Hepatitis B Virus - associated Glomerulonephritis

H B virus (HBV) infection has been shown to induce several extra-hepatic lesions, especially through deposition of immune complexes in different organs (1-5). The exact mechanisms through which certain patients with chronic HBV infection develop glomerulonephritis are not well understood. However, several reports have suggested a role for hepatitis B surface antigen (HBsAg). The diagnosis of HBV-associated glomerulonephritis is done by serologic evaluations for HBV antigens or antibodies, by immunohistochemical demonstration of HBV-related antigens, as well as immune complexes in kidney biopsy (6). The isolation of immune complexes from renal biopsies suggests that this complication may represent a hypersensitivity reaction to the viral infection. HBV-related nephropathy is one of the manifestations of HBV infection of which overwhelming observations have been reported in the literature by authors from all over the world (7-9). The association between chronic HBV infection and glomerular diseases was first described by Combes et al. in 1971 (10), and since then several morphological patterns for glomerular lesions, including membranous nephropathy, minimal change nephropathy, mesangial proliferative glomerulonephritis, membranoproliferative glomerulonephritis, and IgA nephropathy, have been reported (6, 11-36). HBV-associated nephropathy (HBVAN) predominantly occurs in childhood and mainly in males (11, 12, 37-40); the number of reports on adult patients is very limited (2, 31, 41). Moreover, data suggests that compared to adults, the prognosis of HBVAN is more favorable in children (10) and progression to renal failure is rare (2, 38, 40). The aim of this article is to review and classify the literature on various aspects of HBVAN to gather the scientific information together and show the existing gaps in our current knowledge on the topic. Hepatitis Monthly 2009; 9(2): 137-145