Acidosis increases magnesiuria in children with distal renal tubular acidosis.

In experimental animals, metabolic acidosis increases renal magnesium (Mg) excretion, whereas metabolic alkalosis reduces it. The objective of this study was to examine renal magnesium handling (U(Mg)) in children with primary distal renal tubular acidosis (DRTA). We measured U(Mg) in 11 children (3 females, 8 males, aged 6.9+/-4.9 years) with primary DRTA. They were studied either during spontaneous acidosis post treatment removal (3 patients) or after ammonium chloride (100 mmol/m2) induced acidosis (8 patients), and then following oral sodium bicarbonate load (4 g/1.73 m2). During acidosis (plasma pH 7.28+/-0.09, bicarbonate 13.2+/-4.3 mEq/l), U(Mg) was elevated (U(Mg/Cr) 0.18+/-0.06 mg/mg, normal values 0.1+/-0.06, P=0.003) although plasma Mg (P(Mg)) was in the normal range (1.93+/-0.31 mg/dl, controls 1.77+/-0.19, P=NS). After acute correction of metabolic acidosis (plasma pH 7.44+/-0.05, bicarbonate 25.6+/-1.6 mEq/l, P<0.001; urine pH 7.52+/-0.28, bicarbonate 86.9+/-39.1 mEq/l), U(Mg) decreased significantly (P=0.003), returning to control values after about 2 h (U(Mg/Cr) 0.09+/-0.06 mg/mg). Bicarbonate load resulted not only in reduction in U(Mg) but also in a decrease in urinary calcium excretion (U(Ca/Cr)) from 0.46+/-0.17 mg/mg to 0.14+/-0.12 mg/mg (P<0.001). We conclude that in children with primary DRTA, urinary Mg excretion is markedly increased and that this defect, like the hypercalciuric defect, is correctable by sodium bicarbonate administration.