Transient distal renal tubular acidosis with nephrogenic diabetes insipidus after general anaesthesia in a dog.

A 3-year-old, 3.5 kg, female spayed Pomeranian was referred due to persistent vomiting, anorexia, polyuria and polydipsia, 7 days after receiving general anaesthetic for a medial patellar luxation correction. Physical examination revealed lethargy, tachypnoea and 7% dehydration. Complete blood count and serum chemistry results were unremarkable, and venous blood gas analysis revealed hypokalaemia and hyperchloraemic metabolic acidosis with a normal anion gap. Urinalysis revealed a urine specific gravity (USG) of 1.005, pH of 7.0 and proteinuria, and the bacterial culture was negative. Based on these results, the dog was diagnosed with distal renal tubular acidosis, and potassium citrate was prescribed to correct metabolic acidosis. In addition, concurrent diabetes insipidus (DI) was suspected because the dog showed persistent polyuria, polydipsia and a USG below 1.006 despite dehydration. After 3 days of initial treatment, acidosis was corrected, and vomiting resolved. Desmopressin acetate and hydrochlorothiazide were also prescribed for DI, but the USG was not normalized. Based on the insignificant therapeutic response, nephrogenic DI was highly suspected. DI was resolved after 24 days. This case report describes the concomitant presence of RTA and DI in a dog after general anaesthesia.

Distal renal tubular acidosis and lethargy associated with zonisamide treatment in a dog with idiopathic epilepsy.

A 3-year-old neutered male golden retriever administered zonisamide for the treatment of seizures showed lethargy and had normal anion gap metabolic acidosis with hypokalaemia, hyperchloremia, and alkaline urine. The serum zonisamide concentration was close to the upper limit, which raised a suspicion of adverse effects of zonisamide. This is the first report showing that the fractional excretion of bicarbonate after compensation for the plasma bicarbonate concentration by a sodium bicarbonate infusion was approximately 5%, indicating distal renal tubular acidosis (RTA). The serum zonisamide concentration decreased, and adverse effects were abated by reducing the zonisamide dosage. Diagnostic therapy with bicarbonate served as a means of compensating for bicarbonate deficiency and contributed to the clinical diagnosis of the condition in zonisamide-associated RTA in dogs.

Metabolic Disorders Associated with Renal Disease in Horses.

This article overviews metabolic disorders associated with renal disease. Included is a discussion of the pathophysiology, clinical signs, and treatment of hyperchloremic metabolic acidosis associated with renal tubular acidosis. Conditions affecting the central nervous system including uremic encephalopathy and hyponatremic encephalopathy secondary to renal disease are presented. Finally, a discussion of the unique features of calcium and phosphorus homeostasis in horses is provided with special emphasis on a recently described syndrome of calcinosis and calciphylaxis of unknown etiology.

Acute kidney injury manifesting as renal tubular acidosis with proximal and distal renal tubular dysfunction in a dog with acute pancreatitis.

OBJECTIVE: To describe the clinical presentation and management of a critically ill dog with profound renal tubular acidosis (RTA) with proximal and distal renal tubular dysfunction. CASE SUMMARY: A 3-year-old neutered female Border Terrier was presented with frequent regurgitation resulting from acute pancreatitis with severe ileus. Venous acid-base analysis and complete urinalysis confirmed the presence of normal anion gap metabolic acidosis with inappropriately alkaline urine (pH 8), consistent with distal RTA. Urinalysis, urine amino acids, and urinary fractional excretion of electrolytes revealed glycosuria (with normoglycemia), aminoaciduria, and increased fractional excretion of sodium, calcium, and phosphate consistent with generalized proximal renal tubulopathy or Fanconi syndrome. The dog responded well to supportive care and alkaline therapy and made a complete recovery. NEW OR UNIQUE INFORMATION PROVIDED: To the authors' knowledge, this is the first description of RTA with proximal and distal renal tubular dysfunction in the veterinary literature. Furthermore, the authors hypothesize that the transient RTA was a manifestation of acute kidney injury secondary to acute pancreatitis, the first report of this in the literature.

Presumptive renal tubular acidosis secondary to topiramate administration in a cat.

OBJECTIVE: To describe renal tubular acidosis (RTA) and secondary acquired hyperaldosteronism in a cat as an adverse effect of topiramate therapy. CASE SUMMARY: An 8-year-old neutered female cat on chronic oral topiramate therapy at a recommended dose (11.9 mg/kg q 8 h) for seizure control was presented with severe metabolic acidosis and hypokalemia. Plasma electrolyte and acid-base analysis identified a severe metabolic acidosis (pH 7.153, reference interval: 7.31-7.46), hypokalemia (2.08 mmol/L [2.08 mEq/L], reference interval: 3.5-4.8 mmol/L [3.5-4.8 mEq/L]), and ionized hypercalcemia (1.85 mmol/L [1.85 mEq/L], reference range: 1.1-1.4 mmol/L [1.1-1.4 mEq/L]). Urinalysis revealed a urine specific gravity of 1.021 and a pH of 7.0. Diagnostic workup suggested distal RTA as a cause of the cat's acid-base and electrolyte disturbances. Aldosterone concentration was moderately increased, suggestive of secondary hyperaldosteronism. The metabolic abnormalities resolved with supportive care and discontinuation of topiramate. NEW OR UNIQUE INFORMATION PROVIDED: Topiramate is suggested to have led to the development severe RTA in a cat.

Transient distal renal tubular acidosis in a dog with gastric-dilatation-volvulus.

A case of distal renal tubular acidosis occurring as a transient complication in a 13-year-old female greyhound dog with gastric-dilatation-volvulus was diagnosed. The acute renal ischemia and inflammatory condition associated with this syndrome could be considered the main underlying mechanisms responsible for the acute, severe, and complicating renal tubular dysfunction.

Acidose tubulaire rénale distale transitoire chez un chien atteint de volvulus et de dilatation gastrique. Un cas d'acidose rénale distale se manifestant comme une complication transitoire chez une chienne Lévrier anglais âgée de 13 ans atteinte de dilatation gastrique-volvulus a été diagnostiqué. L'ischémie rénale aiguë et l'affection inflammatoire associées à ce syndrome pourrait être considérées comme les principaux mécanismes sous-jacents responsables de la dysfonction tubulaire rénale grave et complexe.(Traduit par Isabelle Vallières).

Hypokalemia and suspected renal tubular acidosis associated with topical carbonic anhydrase inhibitor therapy in a cat.

OBJECTIVE: To describe the occurrence of hypokalemia, metabolic acidosis, and suspected renal tubular acidosis associated with the administration of topical ophthalmic carbonic anhydrase inhibitor (CAI) in a cat. CASE SUMMARY: A 2-year-old, 5.3 kg, male, castrated, domestic short-haired cat developed hyporexia 6 weeks after starting topical ophthalmic dorzolamide 2% therapy for treatment of ocular hypertension. Two weeks later, the cat was evaluated for severe weakness, cervical ventroflexion, and anorexia. Plasma electrolyte and acid-base measurement revealed hypokalemia (K+ = 2.9 mmol/L; reference interval 3.8-5.4 mmol/L) and metabolic acidosis (plasma HCO3- = 9.8 mmol/L; reference interval 15-23 mmol/L) in the presence of a urine pH of 7.5 (reference interval 6.5-7.5). The pH abnormalities were consistent with a renal tubular acidosis. Clinical and biochemical abnormalities resolved with short-term supportive care, potassium supplementation, and discontinuation of dorzolamide therapy. NEW OR UNIQUE INFORMATION PROVIDED: This is the first report of hypokalemia and metabolic acidosis associated with topical CAI therapy in a cat.

Distal renal tubular acidosis associated with concurrent leptospirosis in a dog.

A 9 yr old spayed female boxer was presented for evaluation of vomiting, lethargy, anorexia, and weight loss. Initial laboratory evaluation revealed a hyperchloremic normal anion gap metabolic acidosis with alkaline urine that was consistent with a diagnosis of distal renal tubular acidosis (RTA). Targeted therapy was initiated with Na bicarbonate (HCO3) and potassium (K) gluconate. Leptospirosis was subsequently diagnosed with paired microagglutination testing (MAT), and doxycycline was added to the other treatments. Clinical signs resolved, and 6 mo after diagnosis, although the dog remained on alkali therapy (i.e., NaHCO3 and K gluconate) and a mild metabolic acidosis persisted, the dog remained otherwise healthy with a good quality of life. To the authors' knowledge, this is the first report to describe the concomitant association of those two disorders. Leptospirosis should be considered for any case of RTA in dogs.

Secondary renal tubular acidosis in a Hereford calf.

A 3-month-old Hereford heifer calf was presented for lethargy. Blood gas analysis and plasma biochemical testing revealed severe metabolic acidosis, azotemia, hyponatremia, hyperchloremia, and normal anion gap. Results of a urinalysis were consistent with acute tubular necrosis with inadequate acidification of urine based on the degree of acidemia. Salmonella enterica serovar agona was cultured from both urine and feces. The calf was treated with intravenous polyionic fluids, bicarbonate, and antimicrobials. Acidosis and azotemia resolved, and 4 months following initial presentation the heifer was clinically normal.

Severe life-threatening hypokalemia in a cat with suspected distal renal tubular acidosis.

OBJECTIVE: Description of the clinical presentation and management of a critically ill cat with profound hypokalemia associated with a suspicion of distal renal tubular acidosis (DRTA) and secondary hyperaldosteronism. CASE SUMMARY: A cat was presented with severe generalized weakness and acute ventilatory failure associated with severe hypokalemia. The acid-base analysis and complete analytical profile of the urine confirmed the presence of a normal anion-gap metabolic acidosis with a urine pH of 7, a disorder consistent with DRTA. The high plasma renin activity, high aldosterone concentration, and low normal plasma aldosterone concentration/plasma renin activity ratio suggested secondary hyperaldosteronism. The management of the patient in the ICU was successful. No identifiable cause could be determined as a cause for the DRTA, so the disorder was assumed to be the primary problem. NEW OR UNIQUE INFORMATION PROVIDED: DRTA is a rare disorder occasionally reported in the veterinary literature; it is especially rare in cats. Complete diagnostic evaluation was necessary to identify the reported disorders as the cause of the clinical presentation. To the author's knowledge, this is the first case reporting DRTA, and a simultaneously documented mineralocorticoid response, as a cause of a life-threatening hypokalemia.

Equine renal tubular disorders.

Renal tubular disorders have been sporadically reported in horses. Only three types of tubular defects have been recognized: (1) nephrogenic diabetes insipidus, attributable to unresponsiveness of the renal tubules to antidiuretic hormone; (2) distal renal tubular acidosis (RTA; type I); and (3) proximal RTA (type II). The following review focuses on RTA and nephrogenic diabetes insipidus.

Transient proximal renal tubular acidosis and Fanconi syndrome in a dog.

A 9-year-old spayed female Labrador Retriever was evaluated for anorexia, lethargy, and vomiting of 5 days' duration. Laboratory abnormalities included azotemia, high liver enzyme activities, hyperchloremic metabolic acidosis, glucosuria, ketonuria, proteinuria, and aminoaciduria. These laboratory abnormalities were diagnostic of proximal renal tubular acidosis and Fanconi syndrome. Results of initial and convalescent serologic tests for leptospirosis were negative. The dog was treated with amoxicillin, sodium bicarbonate, and potassium citrate at discharge. Repeated evaluations revealed resolution of the acidosis, azotemia, proteinuria, glucosuria, ketonuria, and high liver enzyme activities. Alkali administration was gradually discontinued, and the dog was clinically normal 8 months after discharge. The dog's clinical condition appeared to have been transient in nature, a phenomenon that is rarely seen in human or veterinary medicine.

Renal tubular acidosis in horses (1980-1999).

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.

Type-II renal tubular acidosis and ventricular tachycardia in a horse.

A 14-year-old Arabian mare was admitted for lethargy, anorexia, and low fecal output. On the basis of laboratory, physical examination, and electrocardiographic findings, diagnoses of type-II renal tubular acidosis (RTA), impaction of the large colon, and ventricular tachycardia were made. Diagnosis of type-II RTA was based on measurement of a low fractional excretion value for potassium and fractional excretion value for sodium within the reference range. In contrast, horses with type-I RTA have high fractional excretion values for sodium and fractional excretion values for potassium within reference ranges. Treatment consisted of intravenous and oral administration of sodium bicarbonate, intravenous administration of fluids, and oral administration of mineral oil and docusate sodium. Acidosis improved, and ventricular tachycardia resolved with resolution of acidosis. Oral administration of bicarbonate was continued after discharge. The mare had several relapses, which were associated with anorexia and low intake of supplemental bicarbonate. The mare was found dead 2 months after discharge.

[Renal tubular acidosis (type 2) in a Friesian mare]. / Renale tubulaire acidose (type 2) bij een friese merrie.

A 2-year-old Friesian mare was examined because she had been sluggish for a few weeks. Blood biochemistry showed that concentrations of creatinine (136 mumol.L-1) and urea nitrogen (6.1 mmol.L-1) in plasma were within their normal limits. Severe metabolic acidosis was apparent; the venous pH was 7.154 and the bicarbonate concentration was 13 mmol.L-1. The base excess amounted to -15.3 mmol.L-1 and the venous pCO2 measured 5.1 kPa. Plasma sodium was normal (135 mmol.L-1) and plasma chloride (113 mmol.L-1) was slightly elevated, but there was a hypokalaemia (2.9 mmol.L-1). The urine had a specific gravity of 1.040 and a pH of 5. These findings indicated type 2 renal tubular acidosis. The blood values returned to normal 3 days after treatment with sodium bicarbonate as a 4.2 per cent solution (3.2 mol in total) and additional bicarbonate (125 g) and potassium chloride (100 g) administered orally.