Post-obstructive urinary concentrating defect. A case study in the role of prostaglandins.
A child with post-obstructive urinary concentrating defect was studied for the possible pathophysiological role of prostaglandins and an eventual therapeutic approach. Increased urinary excretion of prostaglandins was corrected by indomethacin, with resultant increased nephrogenous cyclic AMP and partial improvement in the concentrating defect. The addition of a thiazide restored urinary concentration. These results add clinical support to the conception of the important role of prostaglandins in the mechanism of post-obstructive hyposthenuria. This therapeutic regimen is advocated for prolonged post-obstructive concentrating defect.
D002675:Child, Preschool; D015237:Dinoprost; D015232:Dinoprostone; D006801:Humans; D006852:Hydrochlorothiazide / Q000627:therapeutic use; D007213:Indomethacin / Q000627:therapeutic use; D007671:Kidney Concentrating Ability; D008297:Male; D011141:Polyuria / Q000188:drug therapy / Q000209:etiology* / Q000652:urine; D011183:Postoperative Complications; D011458:Prostaglandins E / Q000652:urine*; D011460:Prostaglandins F / Q000652:urine*; D014524:Urethral Obstruction / Q000150:complications* / Q000601:surgery
D011458:Prostaglandins E; D011460:Prostaglandins F; D006852:Hydrochlorothiazide; D015237:Dinoprost; D015232:Dinoprostone; D007213:Indomethacin