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.