Abstract
AbstractMembranous nephropathy (MN) is an important glomerular disease characterized by podocyte injury and protein‐uria. The understanding of cellular and molecular mechanisms involved in the pathogenesis of MN has come from studies in the Heymann nephritis model of MN in the rat. MN involves the in situ formation of subepithelial immune deposits of antibodies reactive to podocyte antigens, activation of complement, and assembly of C5b‐9 on podo‐cyte plasma membranes. The podocyte responds to C5b‐9 attack by activating protein kinases, phospholipases, oxidants, transcription factors, growth factors, stress pathways, proteinases, and other mediators. These signals impact on metabolic pathways, structure/function of lipids, proteins in the cytoskeleton and slit diaphragm, and turnover of extracellular matrix components. Some effects of C5b‐9 affect podocyte functions adversely, while other effects may limit injury or promote recovery. Increased understanding of pathogenic antigens, complement activation, and changes in podocyte biology induced by C5b‐9 is an opportunity for new diagnostic and concept‐driven therapeutic approaches to this disease.
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