Reduction of urinary protein and prostaglandin E2 excretion in the nephrotic syndrome by non-steroidal anti-inflammatory drugs.
Seven salt depleted patients with the idiopathic nephrotic syndrome were treated with various non-steroidal anti-inflammatory drugs. Indomethacin, diclofenac-sodium and flurbiprofen decreased proteinuria, glomerular filtration rate, plasma renin activity and renal prostaglandin E2 excretion by 59%, 19%, 55% and 68% respectively. Sulindac induced no major changes in proteinuria, glomerular filtration rate, plasma renin activity and renal prostaglandin E2 excretion. The relative change in proteinuria and glomerular filtration rate during non-steroidal anti-inflammatory drug treatment correlated strongly with that of the renal prostaglandin E2 excretion (r = 0.89 and r = 0.70, respectively p less than 0.05). It is likely that the anti-proteinuric effect of non-steroidal anti-inflammatory drugs is dependent on their potency to inhibit renal prostaglandin synthesis and it is suggested that this effect is mediated by lowering transcapillary glomerular hydraulic pressure.
D000328:Adult; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D004008:Diclofenac / Q000627:therapeutic use; D015232:Dinoprostone; D005480:Flurbiprofen / Q000627:therapeutic use; D005919:Glomerular Filtration Rate; D006801:Humans; D007213:Indomethacin / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D009404:Nephrotic Syndrome / Q000150:complications* / Q000652:urine; D011458:Prostaglandins E / Q000652:urine*; D011507:Proteinuria / Q000188:drug therapy* / Q000209:etiology; D012083:Renin / Q000097:blood; D013467:Sulindac / Q000627:therapeutic use
D000893:Anti-Inflammatory Agents; D011458:Prostaglandins E; D004008:Diclofenac; D013467:Sulindac; D005480:Flurbiprofen; D012083:Renin; D015232:Dinoprostone; D007213:Indomethacin