Effects of sulindac and naproxen in patients with chronic glomerular disease.
Eight patients with chronic glomerulonephritis were treated with either naproxen or sulindac in an open randomized study to observe their effects on the urinary excretion of prostaglandins and renal function. Both drugs were given for 7 days. Naproxen caused a decrease (p less than 0.01) of 80% in prostaglandin PGE2 and decrease (p less than 0.01) of 55% in prostaglandin PGF2 alpha. Sulindac caused a decrease (p = 0.01) of 37% in PGE2 and a decrease (p less than 0.05) in PGF2 alpha of 13%. The decrease in urinary excretion of prostaglandins were greater (p less than 0.05) during the naproxen treatment. Naproxen caused a decrease (p less than 0.05) in 24-hour creatinine clearance of 14 ml/min, an increase (p less than 0.05) in plasma urea of 1.0 mmol/l, an increase (p less than 0.05) in plasma potassium of 0.4 mmol/l and a decrease (p less than 0.01) in 24-hour urinary excretion of albumin of 11 mumol. Sulindac did not change any of these parameters significantly. In conclusion, sulindac affects renal prostaglandin synthesis to a significantly minor degree than naproxen and contrary to naproxen it does not influence the renal function in patients with chronic glomerular disease.
D000328:Adult; D002908:Chronic Disease; D002986:Clinical Trials as Topic; D003404:Creatinine / Q000378:metabolism; D015237:Dinoprost; D015232:Dinoprostone; D005260:Female; D005921:Glomerulonephritis / Q000378:metabolism* / Q000652:urine; D006801:Humans; D007192:Indenes / Q000494:pharmacology*; D007668:Kidney / Q000187:drug effects* / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D009288:Naproxen / Q000494:pharmacology*; D011458:Prostaglandins E / Q000652:urine; D011460:Prostaglandins F / Q000652:urine; D011897:Random Allocation; D013467:Sulindac / Q000494:pharmacology*
D007192:Indenes; D011458:Prostaglandins E; D011460:Prostaglandins F; D013467:Sulindac; D009288:Naproxen; D003404:Creatinine; D015237:Dinoprost; D015232:Dinoprostone