Role of hepatitis B virus infection in pathogenesis of IgA nephropathy.

Aim: To investigate the role of hepatitis B virus (HBV) in the pathogenesis of IgA nephropathy (IgAN).

Methods: HBV antigens (HBAg, or HBsAg, HBcAg, and HBeAg) in renal tissues with IgAN were detected by immunohistochemical technique. The distribution and localization of HBV DNA were observed by using in situ hybridization. Southern blot analysis was performed to reveal the state of renal HBV DNA.

Results: Among 100 patients with IgAN, HBs antigenemia was detected in 18 patients (18.00 %). HBAg in renal tissues was detected in 31 patients (31.00 %), the positive rate of HBAg, HBsAg and HBcAg was 64.52 % (20/31), 32.26 % (10/31), 32.26 % (10/31), respectively in glomeruli. HBcAg was also found in tubular epithelia and interstitia, which was 45.16 % (14/31) and 6.45 % (2/31), respectively. Five out of six cases with positive HBV DNA by in situ hybridization were proved to be HBV DNA positive by Southern blot analysis, and all were of the integrated form. Eight specimens were demonstrated to be HBV DNA positive by in situ hybridization, which was localized in the nuclei of tubular epithelial cells and glomerular mesangial cells as well as in infiltrated interstitial lymphocytes.

Conclusion: There is a relationship between HBV infection and IgAN. In addition to the humoral immune damage mediated by HBAg-HBAb immune complex, the cellular mechanism mediated by HBV originating from renal cells in situ may be also involved in the pathogenesis of IgAN.