PRIMARY GLOMERULONEPHRITIS WITH DETECTABLE GLOMERULAR HEPATITIS-B VIRUS-ANTIGENS

Citation
Fmm. Lai et al., PRIMARY GLOMERULONEPHRITIS WITH DETECTABLE GLOMERULAR HEPATITIS-B VIRUS-ANTIGENS, The American journal of surgical pathology, 18(2), 1994, pp. 175-186
Citations number
33
Categorie Soggetti
Pathology,Surgery
ISSN journal
01475185
Volume
18
Issue
2
Year of publication
1994
Pages
175 - 186
Database
ISI
SICI code
0147-5185(1994)18:2<175:PGWDGH>2.0.ZU;2-P
Abstract
The glomerular pathology and hepatitis B virus (HBV) antigens in renal biopsies were investigated in 100 consecutive patients with both prim ary glomerulonephritis and positive serology for hepatitis B surface a ntigen (HBsAg). Glomerular HBV antigens including HBsAg, hepatitis B c ore antigen (HBcAg), and hepatitis B e antigen (HBeAg) were examined i n frozen tissue using both polyclonal and monoclonal antibodies. HBV s erology and glomerular antigens were correlated. Using monoclonal anti bodies, at least one of the three HBV antigens was detectable in glome ruli in 39% of the cases. These findings correspond mainly to detectab le glomerular HBsAg and HBeAg in 22.3 and 28.4% of cases, respectively . A good correlation was found between glomerular and serum HBeAg but not observed for HBsAg. Serum HBcAg was not examined and not correlate d with glomerular staining. When the diagnosis of HBV-related glomerul onephritis was based strictly on detectable glomerular antigens, three distinctive morphologies were identified: membranous nephropathy, mes angiocapillary glomerulonephritis, and mesangial proliferative glomeru lonephritis with immunoglobulin A (IgA) deposits (IgA nephropathy). Ea ch of these lesions may be seen in pure form or occasionally in overla pping form leading to double glomerulopathies. Glomerular HBeAg and HB sAg were associated with subepithelial and mesangial immune complexes, respectively. Rare overlap between membranous nephropathy and IgA nep hropathy further emphasized the distinctive pathology of HBV-related g lomerulonephritis and the independent etiological role of HBeAg and HB sAg. In other glomerulonephritis, which rarely demonstrated glomerular HBV antigens, the pathogenetic role of chronic HBV infection remains to be proven.