Relationship between urine ammonium ion excretion and urine anion gap 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 less than 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.(ABSTRACT TRUNCATED AT 250 WORDS)     

Distal renal tubular acidosis and hepatic lipidosis in a cat

Clinical and laboratory evidence of hepatic failure was found in a chronically anorectic cat. Simultaneous blood and urine pH determinations established a diagnosis of distal renal tubular acidosis. The cat did not respond to treatment. Necropsy revealed distal tubular nephrosis and hepatic lipidosis. The finding of distal renal tubular acidosis in a cat with hepatic lipidosis emphasizes the importance of complete evaluation of acid-base disorders in patients.     

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.     

Suspected renal tubular acidosis in two dogs

Clinical signs of hyperventilation, muscle weakness and lethargy were recognised in a one-year-old female Bichon Frise and a three-year-old male Poodle. One dog was also hyperexcitable and pyrexic. The diagnosis of renal tubular acidosis was confirmed by demonstrating the tendency to an elevated urine pH, a low blood pH and low blood bicarbonate level, and by eliminating other causes of metabolic acidosis. Both dogs were treated with oral sodium bicarbonate resulting in improvement in their clinical condition and a return to near normal blood pH and bicarbonate levels.     

Suspected renal tubular acidosis in two dogs

Clinical signs of hyperventilation, muscle weakness and lethargy were recognised in a one-year-old female Bichon Frise and a three-year-old male Poodle. One dog was also hyperexcitable and pyrexic. The diagnosis of renal tubular acidosis was confirmed by demonstrating the tendency to an elevated urine pH, a low blood pH and low blood bicarbonate level, and by eliminating other causes of metabolic acidosis. Both dogs were treated with oral sodium bicarbonate resulting in improvement in their clinical condition and a return to near normal blood pH and bicarbonate levels.     

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.     

Effects of general anesthesia and surgery on renal function in healthy dogs

OBJECTIVES: To evaluate renal function in healthy dogs undergoing general anesthesia and ovariohysterectomy without concurrent IV administration of fluids. ANIMALS: 35 healthy client-owned dogs. PROCEDURE: Dogs were medicated with promazine hydrochloride (0.05 mg/kg of body weight, SC) approximately 45 minutes before induction of anesthesia with thiopental sodium (10 to 15 mg/kg, IV). Anesthesia was maintained with 2% halothane in oxygen. Ovariohysterectomies were performed by senior veterinary students under the direct supervision of a veterinary surgeon. Renal function was assessed (serum urea and creatinine concentrations, fractional clearance of sodium, urine alkaline phosphatase [ALP] and gamma-glutamyltransferase [GGT] activities, urine specific gravity, and enumeration of renal tubular epithelial cells in urine sediment) prior to and 24 and 48 hours after surgery. RESULTS: Duration of general anesthesia ranged from 80 to 310 minutes. Urine specific gravity and ALP activity and serum urea and creatinine concentrations did not change over time. Fractional clearance of sodium decreased 24 and 48 hours after surgery, whereas urine GGT activity and the ratio of urine GGT activity to urine creatinine concentration increased 24 hours after surgery, compared with presurgery values. Renal tubular epithelial cells increased in number in urine sediment from 11 of 35 (31.4%) dogs and 5 of 35 (14.3%) dogs 24 and 48 hours after surgery, respectively. However, this increase was not clinically relevant. CONCLUSIONS AND CLINICAL RELEVANCE: Intravenous administration of fluids to healthy dogs undergoing general anesthesia and elective surgery may not be necessary for maintenance of renal homeostasis.     

Early renal ultrasonographic findings in dogs with experimentally induced ethylene glycol nephrosis

Renal ultrasonographic changes were evaluated in 5 dogs administered 10 ml of commercial antifreeze (95% ethylene glycol)/kg of body weight, PO, and in 2 dogs given placebos. Studies were made prior to and after ingestion on an hourly basis over a period of 8 to 10 hours. All dogs were anesthetized immediately after toxin or placebo ingestion for the duration of the study. Renal cortical echogenicity was evaluated in comparison with that of the adjacent liver and spleen. Echogenicity of the renal medulla and definition of the corticomedullary junction were assessed. Within 4 hours after ethylene glycol administration, renal cortical echogenicity of all intoxicated dogs increased from normal to surpass that of liver and approach or equal that of the spleen. Medullary echogenicity in all intoxicated dogs progressively increased over the course of the study, with changes recognized within 5 hours after ethylene glycol administration. An ultrasonographic pattern consisting of nearly equal, marked increase in cortical and medullary echogenicity and relatively hypoechoic corticomedullary junction and central medullary regions was recognized concurrent with the development of anuria in 3 of the 5 intoxicated dogs. Mild, transient increases in cortical and medullary echogenicity were observed in anesthetized control dogs. However, no statistical difference (P less than 0.05) was detected between baseline, peak, and terminal echogenicity values in these dogs. Blood and urine samples were collected hourly from intoxicated dogs to coincide with ultrasonographic studies. Most clinicopathologic values derived from these samples were not statistically different (P less than 0.05) from those reported in a study that used a similar intoxication protocol in nonanesthetized dogs.     

Decreased colostral immunoglobulin absorption in calves with postnatal respiratory acidosis

The effect of postnatal acid-base status on the absorption of colostral immunoglobulins by calves was examined in 2 field studies. In study 1, blood pH at 2 and 4 hours after birth was related to serum IgG1 concentration 12 hours after colostrum feeding (P less than 0.05). Decreased IgG1 absorption from colostrum was associated with respiratory, rather than metabolic, acidosis, because blood PCO2 at 2 and 4 hours after birth was negatively related to IgG1 absorption (P less than 0.05), whereas serum bicarbonate concentration was not significantly related to IgG1 absorption. Acidosis was frequently observed in the 30 calves of study 1. At birth, all calves had venous PCO2 value greater than or equal to 60 mm of Hg, 20 of the calves had blood pH less than 7.20, and 8 of the calves had blood bicarbonate concentration less than 24 mEq/L. Blood pH values were considerably improved by 4 hours after birth; only 7 calves had blood pH values less than 7.20. Calves lacking risk factors for acidosis were examined in study 2, and blood pH values at 4 hours after birth ranged from 7.25 to 7.39. Blood pH was unrelated to IgG1 absorption in the calves of study 2. However, blood PCO2 was again found to be negatively related to colostral IgG1 absorption (P less than 0.005). Results indicate that postnatal respiratory acidosis in calves can adversely affect colostral immunoglobulin absorption, despite adequate colostrum intake early in the absorptive period.     

Effects of corticosteroid treatment on survival time in dogs with chronic hepatitis: 151 cases (1977-1985)

Medical records of 151 dogs with chronic hepatitis were reviewed. Corticosteroid treatment had a statistically significant (P less than 0.005) effect on improving survival time when corticosteroid-treated dogs were compared with untreated dogs. Dogs dying within 1 week of examination represented 37.1% of the cases, and when compared with those living more than 1 week, serum glucose concentration was significantly lower (P less than 0.001); prothrombin time and partial thromboplastin time were significantly longer (P less than 0.001); blood ammonia concentration after oral administration of ammonium chloride was significantly higher (P less than 0.05); and necrosis severity and fibrosis severity were significantly greater (P less than 0.05 and P less than 0.022, respectively). The best predictors of early death were low normal serum glucose concentration (P less than 0.001) and prolonged prothrombin time (P less than 0.030), which was abnormal in 60.0% of dogs dying early. Partial thromboplastin time, which was increased in 92.0% of dogs dying early and in 42.6% of dogs living more than 1 week, was a less reliable predictor. Plasma ammonia concentration after oral administration of NH4Cl was least reliable in predicting early death. In dogs living more than 1 week, hypoalbuminemia was a predictor of shorter survival time (P less than 0.003). Of all the histologic features evaluated, only necrosis severity and fibrosis severity were accurate predictors of early death. The presence of bridging fibrosis was a predictor of shorter survival time in dogs living more than 1 week (P less than 0.0002).     

Effect of administration of nonsteroidal anti-inflammatory drugs before surgery on renal function in clinically normal dogs

OBJECTIVES: To investigate renal function in clinically normal dogs undergoing general anesthesia for ovariohysterectomies that received nonsteriodal antiinflammatory drugs (NSAID) before surgery. ANIMALS: 40 clinically normal dogs. PROCEDURE: After induction of anesthesia, dogs were given an analgesic. Renal function was assessed before surgery and 24 and 48 hours after surgery by means of serum urea and creatinine concentrations, fractional clearance of sodium (FC(Na)), urine gamma-glutamyltransferase (GGT) and alkaline phosphatase (ALP) activities, and urine analysis. Ten dogs in each of 4 groups received ketorolac tromethamine (0.5 mg/kg of body weight), ketoprofen (1 mg/kg), carprofen (4 mg/kg), or morphine (0.1 mg/kg; control group). RESULTS: Duration of general anesthesia ranged from 1.75 to 5 hours, with a mean of 3 hours. Two ketorolac- and 2 ketoprofen-treated dogs had transient azotemia. A significant decrease in the FC(Na) between before surgery and 24 hours after surgery, and between before surgery and 48 hours after surgery, was found in ketoprofen- and carprofen-treated dogs. Ketorolac-, ketoprofen-, and morphine-treated dogs had a decrease in urine specific gravity. Two ketorolac, 1 ketoprofen-, 1 carprofen-, and 4 morphine-treated dogs had increases in renal tubular epithelial cells on urine sediment examination 24 hours after surgery. CONCLUSIONS AND CLINICAL RELEVANCE: In clinically normal dogs undergoing general anesthesia and elective surgery, the use of NSAID as analgesics is not contraindicated. Compared with ketorolac or ketoprofen, carprofen had the least effect on renal function and integrity.     

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.     

Multiple endocrine abnormalities in Basenji dogs with renal tubular dysfunction

Three Basenji dogs with renal tubular dysfunction were studied. Hyposthenuria and diminished urine concentrating ability, indicative of nephrogenic diabetes insipidus, were documented. Metabolic acidosis, hyperchloremia, and reduction in glomerular filtration rate also were detected in all dogs. In addition, an exaggerated response to the adrenocorticotropin test and hyperaldosteronism, believed to be secondary to decreased effective circulating blood volume, were detected in all 3 dogs. Thyroxine values were decreased in all dogs and could be correlated with histopathologic changes of the thyroid gland in 2 dogs. Gastropathy and hypergastrinemia were identified in 2 dogs. Diffuse lymphocytic-plasmacytic enteritis was evident in 2 dogs. It was concluded that a urine concentrating defect that may be secondary to hypercortisolism exists in Basenji dogs with renal tubular dysfunction.     

The Effect of Experimental Cystitis and Iatrogenic Blood Contamination on the Urine Protein/Creatinine Ratio in the Dog

The effect of experimentally induced cystitis and iatrogenic blood contamination on the urine protein/creatinine ratio (U P/C) was evaluated in 17 dogs. Before they were included in the study, all dogs were judged to be healthy on the basis of physical examination, serum concentrations of urea nitrogen and creatinine, complete urinalysis, and a U P/C less than 0.4. A single urine sample was contaminated with increasing quantities of canine fresh whole blood (PCV = 42%; total protein = 6.2 g/dl). When added blood was equal to or greater than 25% of the total urine sample volume, the U P/C exceeded 3.5, a finding consistent with nephrotic range proteinuria. When added blood was 10% of the total urine sample volume, the U P/C was less than 1.8. Eleven Beagles underwent routine laparotomy during which a cystotomy was done. The median U P/Cs on postoperative days 1 and 2 were significantly increased compared with preoperative values (P less than 0.05); no U P/C exceeded 2.0. Renal biopsies performed on postoperative day 3 eliminated renal proteinuria as a source of urine protein. Five dogs had bacterial cystitis experimentally induced. At 72 and 96 hours after bacterial inoculation, the median U P/Cs were significantly increased (P less than 0.05); individual values ranged from 1.5 to 40.8. Renal biopsies performed between 5 and 6 days after inoculation eliminated renal proteinuria as a source of urine protein. Cytologic evaluation of urine sediment in each group did not correlate with the magnitude of the increase in the U P/C. The U P/C significantly increased in each model of lower urinary tract inflammation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of bacterial direct-fed microbials on ruminal fermentation,blood variables,and the microbial populations of feedlot cattle

A study was conducted to determine whether bacterial direct-fed microbials (DFM) could be used to minimize the risk of acidosis in feedlot cattle receiving high concentrate diets. Six ruminally cannulated steers, previously adapted to a high concentrate diet, were used in a double 3 x 3 Latin square to study the effects of DFM on feed intake, ruminal pH, and ruminal and blood characteristics. Steers were provided ad libitum access to a diet containing steam-rolled barley, barley silage, and a protein-mineral supplement at 87, 9, and 4% (DM basis), respectively. Treatments were as follows: control, Propionibacterium P15 (P15), and Propionibacterium P15 and Enterococcus faecium EF212 (PE). The bacterial treatments (10(9) cfu/g) plus whey powder carrier, or whey powder alone for control, were top-dressed once daily at the time of feeding (10 g/[steer/d]). Periods consisted of 2 wk of adaptation and 1 wk of measurements. Ruminal pH was continuously measured for 6 d using indwelling electrodes. Dry matter intake and ruminal pH (mean, minimum, hours, and area pH < 5.8 or < 5.5) were not affected by treatment (P > 0.05). However, supplementation with P15 increased protozoal numbers (P < 0.05) with a concomitant increase in ruminal NH3 concentration (P < 0.01) and a decrease in the number of amylolytic bacteria (P < 0.05) compared with the control. Streptococcus bovis, enumerated using a selective medium, was numerically reduced with supplementation of PE. Although blood pH and blood glucose were not affected by DFM supplementation, steers fed PE had numerically lower concentrations of blood CO2 than control steers, which is consistent with a reduced risk of metabolic acidosis. Although the bacterial DFM used in this study did not induce changes in DMI or ruminal and blood pH, some rumen and blood variables indicated that the bacterial DFM used in this study may decrease the risk of acidosis in feedlot cattle.     

Uric acid and phosphorus excretion in dogs with lymphosarcoma

Serum uric acid and phosphorus concentrations were determined for 27 dogs with multicentric lymphosarcoma before and after chemotherapy. Mean serum uric acid values in dogs before treatment were significantly higher (P less than 0.05) than those of a control group of healthy dogs. Serum uric acid values did not change after treatment. Of the 27 dogs, 13 had 24-hour urine collections to determine endogenous creatinine clearance and quantitation of uric acid and phosphorus excretion before and after treatment for lymphosarcoma. Mean values for 24-hour creatinine clearance before and after treatment were statistically similar in dogs with lymphosarcoma, although the values were lower than those in a normal range. Total urinary phosphorus excretions were increased significantly (P less than 0.01) after treatment without change in fractional excretion. Chemotherapeutic agents used accounted for the significant (P less than 0.05) increase in urine volume after treatment and may have affected the excretion of uric acid and phosphorus. Seemingly, dogs with uncomplicated lymphosarcoma rarely have renal dysfunction or clinically important alterations in uric acid or phosphorus excretion secondary to rapid tumor lysis. However, preexisting renal disease or systemic complications, such as hypercalcemia, may be associated with increased risk of further renal impairment during treatment.     

Effect of ammonium chloride on the bicarbonate buffer system in heat-stressed broilers

1. The effects of ammonium chloride (NH4Cl) on the bicarbonate buffer system and plasma lactate in heat-stressed broilers were investigated. 2. The infusion of a 10 g/l solution of NH4Cl into the crop during a 90 min thermoneutral period produced a metabolic acidosis resulting from a reduction in blood bicarbonate concentration. Blood bicarbonate continued to decrease in NH4Cl-treated birds and reached values which were 30% of controls by the end of a 90 min heat stress period. 3. By the end of heat stress, plasma lactate concentrations were lower in NH4Cl-infused birds than in controls.     

Thyrotropin-releasing hormone stimulation testing in healthy dogs

Serum triiodothyronine (T3) and thyroxine (T4) concentrations were determined after IV administration of 200 micrograms of thyrotropin-releasing hormone (TRH) to 10 healthy euthyroid dogs. Significant (P less than 0.05) changes were not found in the T3 concentration throughout an 8-hour sampling interval. All dogs had a significant increase (P less than 0.05) in the T4 concentration at 4, 5, 6, 7, and 8 hours after TRH administration. The largest increase in the serum T4 concentration occurred 4 hours after TRH injection. From 4 to 8 hours after TRH administration, the mean increase above basal T4 concentrations was 13.9 +/- 5.4 ng/ml.     

Serum concentrations of thyroxine, 3,5,3'-triiodothyronine, thyrotropin, and prolactin in dogs before and after thyrotropin-releasing hormone administration

Serum concentrations of thyrotropin (TSH), prolactin, thyroxine, and 3,5,3'-triiodothyronine in 15 euthyroid dogs and 5 thyroidectomized and propylthiouracil-treated dogs after thyrotropin-releasing hormone (TRH) administration were measured. Although thyroidectomized and propylthiouracil-treated dogs had higher (P less than 0.01) base-line concentrations of TSH in serum than did euthyroid dogs, concentrations of TSH after TRH administration varied at 7.5, 15, and 30 minutes with 14 of 45 samples obtained from healthy dogs having lower TSH concentrations than before TRH challenge. Similarly, concentrations of 3,5,3'-triiodothyronine in the serum of euthyroid dogs 4 hours after TRH administration were similar (P less than 0.05) to concentrations before TRH challenge. Although the mean concentration of thyroxine in serum was elevated (P less than 0.05) 4 hours after administration of TRH to euthyroid animals, as compared with base-line levels, the individual response was variable with concentrations not changing or decreasing in 4 dogs. Therefore, the TRH challenge test as performed in the current investigation was of limited value in evaluating canine pituitary gland function. Although mean concentrations of TSH in serum were higher (P less than 0.05) in euthyroid dogs after TRH administration, the response was too variable among individual animals for accurate evaluation of pituitary gland function. Concentrations of prolactin in the sera of dogs after TRH administration, confirmed previous reports that exogenously administered TRH results in prolactin release from the canine pituitary and indicated that the TRH used was biologically potent.     

Alterations in epinephrine-induced arrhythmogenesis after xylazine and subsequent yohimbine administration in isoflurane-anesthetized dogs

Effects of xylazine (1.1 mg/kg of body weight, IV bolus, plus 1.1 mg/kg/h infusion) and subsequent yohimbine (0.125 mg/kg, IV bolus) administration on the arrhythmogenic dose of epinephrine (ADE) in isoflurane (1.8% end-tidal)-anesthetized dogs were evaluated. The ADE was defined as the total dose of epinephrine that induced greater than or equal to 4 premature ventricular contractions within 15 seconds during a 3-minute infusion period or within 1 minute after the end of infusion. Total ADE values during isoflurane anesthesia, after xylazine administration, and after yohimbine injection were 36.6 +/- 8.45 micrograms/kg, 24.1 +/- 6.10 micrograms/kg, and 45.7 +/- 6.19 micrograms/kg, respectively. Intravenous xylazine administration significantly (P less than 0.05) increased blood pressure and decreased heart rate, whereas yohimbine administration induced a significant (P less than 0.05) decrease in blood pressure. induced a significant (P less than 0.05) decrease in blood pressure. After yohimbine administration, the ADE significantly (P less than 0.05) increased above that after isoflurane plus xylazine administration. After yohimbine administration, blood pressure measured immediately before epinephrine-induced arrhythmia was significantly (P less than 0.05) less than the value recorded during isoflurane plus xylazine anesthesia. Heart rate was unchanged among treatments immediately before epinephrine-induced arrhythmia. Seemingly, yohimbine possessed a protective action against catecholamine-induced arrhythmias in dogs anesthetized with isoflurane and xylazine.