PATHOPHYSIOLOGICAL ROLE OF MAGNESIUM IN FAMILIAL BARTTERS-SYNDROME

We studied three siblings with Bartters syndrome associated with hypom agnesemia; two of them showing marked hypomagnesemia and the other mil d hypomagnesemia. Urinary potassium, sodium and chloride excretions we re determined and distal fractional chloride reabsorption and free wat er clearance on water loading test were compared before and after magn esium supplementation. Baseline urinary potassium and magnesium excret ions were elevated in spite of the decreased plasma levels, whereas di stal fractional chloride reabsorption and free water clearance were de pressed in all patients. Magnesium repletion resulted in significant d ecrease in urinary potassium, sodium and chloride and subsequent incre ase in plasma potassium in all patients. However, neither distal fract ional chloride reabsorption nor free water clearance was affected. Hyp omagnesemia 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 a ctive reabsorption of chloride in Henle's loop.