Renal Tubular Acidosis

Luis G. Arroyo • Krista E. EsteU • Monica Aleman

Renal tubular acidosis (RTA) occurs due to improper functioning of the renal tubules and is characterized by hyperchloremic metabolic acidosis with a normal anion gap.

Two types of RTA have been reported in dogs, cats, and horses, and both types result in a hyperchloremic metabolic acidosis with a normal anion gap.^3-6 Type I develops when distal tubular excretion of hydrogen ions (H⁺) is compromised, and affected patients are unable to produce acidic urine. Type II results from decreased proximal tubular bicarbonate resorp­tion and subsequent urinary loss of bicarbonate. Normally, H⁺ is excreted when bicarbonate is reabsorbed in the proximal tubules. Thus, acidosis with both type I and type II RTA results from decreased H⁺ excretion. Hyperchloremia develops as a result of an increased renal absorption of chloride ions subsequent to bicarbonate loss. Type I RTA results in more severe acidosis and electrolyte abnormalities, since the distal tubule is responsible for maximal acidification of the urine.

Equine RTA has been sporadically reported, mostly in North America and Europe. Across the literature, there is no obvious sex predilection. Quarter Horses (QHs) (n = 11), QH-crosses (n = 4), Friesians (n = 6), and Arabians (n = 5) accounted for approximately 70% of RTA cases.^1,2,7,9-18 Affected horses range in age from 2 months to 27 years. Several genetic mutations in ion transport genes have been associated with heritable forms of RTA in humans, but there is no documented evidence of an inherited form in horses.

Typical presenting complaints and clinical signs include dullness, anorexia or poor appetite, weight loss, poor perfor­mance, weakness, decreased borborygmi and fecal output, and mild colic signs of variable duration. Vital parameters are generally within normal ranges, and horses do not appear clinically dehydrated. Hematologic and clinical chemistry abnormalities are usually mild or within reference ranges, with the exception of electrolyte concentrations and acid-base balance. Electrolyte concentrations and acid-base balance abnormalities can be profoundly abnormal but are variable between cases.

■ TABLE 34.1

Classification of Type I and Type II Renal Tubular Acidosis

Treatment consists primarily of intravenous (IV) and oral administration of sodium bicarbonate (NaHCO₃). For initial correction of acidosis, IV NaHCO₃ must be administered aggressively, and large amounts (3000 to 9000 mEq) are often required to return plasma bicarbonate concentration to values above 20 mEq/L. Half the estimated bicarbonate deficit is generally replaced with IV NaHCO₃ over 6 to 12 hours, and the remaining deficit is replaced with a combination of IV and oral NaHCO₃ (initial oral dose: 100 to 150 g twice daily; 1 g contains 12 mEq NaHCO₃). Close monitoring of serum electrolyte concentrations and acid-base balance is required to adjust the rate of IV NaHCO₃ replacement. Marked improve­ment in attitude and appetite usually accompanies correction of the acidosis, but relapse after discontinuation of IV therapy can occur. Continued oral administration of NaHCO3 for months to years may be required for maintenance of a normal acid-base status. Because potassium excretion is proportional to bicarbonate delivery to the distal tubule, initial correction of acidosis with NaHCO₃ promotes kaliuresis and may exac­erbate potassium depletion. Therefore, concurrent supplementa­tion with IV or oral potassium chloride (KCl) is advisable during initial correction of the acidosis. Complications associated with rapid correction of acidosis have not been described, but transient diarrhea ± mild colic may develop if large quantities of NaHCO₃ (>200 g) are given by nasogastric tube to horses that are completely anorectic.

Recurrence of metabolic acidosis also can occur when oral NaHCO₃ is discontinued, especially in horses that have evidence of renal damage. Relapses can be immediate or delayed for weeks to months. Reinstitution of NaHCO₃ supplementation usually corrects the metabolic abnormalities and accompanying depression and anorexia. The short-term prognosis for horses with RTA is good, with some horses reported to recover and compete successfully, but the long-term prognosis is still largely undocumented.^2,9,10,20