Studies in primary hypomagnesaemia: evidence for defective carrier-mediated small intestinal transport of magnesium.

A 4 year old male with primary hypomagnesaemia was studied using balance and steady-state perfusion techniques. Magnesium balance was negative and could be accounted for by increased faecal losses, renal conservation being normal; calcium balance was normal. After oral magnesium therapy magnesium balance became positive. The perfusion studies demonstrated net loss of magnesium into the intestinal lumen when low concentrations (1 and 2 mmol/l) of magnesium were perfused in contrast with control subjects; whereas at high concentrations (10 mmol/l a net absorption of a magnitude similar to control values was observed. In the control subjects sequential perfusion of increasing concentrations of magnesium demonstrated a curvilinear relationship between rates of absorption and the lower concentrations (1, 2, and 4 mmol/l) with an apparent Km and Vmax of 4.5 mmol/l and 91 nmol/min/cm respectively. At the higher concentrations (6 and 10 mmol/l) the relationship was linear. These data suggest that two separate transport systems participate in the absorption of magnesium from the proximal small intestine; a carrier-mediated system which saturates at low intraluminal concentrations, and a simple diffusional process. The possibility of the second transport system being a carrier-mediated process with a very much higher Km cannot be excluded. In primary hypomagnaesaemia the results suggest that the primary abnormality is a defect in carrier-mediated transport of magnesium from low intraluminal concentrations of magnesium.