[The immune complex pathogenesis of experimental membranous glomerulopathy (Heymann nephritis) and its significance in human glomerular disease].

Glomerular subepithelial immune deposits are the hallmark of human membranous glomerulopathy, and of its corresponding experimental rat model, Heymann nephritis (HN). The pathogenesis of HN is now understood in some detail, and recent data on this issue are reviewed in this summary. Immune deposits in HN are caused by the interaction of certain epitopes on the nephritogenic antigen, the glycoprotein gp 330, which is a resident molecule of the clathrin coated pits of glomerular visceral epithelial cells, and specific anti-gp 330 IgG. This step is followed within minutes by detachment of the immune complexes and rapid and firm cross-linking to the glomerular basement membrane, thus preventing its endocytosis by the epithelial cells. Immune complexes accumulate locally to form large immune deposits by repeated cycles of antibody binding to newly synthetized gp 330 antigen, shedding and immobilization in the basement membrane. Also human kidneys contain a gp 330-related (but not identical) protein which appears to be not involved in the formation of immune deposits. However, recent data suggest that also in the human disease similar pathogenic mechanisms as in HN could be involved.