Renal acidification in children with idiopathic hypercalciuria.

Distal renal tubular acidosis is frequently associated with hypercalciuria. To further investigate the cause-and-effect relationships between the two conditions, we examined 20 children (5 to 18 years of age) with idiopathic hypercalciuria for evidence of renal tubular acidosis. Serum electrolytes and urine citrate levels were normal in all subjects. After a single dose of furosemide, 1 of the 20 subjects did not show 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 mmHg after urine alkalinization with orally administered acetazolamide, a finding compatible with a rate-dependent distal renal tubular acidosis. These four subjects underwent acute acid loading with arginine hydrochloride. In all four subjects urine pH decreased < 5.5 but urinary ammonium excretion failed to increase normally; this supports the 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 conclude that distal acidification abilities seem to be intact in children with hypercalciuria in the absence of nephrolithiasis. We speculate that calcium precipitation may lead to tubular damage, including distal renal tubular acidosis.