RENAL ACIDIFICATION IN CHILDREN WITH IDIOPATHIC HYPERCALCIURIA

Distal renal tubular acidosis is frequently associated with hypercalci uria. To further investigate the cause-and-effect relationships betwee n the two conditions, we examined 20 children (5 to 18 years of age) w ith idiopathic hypercalciuria for evidence of renal tubular acidosis. Serum electrolytes and urine citrate levels were normal in all subject s. After a single dose of furosemide, I of the 20 subjects did not sho w a decrease in urine pH < 5.5, which suggests an acidification defect in the cortical collecting duct. Three other patients failed to show an increase in urine-minus-blood partial pressure of carbon dioxide > 20 mm Hg after urine alkalinization with orally administered acetazola mide, a finding compatible with a rate-dependent distal renal tubular acidosis. These four subjects underwent acute acid loading with argini ne hydrochloride. In all four subjects urine pH decreased < 5.5 but ur inary ammonium excretion failed to increase normally; this supports th e diagnosis of a defect in distal acidification. Four of six patients with nephrolithiasis had evidence of distal renal tubular acidosis, in contrast to none of the 14 patients without stones (p = 0.003). We co nclude that distal acidification abilities seem to be intact in childr en with hypercalciuria in the absence of nephrolithiasis. We speculate that calcium precipitation may lead to tubular damage, including dist al renal tubular acidosis.