Page 966 - Equine Clinical Medicine, Surgery and Reproduction, 2nd Edition

Urinary system 941

VetBooks.ir RENAL TUBULAR DISORDERS

RENAL TUBULAR ACIDOSIS
in type II RTA. Blood urea nitrogen and creatinine
should be normal unless dehydration is present.
Definition/overview Otherwise, elevations in blood urea and creatinine
Renal tubular acidosis (RTA) is an uncommon con- indicate concurrent renal disease. Urine pH is neu-
dition in which renal tubules are unable to acidify tral to alkaline in type I RTA and alkaline to acidic
urine, resulting in a continued state of metabolic in type II RTA.
acidosis. Despite profound metabolic acidosis, urine Ammonium chloride loading has been used to
pH remains neutral or alkaline. Normal horses have detect type I RTA. Ammonium chloride delivery
alkaline urine, which should acidify and excrete (0.1 g/kg in 6 litres of water given orally to a horse
hydrogen ions in cases of acidosis. that has been kept off feed and water for at least
7 hours) should acidify the urine in normal horses,
Aetiology/pathophysiology whereas in type I RTA the urine remains alkaline.
Although many cases appear idiopathic, RTA is Diagnosis of type II RTA is based on clinical and
probably a secondary condition. Two types of RTA laboratory findings and following exclusion of type
have been reported in horses: type I (distal tubular I RTA. The distinction between the two types of
acidosis) and type II (proximal tubular acidosis). RTA is not critical, because the treatment and prog-
Type I RTA develops when the patient is unable nosis are similar.
to acidify urine because of inadequate hydrogen
ion secretion in distal renal tubules. Type II RTA Management
is associated with an inability of the proximal renal Treatment of RTA consists of i/v administration of
tubules to resorb bicarbonate, which is subsequently sodium bicarbonate to correct the metabolic acido-
lost in urine. Hyperchloraemia and hypokalaemia sis. Initial treatment should be administered gradu-
occur concurrently, indicating that RTA is caused ally to replace the estimated bicarbonate deficit
by disturbances in strong ion metabolism in renal (0.3 × body weight [kg] × base deficit = bicarbonate
tubules. Type II RTA is often a self-limiting disease. deficit in mmol/l). The initial goal is to return plasma
bicarbonate concentration to values above 20 mEq/l
Clinical presentation and blood pH above 7.3, which usually does not
Anorexia, weight loss, depression and weakness are require the administration of the whole calculated
the main presenting complaints. Ataxia, poor per- bicarbonate deficit. Thereafter, losses are controlled
formance, ill-thrift, tachypnoea and tachycardia by oral administration of sodium bicarbonate (50–
have also been reported. 150 g q12–24 h). Oral potassium supplementation is
often necessary during the initial stages of the treat-
Differential diagnosis ment. Diarrhoea may be observed after high doses of
Differential diagnoses include renal failure, uroperi- oral sodium bicarbonate, but usually resolves if the
toneum, exertion, renal calculi, neurological disor- dose is decreased. Serum electrolyte levels and blood
ders and malabsorption/maldigestion syndrome. gases should be monitored regularly.

Diagnosis Prognosis
Electrolyte and acid–base disturbances are the The prognosis is based on the severity of the under-
main haematological abnormalities. Severe hyper- lying renal disorder, and the duration of response to
chloraemic metabolic acidosis with a low strong ion initial therapy. The short-term prognosis is usually
difference is characteristic. Hyponatraemia and/ good with proper treatment. Several horses have
or hypokalaemia may also be present. Fractional been reported to recover completely with bicarbon-
excretion of sodium is usually high in type I RTA, ate supplementation. Relapses are common if renal
while the fractional excretion of potassium is low disease is present.