[Hepatitis B virus infection and pathogenesis of glomerulonephritis]

In order to investigate the role of hepatitis B virus (HBV) infection in the pathogenesis of HBV associated glomerulonephritis, 50 cases of glomerulonephritis with positive HBV infection marker antigenemia and/or HBAg detected by immunohistochemistry in renal tissue were collected. The distribution and localization of HBV DNA were observed by using in situ hybridization. In addition, Southern blot analysis was performed in 23 of the 50 cases to reveal the state of renal HBV DNA. Thirty Six cases (72%) were found to be HBV DNA positive by in situ hybridization, which was localized in the nucleus of tubular cells. In 26 cases HBV DNA was simultaneously detected in the nucleus of glomerular mesangial and epithelial cells as well as in the mesangial matrix. Seventeen of the 23 cases proved to be HBV DNA positive by Southern blot analysis. In which 3 cases were identified as having non-replicating free HBV DNA, while 14 cases (82%) were of the integrated form. Since there was abundant evidence of the renal tissue being infected with HBV, it was considered that the HBAg deposited on glomeruli not only originated from circulation but also from the HBV infected glomerular cells. In addition to the humoral immune injury mediated by HBAg-HBAb immune complex, the cellular mechanism mediated by target antigen (HBcAg) may be also involved in the pathogenesis of HBV associated glomerulonephritis.