The Effect of Indomethacin on Proteinuria and Kidney Function in the Nephrotic Syndrome

Abstract

In 19 nephrotic patients on a dietary intake of 20 mEq sodium/24 hours, indomethacin caused an immediate decrease in glomerular filtration rate (GFR) and urinary protein excretion, an effect completely reversible upon withdrawal of the drug. As a consequence of lower protein excretion, there was eventually a rise in GFR. It is proposed that the therapeutic effect of indomethacin in nephrotic syndrome is caused by its inhibiting action on renal prostaglandin synthesis, thereby potentiating the effect of the renin-angiotensin system on the kidney. The difference between the decrease in GFR (mean 35%) and proteinuria (mean 55%) and the more selective proteinuria during indomethacin administration may be explained by quantitative and qualitative differences in protein leakage between outer cortical and inner cortical nephron populations.