The Pathogenesis of Autologous Immune Complex Glomerulonephritis in Rats

Abstract

Over 11 years has elapsed since the term autologous immune complex nephritis (AICN) was initially proposed to describe the pathogenetic mechanisms operative in an experimental membranous glomerulopathy induced in rats by active immunization with renal tubular epithelial (RTE) antigens in Freund’s complete adjuvant. In this experimental model, which was originally described by Heymann and co-workers (Heymann et al., 1959), it was envisaged that circulating immune complexes (CIC) composed of autoantibodies to a specific proximal RTE antigen (designated RTE α₅) and autologous RTE α₅ deposited continuously in the glomerular capillaries (Edgington et al., 1967a). These CIC ultimately localized in the subepithelial space and provoked the typical morphologic and clinical features of membranous glomerulopathy including granular deposits of immunoglobulin and subepithelial electron-dense deposits in glomeruli (Glassock et al., 1968). Since then, a number of additional autologous antigen-antibody systems capable of evoking glomerular injury have been described in both animals and man (Naruse et al., 1973; Couser et al., 1974; O’Regan et al., 1976).