman Pinschers had no clinical or laboratory evidence of hepatic disease.

The influence of a maintenance diet (44.4% dry weight protein) and 2 reduced protein diets (8.2 and 17.2% dry weight protein) on acid-base, electrolyte, and divalent ion balance of dogs with experimentally induced chronic renal failure was studied for 40 weeks. Moderate-to-severe hyperchloremic metabolic acidosis developed in dogs fed the 8.2% protein diet, but not in the groups fed the 17.2% and 44.4% protein diets. Serum sodium and potassium concentrations were not altered significantly by the diets. Mean serum calcium concentrations increased significantly in the 3 groups after renal failure was induced; however, serum calcium concentration generally did not exceed the normal range. Dogs fed reduced protein diets had smaller serum magnesium and phosphorus concentrations than did the dogs fed the maintenance diet. Microscopic alterations in bone morphology consistent with canine renal osteodystrophy were not detected after 40 weeks of renal failure in dogs fed the 17.2% and 44.4% protein diets. Examination of skull radiographs of the dogs prepared 40 weeks after renal failure was induced revealed that the lamina dura dentes were visible in all groups. It was concluded that the 8.2% protein diet was of therapeutic benefit in management of altered divalent ion metabolism in dogs with chronic renal failure. However, the high frequency of concomitant acidosis indicated that appropriate alkalinization therapy should be included with this diet. Adverse effects of feeding the 17.2% protein diet were not detected. However, it was less effective than the 8.2% protein diet in minimizing development of hypermagnesemia and skeletal changes consistent with renal osteodystrophy.

The influence of a maintenance diet containing 44.4% dry weight protein and 2 reduced protein diets containing 8.2% and 17.2% dry weight protein on morbidity, mortality, and renal function of dogs with induced chronic renal failure was studied for 40 weeks. The diets differed in mineral and electrolyte composition in addition to differences in protein, carbohydrate, and fat content. Dogs fed the 44.4% protein diet had a higher mortality (6 of 11) than did dogs fed the 8.2% (1 of 6) or 17.2% (0 of 6) protein diets. Dogs fed the 44.4% protein diet died of uremic complications. An occlusive portal vein thrombus caused death of the nonsurvivor fed the 8.2% protein diet. Clinical signs of uremia were detected only in nonsurvivors fed the 44.4% protein diet. Surviving dogs fed the maintenance diet were less active and had poorer hair than did dogs fed reduced protein diets. Inulin clearance rate and urinary protein excretion were lower in most dogs fed reduced protein diets than in dogs fed the maintenance diet. Despite the greater decrease in renal function, serum urea nitrogen concentrations were markedly lower in dogs fed the 8.2% and 17.2% protein diets than in dogs fed the 44.4% protein diet. Seemingly, the reduced protein renal failure diets were of benefit in preventing or reducing morbidity and mortality associated with the uremic syndrome and in reducing serum urea nitrogen concentrations as compared with that of the higher protein diet. The potential benefits of dietary protein restriction in dogs with chronic renal failure prevailed over potential adverse affects of excessive protein consumption.

Renal specimens obtained by biopsy and/or at necropsy from 4 dogs with nephrotic syndrome were studied using light, immunofluorescence, and electron microscopies. The glomerulonephritis observed in these dogs was considered an idiopathic immune complex glomerulonephritis associated with multisystem involvement because causes of glomerulonephritis in these dogs could not be established. Immunoglobulin A was observed in granular deposits in the mesangial and subendothelial regions of the glomeruli. The relationship of the clinical and pathologic features of this disease in dogs to various renal syndromes in human beings are described.