On the pathogenetic role of prostaglandins in Bartter's syndrome.

Abstract

Two patients, one with Bartter's syndrome and one with severe abuse of diuretics, were investigated before and after indomethacin treatment. Before indomethacin the two patients showed a similar pattern of hypokalaemic alcalosis, secondary hyperaldosteronism, and increased urinary excretion of PGE2 and kallikrein. After a few days on peroral indomethacin medication the hypokalaemia was significantly improved, the plasma renin activity, and the urinary excretion of aldosterone, PGE2 and kallikrein were normalized in both patients. It is concluded that the beneficial effect of indomethacin cannot be used as a proof of prostaglandin overproduction as the primary defect in Bartter's syndrome.