Reduction of urinary protein and prostaglandin E2 excretion in the nephrotic syndrome by non-steroidal anti-inflammatory drugs

Clin Nephrol. 1986 Feb;25(2):105-10.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Anti-Inflammatory Agents / therapeutic use*
  • Diclofenac / therapeutic use
  • Dinoprostone
  • Flurbiprofen / therapeutic use
  • Glomerular Filtration Rate
  • Humans
  • Indomethacin / therapeutic use
  • Male
  • Middle Aged
  • Nephrotic Syndrome / complications*
  • Nephrotic Syndrome / urine
  • Prostaglandins E / urine*
  • Proteinuria / drug therapy*
  • Proteinuria / etiology
  • Renin / blood
  • Sulindac / therapeutic use

Substances

  • Anti-Inflammatory Agents
  • Prostaglandins E
  • Diclofenac
  • Sulindac
  • Flurbiprofen
  • Renin
  • Dinoprostone
  • Indomethacin