Prostaglandin synthetase inhibitors in Bartter's syndrome. Effect on immunoreactive prostaglandin E excretion

R. E. Bowden, J. R. Gill Jr, N. Radfar, A. A. Taylor and H. R. Keiser

Urinary excretion of immunoreactive prostaglandin E (iPGE) was measurably increased in five of seven patients with Bartter's syndrome. The effects of indomethacin were compared with those of either aspirin or ibuprofen in four patients. Indomethacin produced notably greater suppression of urinary iPGE, greater sodium and potassium retention, greater increases in serum potassium, and decreases in plasma renin activity and in creatinine clearance than the other inhibitors. This demonstration that there is a close correlation between the suppression of urinary iPGE excretion and the extent of correction of the clinical abnormalities in Bartter's syndrome, regardless of the chemical structure of the prostaglandin synthetase inhibitor, is further evidence for the importance of prostaglandins in the pathogenesis of this syndrome.