Figure 925

The mechanisms of renal complications induced by hepatitis C virus (HCV) infection, with or without associated mixed cryoglobulinemia, according to our hypothesis. As illustrated, the prevalent pathogenetic mechanism is the deposition in the glomerulus of a monoclonal IgM rheumatoid factor (RF) with particular affinity for the glomerular matrix, which is produced by permanent clones of B lymphocytes infected by HCV. It is unknown whether the IgM RF deposits in the glomerulus alone, with subsequent in situ binding of IgG (perhaps bound already to viral antigens, or as a complex composed of HCV antigens, IgG anti-HCV antibodies, and IgMk RF). Only recently have specific HCV-related proteins been detected in glomerular structures using indirect immunochemistry. As depicted on the left, it is possible that in a minority of cases immune complexes composed of HCV antigens and anti-HCV IgG antibodies can deposit directly in the glomerular structures, in the absence of a concomitant type II MC with a monoclonal IgM RF. This deposition induces an immune-complex glomerulonephritis similar to that described in patients infected with the hepatitis B virus. (Adapted from D'Amico [21].)

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