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 > 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.

Four consecutive 6-hour urine sample collections were performed on 7 healthy adult Holstein cows fed a diet of coastal Bermuda hay with ad libitum water consumption. Urine (via indwelling urinary catheter) and venous blood samples were collected at 6, 12, 18, and 24 hours. Total 24-hour urine production for the 7 cows ranged from 4,515 to 7,130 ml/d (mean +/- SD, 5,633 +/- 946 ml/d) or 0.02 to 0.04 ml/kg of body weight/d (mean +/- SD, 0.03 +/- 0.007 ml/kg/d). Renal clearance (C) of creatinine (Cr), sodium (Na), calcium (Ca), and magnesium (Mg) varied significantly (P less than 0.05) among individuals, but did not vary significantly among the four 6-hour collection periods. Clearance of chloride (Cl) and phosphorous (P) did not vary significantly either among individuals or among the four 6-hour periods. Clearance of potassium (K) varied significantly (P less than 0.05) among individuals and among the four 6-hour periods. Creatinine clearance was significantly (P less than 0.01) correlated with CCl, CCa, CP, and CMg when all data were considered. Significant (P less than 0.05) correlations were also found between CCl, and CK, CCa, CP, and CMg; between CCa and CP and CMg; and between CP and CMg. Fractional excretion (FE) of Na, K, Cl, Ca, P, and Mg did not vary significantly among the four 6-hour periods. Fractional excretion of Na, Ca, and Mg (P less than 0.01) and K and P (P less than 0.05) varied significantly within individuals among the 6-hour periods. Mean FE values, calculated by averaging values for each of the 4 collection periods for all 7 cows, ranged from 0.05 to 0.78% for FENa; 129.33 to 670.40% for FEK; 1.23 to 6.23% for FECl; 0.17 to 4.44% for FECa; 0.36 to 1.14 for FEP; and 4.96 to 11.73% for FEMg. Linear relationships between the clearance and fractional excretion of electrolytes were observed on base-10 logarithmically transformed data for Na, Ca, P, and Mg. Linear relationship was not found between CK and FEK or between CCl and FECl.

Gentamicin sulfate-induced nephrotoxicosis was compared in 2 groups of horses fed different rations. Four horses were fed only alfalfa hay, and 4 other horses were fed only whole oats. Seven days after initiation of the diet, all horses were given gentamicin IV (5 mg/kg of body weight) every 12 hours for 22 days. Urinary gamma-glutamyltransferase to urinary creatinine (UGGT:UCr) ratio was calculated daily, and serum concentration of gentamicin was measured at 1 and 12 hours after drug administration. Results indicated that horses fed oats had greater renal tubular damage than did horses fed alfalfa. Mean UGGT:UCr for horses fed alfalfa was 47.1 +/- 18.8 and was 100.0 +/- 19.0 for horses fed oats (P = 0.007). The UGGT:UCr in horses fed oats was > 100 for a total of 54 days; horses fed alfalfa had UGGT:UCr > 100 for only 7 days. Two horses not given gentamicin were fed only oats and 2 were fed only alfalfa. These horses had mean UGGT:UCr of 17.6 +/- 2.2 and 30.5 +/- 3.0, respectively. Mean peak and trough concentrations of gentamicin were statistically different for horses fed oats and those fed alfalfa (peak 23.16 +/- 1.87 and 14.07 +/- 1.79 microgram/ml, respectively [P = 0.0001], and trough, 1.81 +/- 0.69 and 0.71 +/- 0.70 microgram/ml, respectively [P = 0.02701)]. Mean half-lives of gentamicin (estimated from peak and trough concentrations) for horses fed alfalfa (2.58 +/- 0.26 hours) and horses fed oats (2.88 +/- 0.27 hours) were not significantly different. Horses fed only oats had greater degree of gentamicin-induced nephrotoxicosis than did those fed only alfalfa.

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 < 0.0001) and sodium (P < 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 urinary excretion in clinically normal cats.

The effects of method of seminal collection and a diuretic on retrograde flow of spermatozoa into the urinary bladder of rams were examined. In experiment 1, semen and urine were collected from 8 rams during the nonbreeding season. Prior to seminal collection, all rams were given furosemide and a sample of urine was obtained during micturition. Semen was then collected from each ram with an artificial vagina or by electroejaculation in alternate weeks for 4 weeks, and the urine released during the first postseminal collection micturition was collected in 4 consecutive samples. The volume of electroejaculates was larger (P < 0.0001) than the volume of ejaculates, but the total number of spermatozoa in the electroejaculate or in the ejaculate were not different (P > 0.1). Urine obtained before seminal collection was azoospermic or contained few, nonmotile spermatozoa (mean +/- SD = 0.053 +/- 0.114 x 10(6)/ml). The adjusted spermatozoal concentration (mean +/- SD = 1.630 +/- 2.258 X 10(6)/ml) in the urine collected after seminal collection was 31 times higher (P < 0.0001) and there were motile spermatozoa in most (97%) of the samples. The spermatozoal concentration in sequential samples of urine was not different (P > 0.1) between samples and was not affected (P > 0.1) by the method of seminal collection. There was a trend, approaching significance (P = 0.052), for an effect of method of seminal collection on the percentage of retrograde flow. Retrograde flow ranged from 0.21 to 19.38% when semen was collected with an artificial vagina and from 0.03 to 94.60% when semen was collected by electroejaculation and varied (P = 0.02) among rams within the 2 methods of seminal collection. In experiment 2, the 8 rams used in experiment 1 were given injections of 0.9% physiologic saline solution or furosemide in alternate weeks prior to seminal collection with an artificial vagina. Furosemide increased (P = 0.009) the volume of urine voided during the first postejaculation micturition, but did not influence (P > 0.1) the time from exposure of rams to the teaser to ejaculation, seminal characteristics, number of spermatozoa in the urine, or the percentage of retrograde flow. There was a trend (P < 0.1) for more rams to have motile spermatozoa in the postejaculation urine after treatment with furosemide. Administration of furosemide prior to seminal collection facilitates the noninvasive collection of pre- and postejaculation samples of urine for the determination of retrograde flow.

The effect of methoxamine on retrograde flow of spermatozoa into the urinary bladder of domestic cats during electroejaculation and the incidence of retrograde flow during the collection of semen with an artificial vagina, or during mating was examined. In experiment 1, urine collected by cystocentesis prior to electroejaculation was azoospermic or contained few, nonmotile spermatozoa, whereas urine collected after electroejaculation contained more (P = 0.002) spermatozoa, and motile spermatozoa were evident in urine obtained from 6 of 8 cats. Administration of methoxamine hydrochloride (200 microgram/kg of body weight, IV) did not affect spermatozoal output or percentage of retrograde flow. Percentage of retrograde flow for control cats ranged from 61.18 to 92.95% (mean +/- SD, 80.00 +/- 14.28%) and for methoxamine-treated cats, ranged from 15.25 to 92.49% (mean +/- SD, 58.10 +/- 32.28%), but the difference was not significant. In experiment 2, an artificial vagina was used to collect semen from 5 of the 8 cats used in experiment 1. Urine collected by cystocentesis after ejaculation contained spermatozoa, and motile spermatozoa were evident in the urine from 4 of 5 cats. The mean (+/- SD) percentage of retrograde flow for these 5 cats was 46.82 +/- 31.67% (range, 14.56 to 90.32%). In experiment 3, each of the 5 cats that were used in experiments 1 and 2 were mated. Spermatozoa were recovered from the vagina of each mated female, and motile spermatozoa were also present in postejaculation urine obtained by cystocentesis from each of the 5 male cats. Mean total number of spermatozoa in the postmating urine was 29.42 +/- 33.58 X 10(6) (range, 0.22 X 10(6) to 76.05 X 10(6) spermatozoa). Anesthesia of cats with ketamine facilitated the obtention of urine by cystocentesis, but did not cause spermatozoal displacement into the urinary bladder. Results of this study confirm the fact that, in cats, appreciable numbers of spermatozoa are lost because of retrograde flow into the urinary bladder during electroejaculation. Recovery of spermatozoa from the urinary bladder after collection of semen with an artificial vagina or following natural mating, indicates that retrograde flow of spermatozoa is not an artifact derived from electrical stimulation but is a component of the ejaculatory process in cats.

To determine the role of thromboxane A2 in the pathogenesis of experimentally induced immune complex glomerulonephritis, 12 concanavalin A-immunized Beagles were infused with 1 mg of concanavalin A via each renal artery and treated twice daily for 8 days with either 30 mg of CGS 12970/kg, PO, a specific thromboxane synthetase inhibitor, or placebo. The effect of treatment was assessed by measuring endogenous creatinine clearance and urine protein and eicosanoid excretion, and by evaluating changes in glomerular morphometric characteristics. On postinfusion day 8, urine protein, thromboxane B2, and 11-dehydro-thromboxane B2 excretion, glomerular epithelial crescent formation, and glomerular cell proliferation in the CGS 12970-treated dogs were significantly decreased when compared with values in the placebo-treated group. Differences were not observed in endogenous creatinine clearance, urine prostaglandin E2 and 6-keto-prostaglandin F1 alpha excretion, or glomerular polymorphonuclear leukocyte infiltration between groups in this study. These findings suggest thromboxane A2 has a role in the development of immune complex glomerulonephritis and that thromboxane synthetase inhibition may be beneficial in attenuating some of the functional and histologic changes associated with immune complex glomerulonephritis.

The urine-blood carbon dioxide tension (PCO2) gradient was measured in 10 healthy mature Beagles after alkalinization of the urine by administration of sodium bicarbonate. The mean (+/- SD) urine-blood PCO2, gradient was 65.92 +/- 14.42 mm of Hg, with range of 38.2 to 82.2 mm of Hg. Mean urine PCO2, was 110.21 +/- 14.19 mm of Hg, with range of 84.1 to 127.3 mm of Hg. Because urine-blood PCO2 gradient < 30.0 mm of Hg or urine PCO2 < 55 mm of Hg in people is diagnostic for a defect in distal nephron acidification, similar values might be applicable to diseases in dogs.

Acidemia stimulates renal ammonia production and excretion. This adaptive response allows increased H+ secretion and generation of new bicarbonate. To determine whether a relationship existed between urine ammonium (NH4+) concentration and excretion and urine anion gap (Na+ + K+ - Cl-), ammonium chloride (NH4Cl) was administered per OS for 5 days to induce systemic acidemia in 12 healthy Beagles. During NH4Cl administration, a strong, statistically significant (P < 0.0001) relationship was apparent between urine NH4+ concentration measured in millimoles per liter and urine anion gap. Regression equation: urine [NH4+] = 8.2 - 0.416 X urine anion gap; r = -0.897. A statistically significant (P = 0.0001) relationship existed between urine NH4+ excretion measured in millimoles per kilogram of body weight per day and urine anion gap. Regression equation: urine NH4+ excretion = 0.74 - 0.38 X urine anion gap; r = -0.768. As urine NH4+ concentration or excretion increased, urine anion gap became more negative. Before NH4Cl administration (no systemic acidemia), a weak, but statistically significant (P = 0.015) relationship was observed between urine NH4+ concentration and urine anion gap. Regression equation: urine [NH4+] = 65.2 - 0.141 X urine anion gap; r = -0.41. However, a relationship was not evident between urine NH4+ excretion and urine anion gap before NH4Cl administration. Hence, urine anion gap is a reliable index of urine NH4+ concentration and excretion only in dogs with metabolic acidosis. In human beings with distal renal tubular acidosis, NH4+ excretion is inappropriately low and results in a positive urine anion gap. Therefore, as a reliable index of NH4+ excretion, urine anion gap may represent an easy and rapid method to aid in the diagnosis of distal renal tubular acidosis in dogs.

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 > 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.