Serum and tissue positivity for hepatitis B virus markers in histopathologically proven glomerulonephropathies

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 less than 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 in situ; 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 less than 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.