TRIPLE-DRUG TREATMENT OF AUTOLOGOUS IMMUNE-COMPLEX GLOMERULONEPHRITIS

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  • 1 January 1980
    • journal article
    • research article
    • Vol. 41  (2) , 218-224
Abstract
Autologous immune complex glomerulonephritis, an established experimental model of membranous glomerulopathy in man, was used to investigate the effect of various drugs on its course. Because immunosuppressive or anti-inflammatory drugs are reported to have little or no effect on autologous immune complex glomerulonephritis a combination of cyclophosphamide, azathioprine and prednisolone was used in this study. Since in this glomerular disease free-circulating anti-Fx1A [tubular brushborder antigen] antibody has pathogenetic significance special attention was paid to the effect of triple-drug treatment on the anti-Fx1A serum titers and the relation between these titers, deposition of immune aggregates in the glomerular basement membrane and the occurrence of proteinuria. Triple-drug treatment could prevent completely deposition of immune aggregates in the glomeruli as well as development of proteinuria when it was started simultaneously with the immunization procedure. If triple-drug treatment was started at the moment when immune deposits appeared along the glomerular basement membrane, a decrease in serum titers of autologous anti-Fx1A antibody, diminished deposition of immune aggregates along basement membranes and a significant decrease of proteinuria were found. In later stages of the disease when proteinuria was fully developed, no beneficial effect of triple-drug treatment could be demonstrated. The beneficial effect of triple-drug treatment on early stages of autologous immune complex glomerulonephritis is caused by a decrease in the level of free-circulating anti-Fx1A antibody.