Figure 71

Renal disease associated with hepatitis B. Infection with hepatitis B virus (HBV) may be associated with a variety of renal diseases [1,2]. Many patients are asymptomatic, with plasma serology positive for hepatitis B surface antigen (HBsAg), hepatitis B core antibody (HBcAb), and hepatitis B antigen (HBeAg). The pathogenetic role of HBV in these processes has been documented primarily by demonstration of hepatitis B antigen-antibody complexes in the renal lesions [1,3,4]. Three major forms of renal disease have been described in HBV infection. In membranous nephropathy, it is proposed that deposition of HBeAg and anti-HBe antibody forms the classic subepithelial immune deposits [1,3-5]. Polyarteritis nodosa is a medium-sized vessel vasculitis in which antibody-antigen complexes may be deposited in vessel walls [1,2]. Finally, membranoproliferative glomerulonephritis is characterized by deposits of circulating antigen-antibody complexes in which both HBsAg and HBeAg have been implicated [3].

recent studies have noted one or more of the following features in over 95% of patients with this disorder: circulating anti-HCV antibodies; polyclonal immunoglobulin G anti-HCV antibodies within the cryoprecipitate; and HCV RNA in the plasma and cryoprecipi-tate [6,7]. Furthermore, evidence exists suggesting direct involvement of HCV-containing immune complexes in the pathogenesis of this renal disease [6]. Sansono and colleagues [12] demonstrated HCV-related proteins in the kidneys of eight of 12 patients with cryoglobulinemia and membranoproliferative glomerulonephritis (MPGN) by indirect immunohistochemistry. Convincing clinical data exist suggesting that HCV is responsible for some cases of MPGN and possibly membranous nephropathy [13-15]. In one report of eight patients with MPGN, purpura and arthralgias were uncommon and cryoglobulinemia was absent in three patients [13]. Circulating anti-HCV antibody and HCV RNA along with elevated transaminases provided strong evidence of an association with HCV infection. Establishing the diagnosis of HCV infection in these diseases is important because of the potential therapeutic benefit of a-interferon treatment [13]. A number of reports exist that demonstrate a beneficial response to chronic antiviral therapy with a-interferon [6,13,16,17]. Even more compelling evidence for a beneficial effect of a-interferon in HCV-induced mixed cryoglob-ulinemia was demonstrated in a randomized prospective trial of 53 patients given either conventional therapy alone or in combination with a-interferon [18]. Because of the likely recurrence of viremia and cryoglobulinemia with cessation of a-interferon therapy after conventional treatment (3 X 106 U three times weekly for 6 mo), extended courses of therapy (up to 18 mo) and higher dosing regimens are being studied [19-21].

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