Since indomethacin diminishes the intensity of proteinuria in glomerulonephritis, experiments were undertaken to identify the morphological elements that might explain the reduction in the permeability of the glomerular capillary wall. In normal rats, the treatment with indomethacin produced first of all in the podocytes morphological signs of a possible activated function and in later stages a reaction of mesangial cells. The possible role of these two types of cells in the production of the basal membrane of the glomerular capillary, and the significance that their ‘activated function’ may have on the permeability of the capillary wall are discussed.

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The concomitant administration of Indomethacin reduced the biochemical signs of the nephrotic syndrome induced in rats by aminonucleoside; in the rats treated with both drugs a morphological picture suggesting activated function of podocytes was found at the electron microscopic examination of the renal glomerular structures, together with the lesions characteristic of the aminonucleoside nephrosis. The possibility is discussed that Indomethacin could modify the permeability of the glomerular capillary wall by stimulating thepodocytes to synthesize basement membrane material.

The effects of indomethacin and lysine acetylsalicylate (L-ASA) were compared in rats in which autologous nephrotoxic serum nephritis had been induced. The aim of this study was to offer support to the hypothesis that indomethacin might reduce proteinuria through increased synthesis of glomerular basement membrane by the podocytes. Both drugs were injected intraperitoneally at the dosage of 4 mg/kg body weight daily during a 6-day period into 40 rats rendered nephritic by rabbit nephrotoxic serum injection. Rats treated with indomethacin showed a marked decrease of proteinuria (tested by the 3% sulfosalicylic acid method) and a clear ultrastructural picture of hyperplasia and hypertrophy of podocytes. Rats given L-ASA showed only a slight correction of proteinuria and less specific ultrastructural modification. These observations suggest that indomethacin decreases proteinuria in nephritic rats not only through its anti-inflammatory activity, but possible also by a peculiar mechanism, namely an increase in podocytic basement membrane synthesis.