Abstract

The response to indomethacin of a patient with Bartter's syndrome and proximal tubular sodium wasting is described. The patient had evidence of excessive prostaglandin activity (elevated urinary prostaglandin E metabolite [PGE-M] excretion) which returned to normal with indomethacin therapy. Indomethacin administration corrected the defect in proximal tubular sodium resorption, but suppressed plasma renin activity and urinary aldosterone excretion only when sufficient dietary sodium was available to allow for extracellular fluid volume (ECFV) expansion. We conclude that the proximal tubular defect in sodium resorption may have been caused by excessive prostaglandin activity and that the sustained hyperactivity of the renin-aldosterone system was mediated by ECFV depletion.