Effects of an extract of Serenoa repens on dogs with hyperplasia of the prostate gland.

OBJECTIVE: To determine effects of an extract of Serenoa repens on dogs with prostatic hyperplasia. ANIMALS: 20 mature male dogs with benign prostatic hyperplasia. PROCEDURE: Dogs were assigned to 3 comparable groups on the basis of prostatic volume per kg of body weight and degree of prostatic hyperplasia determined histologically. Dogs in 2 groups were treated for 91 days (8 received 500 mg, PO, q 8 h [1,500 mg/d], and 6 received 100 mg, PO, q 8 h [300 mg/d]). The control group of 6 dogs did not receive medication. Effects of treatment on prostatic volume, prostatic weight, prostatic histologic characteristics, radiographic and ultrasonographic assessment of prostatic size, results of CBC, serum biochemical analyses, and urinalysis, serum testosterone concentration, and semen characteristics were determined. At the termination of the study, all dogs were euthanatized, and necropsies were performed. Investigators conducting tests and interpreting results were not aware of treatment group of each dog. RESULTS: Treatment did not affect prostatic weight, prostatic volume, or prostatic histologic scores, libido, semen characteristics, radiographs of the caudal portion of the abdomen, prostatic ultrasonographs, or serum testosterone concentrations. Results of CBC, serum biochemical analyses or urinalysis, and body weights did not change during treatment. CONCLUSIONS AND CLINICAL RELEVANCE: Treatment with an extract of S repens for 91 days did not significantly affect the prostate gland of dogs. Adverse effects were not evident. Although products containing extracts of S repens are widely advertised for men with prostatic hyperplasia, beneficial or harmful effects of this plant extract were not found in dogs with prostatic hyperplasia.

Effects of dietary polyunsaturated fatty acid supplementation in early renal insufficiency in dogs.

Dietary supplementation with polyunsaturated fatty acids (PUFAs) alters the course of experimental kidney disease in dogs. In particular, supplementation with omega-6 PUFAs hastens the decline of kidney function, and omega-3 PUFAs are renoprotective. We investigated the early stages of renal insufficiency to determine whether PUFA supplementation altered the magnitude of hypercholesterolemia or glomerular hemodynamics. Two months after 11/12 nephrectomy, dogs were randomly divided into three groups of 6 animals each. Each group of dogs was then fed a low-fat basal diet supplemented with one of three sources of lipid to achieve a final concentration of 15% added fat. Fat sources were rich in omega-3 PUFAs (menhaden fish oil, group FO), omega-6 PUFAs (safflower oil, group SO), or saturated fatty acids (beef tallow, group C). Early in renal insufficiency, before significant kidney damage, group FO had a lower (P<.05) serum cholesterol concentration and tended to have a lower urinary prostaglandin E2 (PGE2) and thromboxane A2 (TxA2) excretion than group C. In contrast, group SO had a higher mean glomerular capillary pressure (P<.05) and more glomerular enlargement (P<.05) and tended to have higher eicosanoid excretion rates than group C. These differences in lipid metabolism, glomerular hypertension and hypertrophy, and urinary eicosanoid metabolism could explain, in part, the beneficial effects of omega-3 PUFAs and the detrimental effects of omega-6 PUFAs when administered on a long-term basis in this model of renal insufficiency.

Beneficial effects of chronic administration of dietary omega-3 polyunsaturated fatty acids in dogs with renal insufficiency.

Dietary supplementation with polyunsaturated fatty acids (PUFA) alters the course of experimental renal disease in rats. However, chronic renal disease in other laboratory animals and in human beings frequently responds differently to experimental manipulations. We investigated the effects of variations in dietary PUFA composition on the chronic course of induced renal disease in dogs. Two months after 15/16 nephrectomy, dogs were randomly divided into three groups of seven animals each. For the next 20 months, each group of dogs was fed a low-fat basal diet supplemented with one of three sources of lipid to achieve a final concentration of 15% added fat. Fat sources provided omega-3 PUFA (menhaden fish oil, group FO), omega-6 PUFA (safflower oil, group SO), or saturated fatty acids (beef tallow, group BT). Throughout the dietary trial, the magnitude of proteinuria and the plasma concentrations of creatinine, cholesterol, and triglyceride were lower in group FO. The mean overall glomerular filtration rate was 0.89+/-0.18 ml/min per kilogram of body weight in group SO, a value that was significantly less (p < 0.05) than the corresponding values for groups BT and FO (1.21+/-0.18 and 1.43+/-0.20 ml/min/kg, respectively). Renal interstitial fibrosis also was significantly elevated in group SO. The extents of mesangial matrix expansion, glomerulosclerosis, and renal interstitial cellular infiltrate were similar in groups BT and SO, but lower (p < 0.05) in group FO. We conclude that supplementation with omega-6 PUFA enhanced renal injury; supplementation with omega-3 PUFA was renoprotective.

Reliability of using random urine samples for "spot" determination of fractional excretion of electrolytes in cats.

OBJECTIVE: To determine whether the "spot" method of determining fractional excretion (FE) of electrolytes in cats is accurate. ANIMALS: 5 clinically normal young adult female cats. PROCEDURE: Cats were acclimated to metabolism cages, and 2 consecutive 72-hour collections of urine were made to determine FE of total calcium, potassium, total magnesium, sodium, and phosphorus by conventional methods, using endogenous creatinine clearance as an estimate of glomerular filtration rate. During collections, small samples of urine were obtained by cystocentesis at 8 AM, 3 PM, and 9 PM for determination of FE of the electrolytes by use of the "spot" method. RESULTS: Values from "spot" determinations were highly variable, compared with 72-hour values, with a high percentage falling outside the range of mean +/- 2 SD for 72-hour FE values. CONCLUSIONS AND CLINICAL RELEVANCE: The "spot" method for determining FE is not precise, and if used, caution and judgement should be exercised in interpretation of the results.

Effects of phosphorus/calcium-restricted and phosphorus/calcium-replete 32% protein diets in dogs with chronic renal failure.

Twenty-four dogs with induced, severe chronic renal failure were allotted to 2 groups of 12 each. Group-A dogs were fed a 0.4% phosphorus (P)/0.6% calcium, 32% protein diet, and group-B dogs were fed a 1.4% P/1.9% calcium, 32% protein diet. Dogs were studied over 24 months to determine clinical status, survival, blood biochemical alterations, glomerular filtration rate (GFR), urinary excretion of P and protein, renal morphologic changes, and renal tissue concentrations of calcium, P, and magnesium. Group-A dogs developed statistically significant differences from group-B dogs in several blood biochemical values (PCV and total solids, calcium, P, potassium, sodium, chloride, total CO2 (TCO2), anion gap, and parathyroid hormone concentrations) and in urinary P excretion. Mean (+/- SEM) GFR values in group-A and group-B dogs were nearly identical when diets were initiated (group A = 0.73 +/- 0.05 ml/min/kg of body weight; group B = 0.72 +/- 0.08 ml/min/kg), but significantly (P = 0.0346) lower GFR developed in group-B than in group-A dogs over time. At 24 months, GFR in survivors was 0.83 +/- 0.08 and 0.63 +/- 0.15 ml/min/kg for dogs of groups A and B, respectively. Other measurements favored the hypothesis that P/calcium restriction was beneficial, but values failed to reach statistical significance. Survival was greater at 24 months in group-A than in group-B (7 vs 5) dogs, and renal tissue concentrations of calcium and P were higher in group-B than in group-A dogs. Differences were not detected between groups in urinary excretion of protein and in the type or severity of renal lesions.(ABSTRACT TRUNCATED AT 250 WORDS)

Influence of dietary source of phosphorus on fecal and urinary excretion of phosphorus and other minerals by male cats.

Twelve male cats were fed 2 diets that differed in the source of P. In diet 1 (1.4% P), 62.7% of P originated from poultry, meat, and fish meal, and the remainder from other organic ingredients of food. In diet 2 (1.6% P), 63.5% of P was derived from neutral monobasic/dibasic salts, and the remainder from other organic ingredients of the food. The P intake was nearly the same with both diets, but there was a significant (P less than 0.05) difference between diets in the percentage of ingested P that was excreted in the urine (14.7 +/- 5.3% for diet 1; 34.9 +/- 8.4% for diet 2), and in 6-day urinary P excretion (774 +/- 290 mg for diet 1; 2,004 +/- 556 mg for diet 2). The P concentrations in urine samples obtained by cystocentesis after cats ate were significantly (P less than 0.05) higher when cats were fed diet 2 than when those same cats were fed diet 1. Plasma P concentrations increased after ingestion of diet 2, but were unchanged after ingestion of diet 1. Seemingly, urinary excretion of P was markedly influenced by dietary composition. Diets with the same P content have potential for different biologic effects because of differences in availability of P.

Effects of three diets on dogs with induced chronic renal failure.

Healthy mixed-bred dogs of both sexes had renal mass surgically reduced and were allowed 2 to 3 months for hypertrophy of the remnant kidney. They were then allotted into 3 groups with equal renal function and were fed 1 of 3 diets that differed in composition. Group 1 dogs (n = 6) were fed moist food that contained 50% protein, 2.34% Ca, and 1.64% P with a P-binding agent (basic aluminum carbonate gel) added. Group 2 dogs (n = 6) were fed a dry diet that contained 24.5% protein, 1.26% Ca, 1.21% P, and the same P-binding agent as used for group 1. Group 3 dogs (n = 7) were fed a moist diet that contained 16.1% protein, 0.38% Ca, and 0.3% P without a P-binding agent. Each group was fed its diet for 92 days and monitored for responses. Mortality associated with uremia occurred in 2 of 6 group 1 dogs, 0 of 6 group 2 dogs, and in 2 of 7 group 3 dogs. Among survivors, clinical signs were seen in the more azotemic dogs of group 1, but not in dogs of groups 2 and 3. The blood urea nitrogen, plasma P concentrations, and PCV values were most favorable in group 3 and least favorable in group 1. Marked differences between groups were not seen in plasma concentrations of protein, albumin, or Ca or in plasma alkaline phosphatase activity. Values for glomerular filtration rate did not change in any group during the experiment.(ABSTRACT TRUNCATED AT 250 WORDS)

Characterization of magnesium-induced urinary disease in the cat and comparison with feline urologic syndrome.

Aggregates of struvite crystals caused urethral obstruction in a high percentage of cats fed moist and dry diets supplemented with Mg oxide. Some of the diets were associated with cystolith formation as well. The percentage of Mg in the experimental diets was a misleading indicator of Mg intake because of differences between moist and dry diets in their caloric density. Magnesium homeostasis was maintained in cats ingesting large quantities of Mg. Tissue (kidney, muscle, and rib) concentrations of Mg were the same in cats fed high Mg and control diets. Plasma Mg concentration was increased only in cats ingesting the largest amount of Mg. Magnesium homeostasis was maintained by a marked increase in urine Mg excretion. However, urine Mg concentration was not directly related to Mg intake, apparently because of differences between diets in intestinal absorption of Mg. Urethral obstruction of experimental cats was not associated with a transient increase in Mg intake, nor did obstructing cats have higher urine Mg concentrations than did nonobstructing cats fed the same diet. This observation indicates that factor(s) other than urine Mg concentration are important in urethral obstruction. Cats with urethral obstruction due to naturally occurring disease, feline urological syndrome (FUS), had markedly lower urine Mg concentrations than cats fed high Mg diets. This finding refutes the theory that cats develop FUS because of primary Mg hyperabsorptive phenomena or because of a primary urinary leak of Mg. It also indicates that factors other than urine Mg concentration are involved in the genesis of naturally occurring urethral obstruction. Another difference between the natural and the induced disease was related to the character of the urinary precipitates. Experimental diets higher in Mg concentration caused urolith formation, which is uncommon with FUS. Lower Mg diets caused obstruction with aggregates of crystals, but mucus was not observed. However, in the experimental disease induced in the present study, urinary precipitates were predominantly or exclusively struvite, as has been reported in the natural disease. Many similarities were seen between the diet-induced disease and FUS, but factors in addition to Mg intake are involved in the natural disease. The importance of Mg, compared with the undefined factors, remains to be established.