[Molecular pathogenesis of experimental membraneous glomerulonephritis (Heymann nephritis)]

The analysis and reassembly of the single steps in the pathogenesis of Heymann nephritis is reasonable well advanced, but still far from being comprehensive. It is established that antibodies against certain epitopes of the megalin/gp330 molecule or RAP are responsible for the formation of glomerular immune deposits. Apparently a second antibody antigen system targeting lipid antigens causes the activation of C5b-9, which triggers the biosynthesis of oxygen-radical-producing enzymes within glomerular epithelial cells. The oxygen radicals cause lipid peroxidation which, by virtue of its toxic products, causes cross-linking of type IV collagen via its NC1 domains. It is possible that this is associated with a distortion and increase of permeability of the glomerular basement membrane, thus causing proteinuria.