To assess the pathogenic significance of hepatitis B virus (HBV) in glomerulonephritis (GN), 98 patients with histopathologically proven glomerulonephropathies were screened for HBV markers, complement components and levels of circulating immune complexes (CICs); and renal biopsies from 31 of them were examined for the presence of hepatitis B surface antigen (HBsAg), and its location, by immunoperoxidase staining. The HBsAg positive rate in the patients (who came from a population with 10% HBsAg positivity) ranged from 51.9% in minimum change nephrotic syndrome (MCNS) to 81.8% in patients with proliferative glomerulonephritis (PGN). Whereas 24.5% of the cases were positive for HBsAg only, 10.2% had anti-HBcIgM with HBsAg, 13.3% had HBeAg with HBsAg and 9.2% had HBsAg, HBeAg and anti-HBcIgM. Complement component C3 levels were decreased in all groups of GN studied, but C4 levels varied. CIC levels were significantly increased (p < 0.01) only in HBsAg-positive MCNS, focal glomerulosclerosis (FGS) and membranous glomerulonephritis (MGN). Of the 31 renal biopsies examined for the deposition of HBsAg, 4 (12.9%) were found to be positive for HBsAg ; 64.5% of biopsied patients were seropositive for HBsAg and 77.4% had CICs. All the four in-situ HBsAg-positive cases were seropositive for HBsAg, HBeAg and anti-HBcIgM with significantly high CIC levels (p<0.01). HBsAg deposition was intracytoplasmic in the mesangial cells of the glomeruli, in the glomerular basement membrane or in the tubules, or in a combination of these sites.


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