THE PATHOGENETIC ROLE OF FREE-CIRCULATING ANTIBODY IN AUTOLOGOUS IMMUNE-COMPLEX GLOMERULONEPHRITIS

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  • 1 January 1980
    • journal article
    • research article
    • Vol. 41  (2) , 205-217
Abstract
Autologous immune complex glomerulonephritis is an established model of chrodnic glomerulonephritis which very closely resembles membranous glomerulopathy in man. The disease can be induced in certain rat strains by immunization with tubular brush-border antigen (Fx1A) in Freund''s complete adjuvant. This procedure is believed to result in circulating immune complexes consisting of anti-Fx1A antibody and Fx1A antigen, which are deposited along the glomerular basement membrane. Since previous studies indicated the presence of Fx1A antigen in the glomerular basement membrane of normal rats and suggested an in situ formation of immune aggregates at this site as the pathogenetic mechanism in heterologous immune complex glomerulonephritis, the validity of the same mechanism in the pathogenesis of autologous immune complex glomerulonephritis was studied. An association was found between the serum titer of autologous anti-Fx1A antibody and the presence of immune aggregates in the glomerular basement membrane. Unilateral perfusion of normal rat kidneys with IgG eluted from kidneys of rats with autologous immune complex glomerulonephritis resulted in a binding of autologous anti-Fx1A antibody at the subepithelial side of the glomerular basement membrane. A pathogenetic role for circulating anti-Fx1A antibody is indicated. Rat anti-Fx1A antibody is able to bind to Fx1A antigens present in the glomerular basement membrane. Although a possible role for circulating immune complexes is not excluded, a pathogenetic mechanism of in situ formation of subepithelial immune aggregates in autologous immune complex glomerulonephritis is strongly suggested.