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1.
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.  相似文献   

2.
Renal tubular acidosis (RTA) is characterized by altered renal tubular function resulting in hyperchloremic metabolic acidosis. The purpose of the study was to describe RTA in 16 horses. No breed or sex predilection was found. The mean age at onset of the disease was 7 years of age. The type of diet had no apparent effect on development of RTA. The most common clinical signs were depression, poor performance, weight loss, and anorexia. Initial blood work revealed a marked hyperchloremic metabolic acidosis in all horses and a compensatory respiratory response in most horses. Sixty-three percent (10/16) of the horses had some evidence of renal damage or disease. Initial treatment consisted of large amounts of sodium bicarbonate given intravenously and orally for the prompt correction of the acidosis. Response to treatment was largely dependent on the rate of sodium bicarbonate administration. Long-term oral supplementation with NaHCO3 was required for the maintenance of normal acid-base status in individual horses. Recurrence of RTA was noted in 56% (9/16) of the horses. Horses with evidence of renal disease had multiple relapses. RTA should be considered as a differential diagnosis in horses with vague signs of depression, weight loss, and anorexia. The pathogenesis of RTA in horses remains uncertain, but prompt recognition and early aggressive intravenous sodium bicarbonate therapy followed by long-term oral supplementation seem to be important to successful management.  相似文献   

3.
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.  相似文献   

4.
To test the acidifying ability of the distal portion of the nephrons in healthy dogs, 0.2 g of NH4Cl/kg of body weight was given PO. Samples for venous blood gas analysis and urine pH were taken hourly for 6 hours. Systemic acidemia developed, as evidenced by a statistically significant (P less than 0.05) decrease in blood pH 1 hour after NH4Cl administration. Four hours after administration, mean urine pH decreased to a low of 5.16 +/- 0.1 and was less than 5.5 3 hours after administration. Changes in urine pH 2 hours after administration were statistically significant (P less than 0.05). In human beings, NH4Cl loading is used to detect patients with distal renal tubular acidosis (defective hydrogen ion secretion by the distal nephrons) and normal acid/base values. Distal renal tubular acidosis is diagnosed if urine pH fails to decrease to less than 5.5 after NH4Cl administration. On the basis of the findings of this study, a similar value would be valid for dogs.  相似文献   

5.
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.  相似文献   

6.
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)  相似文献   

7.
8.
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.  相似文献   

9.
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.  相似文献   

10.
In a previous cross-sectional study of feline chronic renal failure (CRF), metabolic acidosis was identified in 52.6 per cent of animals with severe renal failure (plasma creatinine concentration >400 micromol/litre). The aim of this longitudinal study was to determine whether metabolic acidosis preceded or accompanied a deterioration in renal function in cats with CRF. Data were analysed from 55 cats with CRF that had been followed longitudinally for at least four months. Twenty-one cases showed deterioration in renal function over the period of the study, as evidenced by significant rises in their plasma creatinine concentrations and decreases in bodyweight. In five of the 21 cases, acidaemia accompanied the deterioration in renal function. Only one of these cats had evidence of metabolic acidosis before renal function deterioration. One other case developed metabolic acidosis without a rise in plasma creatinine concentration. These data suggest that biochemical evidence of metabolic acidosis does not generally occur until late in the course of feline CRF.  相似文献   

11.
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.  相似文献   

12.
Potassium depletion in cats: renal and dietary influences   总被引:1,自引:0,他引:1  
Excessive urinary potassium loss was diagnosed in 7 cats with persistent hypokalemia and high serum creatinine concentrations. Renal tubular acidosis (proximal or distal) was not evident in the affected cats. Plasma aldosterone concentrations and plasma renin activities in affected cats were not significantly different from control values. Potassium depletion and hypokalemia were attributed to the combined effects of decreased dietary potassium intake and excessive urinary potassium losses. It was concluded that increased urinary potassium excretion may represent a basic response to renal dysfunction in cats. Data suggested that dietary potassium supplementation improved renal function in most cats in this study.  相似文献   

13.
Pregnancy toxemia and ketosis of ewes and does   总被引:2,自引:0,他引:2  
Pregnancy toxemia of ewes and does appears to occur when the animal cannot meet the glucose demands of the fetal-placental unit and hypoglycemia develops. There is individual variation in susceptibility, and there may be basic differences in glucose metabolism between susceptible animals and nonsusceptible animals. Increased serum NEFA and ketone body concentrations accompany the disease, but clinical signs do not appear to develop in the absence of hypoglycemia. The diagnosis is based on history, clinical signs, and the finding of ketone bodies in the urine. Numerous metabolic abnormalities develop subsequent to hypoglycemia and hyperketonemia, and these affect the prognosis. Important secondary abnormalities include acidosis, dehydration, and renal failure. Therapy is frequently unsuccessful, but frequent administration of small doses of glucose appears to be beneficial, if the other abnormalities, such as acidosis and dehydration, are controlled. Prevention can be readily achieved by nutritional means and is far more rewarding than therapy. Ewes and does must be fed in relation to their changing energy needs throughout the reproductive cycle.  相似文献   

14.
Renal electrolyte and net acid excretion were characterized during generation and maintenance of hypochloremic metabolic alkalosis in a ruminant model. Two phases of renal response with regard to sodium and net acid excretion were documented. An initial decrease in net acid excretion was attributable to increase in bicarbonate excretion with associated increase in sodium excretion. As the metabolic disturbance became more advanced, a second phase of renal excretion was observed in which sodium and bicarbonate excretion were markedly decreased, leading to increase in net acid excretion and development of aciduria. Throughout the metabolic disturbance, chloride excretion was markedly decreased; potassium excretion also decreased. These changes were accompanied by increase in plasma renin and aldosterone concentrations. There was apparent failure to concentrate the urine optimally during the course of the metabolic disturbance, despite increasing plasma concentration of antidiuretic hormone.  相似文献   

15.
Complex clinical and clinico-biochemical examination of the blood, urine and rumen liquor in a herd of dairy cows revealed chronical metabolic acidosis accompanied by rumen dysfunction and by a reduced butterfat content of milk. During the first examination of the acid-base state of the blood was almost at a standard level. An increased level of urea in blood plasma and a higher GOT transaminase activity testified to an excessive load on the liver. Urine pH was considerably deviated towards the acidic side and inorganic phosphorus was present in urine in a greater concentration. The pH of rumen liquor was slightly shifted towards alkalinity owing to the release of NH3 from urea in the food ration. The diagnosis--suspect chronical metabolic acidosis--was determined on the basis of the first examination. Chronical metabolic acidosis was definitely proved by the second examination when urea had been excluded from the feed ration. Repeated examinations revealed chronical metabolic acidosis which had originally been accompanied by a higher rumen liquor pH. On the basis of case histories and mechanisms of chronical acidosis, measures were proposed, resulting in an increase of the butterfat content of milk. Chronical metabolic disorders often follow a long-lasting latent pattern, manifesting themselves as a reduced milk yield and lower resistance; the clinical form of disease appears only at a later stage. The system of preventive diagnostics provides information on the changes in the composition of internal medium and of the faeces before a drop occurs in milk and fat production. These measures prevent metabolic disorders and high losses of produce which otherwise remain hidden for a long time.  相似文献   

16.
The effects of two reduced-protein diets and a canine maintenance diet on renal function, nutrition, serum and urine acid-base and electrolyte values, and divalent ion metabolism were compared in Beagle dogs with induced chronic renal failure. Two reduced-protein (18%) diets differed in their protein sources. One 18% protein diet was formulated using egg protein as the only protein source. The other 18% protein diet was formulated using a mixture of animal and vegetable proteins. The 42% protein diet contained a mixture of animal and vegetable protein sources. Results of this study indicate that the egg-based and mixed protein-based diets had similar effects on most clinical and laboratory evaluations in dogs with chronic renal failure. However, the egg protein diet appeared to promote hyperchloremic metabolic acidosis. Both reduced-protein diets were beneficial in reducing azotemia, polyuria, hypermagnesemia, and fractional excretion of phosphorus compared with the 42% protein diet.  相似文献   

17.
BACKGROUND: Chronic renal failure (CRF) is a common disease in dogs, and many metabolic disorders can be observed, including metabolic acidosis and calcium and phosphorus disturbances. Acidosis may change the ionized calcium (i-Ca) fraction, usually increasing its concentration. OBJECTIVE: In this study we evaluated the influence of acidosis on the serum concentration of i-Ca in dogs with CRF and metabolic acidosis. METHODS: Dogs were studied in 2 groups: group I (control group = 40 clinically normal dogs) and group II (25 dogs with CRF and metabolic acidosis). Serum i-Ca was measured by an ion-selective electrode method; other biochemical analytes were measured using routine methods. RESULTS: The i-Ca concentration was significantly lower in dogs in group II than in group I; 56% of the dogs in group II were hypocalcemic. Hypocalcemia was observed in only 8% of dogs in group II when based on total calcium (t-Ca) concentration. No correlation between pH and i-Ca concentration was observed. A slight but significant correlation was detected between i-Ca and serum phosphorus concentration (r = -.284; P = .022), as well as between serum t-Ca and i-Ca concentration (r = .497; P < .0001). CONCLUSION: The i-Ca concentration in dogs with CRF and metabolic acidosis varied widely from that of t-Ca, showing the importance of determining the biologically active form of calcium. Metabolic acidosis did not influence the increase in i-Ca concentration, so other factors besides acidosis in CRF might alter the i-Ca fraction, such as hyperphosphatemia and other compounds that may form complexes with calcium.  相似文献   

18.
Ureterocolonic anastomosis (UCA) was performed in 10 dogs with transitional cell carcinoma of the urinary bladder trigone or the urethra, or both. All grossly visible tumor was excised. All of the dogs recovered from anesthesia and surgery and had anal continence with no urine leakage. One dog died of undetermined causes 7 days after surgery. Nine dogs survived 1 to 5 months. The owners of eight of the dogs considered their dog's quality of life to be acceptable. Four dogs were euthanatized because of neurologic disease, three of which also had nausea and vomiting. The neurologic and gastrointestinal signs may have been caused by hyperammonemia, metabolic acidosis, and uremia. Blood ammonia levels were elevated in two dogs with neurologic signs. Hyperchloremic metabolic acidosis that was reversible with bicarbonate therapy was diagnosed in five dogs. All of the dogs were azotemic because of intestinal recycling of urea. Serum creatinine concentrations increased in four dogs after surgery. Drug-induced renal disease may have developed in two dogs. Pyelonephritis developed in five kidneys, two of which had outflow obstruction and two had bilateral hydroureteronephrosis before the UCA. In this small number of dogs, surgical excision of transitional cell carcinoma was not curative with six dogs having confirmed metastatic lesions at the time of death.  相似文献   

19.
Chloride Ion in Small Animal Practice: The Forgotten Ion   总被引:1,自引:0,他引:1  
The Physiology of chioride ion and its relationship to clinical disorders in small animall practice is reviewed. Chioride is the major anion in the extracellular fluid and is important in the metabolic regulation of acid-base balance. A new clinical approach is used to assess chloride ion changes after accounting for changes in free water. Using this approach chloride disorders can be divided into corrected and artifactual. Changes in free water are solely responsible for the chioride ion changes in artifactual disorders, whereas in corrected chloride disorders, chloride ion itself changes. Corrected hypochioremia is associated with increases in the strong ion differece (SID) and metabolic alkalosis and is caused by administration of solution containing a high concentration of sodium relative to chioride (e.g., Sodium bicarbonate) or the excessive loss chioride relative to sodium (e.g., vomiting of stomach contents). Administration of chioride is correction of hypochioremic metabolic alkalosis. Corrected hyperchioremia is associated with a decreased SID and metabolic acidosis and is usually the result of excessive loss of sodium relative to chloride (e.g., diarrhea), chioride retention (e.g., renal tubular acidosis), or therapy with solutions containing a high concentration of chioride relative to sodium (e.g.,0.9% sodium chloride;3–24% hypertonic saline). Treatment with sodium bicarbonate should be attempted in patients with corrected hyperchioremia and a plasma pH beiow 7.2.  相似文献   

20.
A 6-year-old spayed female Jack Russell Terrier presented with a 1-month history of lethargy, anorexia, vomiting and weight loss. The dog was fed beef and chicken jerky treats daily in addition to a commercial diet. Laboratory tests revealed azotemia, hypokalemia, hyperchloremia, metabolic acidosis and glucosuria with normoglycemia. Urine amino acid analysis showed significant amino acid loss into the urine. Thus, Fanconi syndrome was diagnosed, and based on the case history and extensive diagnostic testing, excessive consumption of jerky treats was strongly suspected as the cause. Glucosuria resolved 7 days after the withdrawal of jerky treats and fluid therapy. Aminoaciduria was substantially, but not completely, improved 3 months after diagnosis. Mild azotemia remained, suggesting chronic renal disease. To the best of our knowledge, this is the first reported case of Fanconi syndrome following the consumption of jerky treats in Japan.  相似文献   

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