Pathophysiological role of magnesium in familial Bartter's syndrome.

We studied three siblings with Bartter's syndrome associated with hypomagnesemia; two of them showing marked hypomagnesemia and the other mild hypomagnesemia. Urinary potassium, sodium and chloride excretions were determined and distal fractional chloride reabsorption and free water clearance on water loading test were compared before and after magnesium supplementation. Baseline urinary potassium and magnesium excretions were elevated in spite of the decreased plasma levels, whereas distal fractional chloride reabsorption and free water clearance were depressed in all patients. Magnesium repletion resulted in significant decrease in urinary potassium, sodium and chloride and subsequent increase in plasma potassium in all patients. However, neither distal fractional chloride reabsorption nor free water clearance was affected. Hypomagnesemia may contribute to urinary potassium wasting and aggravate urinary sodium and chloride wasting in familial Bartter's syndrome by a mechanism independent of the defect in free-water formation by the active reabsorption of chloride in Henle's loop.