title: Indomethacin in Bartter's syndrome: does the syndrome represent a state of hyperprostaglandinism?
abstract: In three patients with Bartter's syndrome, indomethacin administration resulted in the disappearance of the hypokalemic alkalosis and in a normalization of the elevated plasma renin activity. Changes in calcium and phosphate metabolism during indomethacin medication seemed to indicate an increase in reabsorption activity of the renal proximal tubulus. A kidney biopsy performed in one of the patients showed, besides hyperplasia of juxtaglomerular cells, hyperplasia of interstitial medullary cells which are presumed to produce prostaglandins. As indomethacin is a well-known inhibitor of prostaglandin synthesis, the observations suggest that an overproduction of renal prostaglandins could well be of pathogenetic significance in Bartter's syndrome.
mesh_terms: D000328:Adult; D000450:Aldosterone / Q000378:metabolism; D001477:Bartter Syndrome / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D006801:Humans; D006929:Hyperaldosteronism / Q000188:drug therapy*; D007213:Indomethacin / Q000494:pharmacology / Q000627:therapeutic use*; D008297:Male; D011188:Potassium / Q000378:metabolism; D011453:Prostaglandins / Q000378:metabolism; D012964:Sodium / Q000378:metabolism; D013577:Syndrome
chemical_list: D011453:Prostaglandins; D000450:Aldosterone; D012964:Sodium; D011188:Potassium; D007213:Indomethacin