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Biomedical subjects

D J Polzin

Publications and source records attributed to D J Polzin.

At least 55 records · Page 3Linked to original sources
PubMed1986

Nonsurgical management of canine obstructive urolithopathy.

Obstruction to urine outflow is a common complication of urolithiasis. However, varying degrees of recovery of renal function may occur following examination of the cause of obstruction. Therefore, in the absence of conclusive evidence of irreversible dysfunction, one should consider efforts to decompress the urinary tract and to eliminate the cause of obstruction. Nonsurgical methods that may be used for management of obstructive urolithiasis include cystocentesis, palpation, urohydropropulsion, and catheterization.

Animals↗
PubMed1986

Medical dissolution of canine struvite uroliths.

Medical therapy is an effective method of canine struvite urolith dissolution. Recommendations include (1) eradication or control of urinary tract infection (if present), (2) use of calculolytic diets, and (3) administration of urease inhibitors to patients with persistent urinary tract infection caused by urease-producing microbes.

Animals↗
PubMed1986

Dissolution of canine ammonium urate uroliths.

Medical therapy that may be effective in promoting dissolution of canine ammonium urate uroliths includes the following: reduction of dietary purines, reduction in in vivo production of uric acid, and alkalinization of urine.

Animals↗
PubMed1984

Medical management of male and female cats with nonobstructive lower urinary tract disease.

This case is typical of recurrent urolithiasis managed by repeated surgery. Retrospective assessment of the disorder indicates the need for quantitative analyses of uroliths removed by cystotomy. Compliance of the owners with recommendations to minimize recurrent urolithiasis might have been beneficial. Results of medical therapy designed to induce dissolution of uroliths in this case are representative of preliminary findings of medical dissolution of naturally occurring struvite uroliths in ten other cats. It is of interest that the uroliths dissolved even though no effort was made to induce diuresis. The underlying cause of UTI in this patient may have been damage to the lower urinary tract induced by previous diagnostic and therapeutic procedures and/or sterile struvite uroliths that compromised local host defense mechanisms. Lack of urease production by the uropathogens suggests that they did not play a causative role in formation of uroliths. The need for preventative therapy of recurrent formation of uroliths after their medical dissolution is worthy of further comment. In this patient, specific measures to prevent urolith recurrence were not initiated because it is a part of a prospective clinical study. In the event uroliths recur, medical therapy designed to induce dissolution of uroliths would be repeated. Need for long-term preventative therapy would be dependent on the time interval between recurrent episodes (weeks, months, or years), and the effectiveness of medical therapy for urolith dissolution. Long-term prophylactic therapy would include urine acidifiers and diets low in magnesium.

Ammonium Chloride↗
PubMed1984

Influence of reduced protein diets on morbidity, mortality, and renal function in dogs with induced chronic renal failure.

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.

Animals↗
PubMed1983

Effects of modified protein diets in dogs with chronic renal failure.

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.

Animal Feed↗
PubMed1983

Influence of modified protein diets on the nutritional status of dogs with induced chronic renal failure.

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.

Animals↗
PubMed1982

Influence of modified protein diets on electrolyte, acid base, and divalent ion balance in dogs with experimentally induced chronic renal failure.

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.

Acid-Base Equilibrium↗
PubMed1981

Acute hepatic necrosis associated with the administration of mebendazole to dogs.

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.

Acute Disease↗