Membranoproliferative glomerulonephritis (MPGN), also known as mesangiocapillary glomerulonephritis, is a pattern of glomerular injury that results from deposition of immune complexes and/or complement in the mesangium and along the glomerular capillary walls. Recently, a classification that emphasizes the pathogenesis of MPGN has been proposed. According to this new classification, MPGN can be divided into immune complex-mediated (Ig) or complement-mediated MPGN. The common causes of Ig-mediated MPGN include chronic infections, autoimmune diseases, and monoclonal gammopathy/dysproteinemias. MPGN that is Ig mediated should lead to work up for infections, autoimmune diseases, and monoclonal gammopathy. Complement-mediated MPGN includes dense deposit disease and proliferative glomerulonephritis with C3 deposits (GN-C3). Dysregulation of the alternate pathway of complement (AP) can result from genetic mutations or development of autoantibodies to complement-regulating proteins with ensuing dense deposit disease or C3 glomerulonephritis. Complement-mediated MPGN should lead to work of the AP of complement. Initial AP screening tests should include serum membrane attack complex (sMAC) levels, AP functional assay, and hemolytic assay, followed by tests for mutations and autoantibodies to complement-regulating proteins. The absence of randomized control studies together with our current knowledge regarding the multiple pathogenic processes highlights the problems for making treatment decisions in this patient population. Evaluation of MPGN according to the underlying pathophysiologic process will help us to evaluate new ways for optimizing the treatment of MPGN based on the etiological process.
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