There is no agreement concerning the primary pathogenetic event leading to Bartter's syndrome. Free water clearance and distal fractional chloride reabsorption were abnormally low in our patient with Bartter's syndrome. This series of investigations in this patient with Bartter's syndrome and hypomagnesemia was undertaken to determine if the defect in chloride transport in the ascending limb and the associated renal potassium wasting was specifically related to potassium depletion, increased prostaglandin production or magnesium depletion. Neither potassium repletion, indomethacin administration nor magnesium repletion had an effect on the defect in free water clearance or in distal fractional chloride reabsorption. However, magnesium infusion eliminated renal potassium wasting. These observations suggest that the proximate cause of Bartter's syndrome in this patient is a primary defect in the reabsorption of sodium chloride in the ascending limb and not renal potassium wasting. however, hypomagnesemia may contribute to the renal potassium wasting seen in this syndrome.