2004Chinese Remedies & ClinicsRequires access

Probing into the relationship of serum hepatitis B virus-negative glomerulonephritis with the hepatitis B virus infection

Xiaoqi Zhang

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Abstract

Objective To study the relationship between hepatitis B virus(HBV) infection and glomerulonephritis, to probe into the origin of renal HBV antigens and its with the relation that pathology change, and to make further research of pathologic mechanism of hepatitis B virus associated glomerulonephritis (HBV-GN) . Method HBV antigens (HBsAg, HBcAg) in 101 cases of renal biopsy specimens with various types of glomerulonephritis were examined by immunohistochemical techniques(S-P). There were 96 patients with negative serum HBV, and 5 patients with positive serum HBV in this study. In situ hybridization was used to detect HBV-DNA in 32 cases, which had erough renal tissues and had received the detection of HBV antigens (HBsAg and/or HBcAg) through immunohistochemical method. Electron microscopy examined 5 patients with membranous nephropathy, who all had received the detection of HBV antigens (HBsAg and/or HBcAg), and only 1 case had HBV antigenemia. Results The deposits of HBV marker in the renal tissue of the serun HBV-negative glomerulonephritis were coincident with those in HBV antigenemia. HBV antigens were frequently found in the tubular cells in addition to the appearance of HBV antigens on the glomeruli in certain glomerulonephritis. The positive rate of HBcAg in the tubular cells was 43.6%, higher than that in glomeruli (23.8%). Pathological change degree of the renal tissue in the group with positive HBcAg in their tubular cells was statistically, significantly, more serious than that in the group with negative HBcAg (P0.05=. Renal HBV-DNA was positive in 8 cases among 27 patients with negative serum HBsAg and/or HBcAg, which mainly deposited in cytoplasm of tubular cells. Electron microscopy revealed that serum HBV-negative MGN (membranous glomerulonephritis) showed a diffuse-thichened glomerular basement membrane (GBM) some electro-dense material deposited in subepithelium, and a fusion occurred in epithelial podocytes; while serum HBV-positive MGN showed an uneven-thickened GBM, and a deposition of small, sporadic electro-dense material (with high density) in the basilemma. Conclusion The results suggested that the HBV infection in serum is not identical with that in renal tissue of certain cases of glomerulonephritis (MGN, MPGN, MsPGN, IgAN ) ; HBV antigen-antibody immunocomplex deposited in renal tissue may develop in situ, aside from originating from the circulation; HBcAg deposition in renal tubules may be related to the severity of nephritides above-mentioned and their pathological changes.

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Objective To study the relationship between hepatitis B virus(HBV) infection and glomerulonephritis, to probe into the origin of renal HBV antigens and its with the relation that pathology change, and to make further research of pathologic mechanism of hepatitis B virus associated glomerulonephritis (HBV-GN) . Method HBV antigens (HBsAg, HBcAg) in 101 cases of renal biopsy specimens with various types of glomerulonephritis were examined by immunohistochemical techniques(S-P). There were 96 patients with negative serum HBV, and 5 patients with positive serum HBV in this study. In situ hybridization was used to detect HBV-DNA in 32 cases, which had erough renal tissues and had received the detection of HBV antigens (HBsAg and/or HBcAg) through immunohistochemical method. Electron microscopy examined 5 patients with membranous nephropathy, who all had received the detection of HBV antigens (HBsAg and/or HBcAg), and only 1 case had HBV antigenemia. Results The deposits of HBV marker in the renal tissue of the serun HBV-negative glomerulonephritis were coincident with those in HBV antigenemia. HBV antigens were frequently found in the tubular cells in addition to the appearance of HBV antigens on the glomeruli in certain glomerulonephritis. The positive rate of HBcAg in the tubular cells was 43.6%, higher than that in glomeruli (23.8%). Pathological change degree of the renal tissue in the group with positive HBcAg in their tubular cells was statistically, significantly, more serious than that in the group with negative HBcAg (P0.05=. Renal HBV-DNA was positive in 8 cases among 27 patients with negative serum HBsAg and/or HBcAg, which mainly deposited in cytoplasm of tubular cells. Electron microscopy revealed that serum HBV-negative MGN (membranous glomerulonephritis) showed a diffuse-thichened glomerular basement membrane (GBM) some electro-dense material deposited in subepithelium, and a fusion occurred in epithelial podocytes; while serum HBV-positive MGN showed an uneven-thickened GBM, and a deposition of small, sporadic electro-dense material (with high density) in the basilemma. Conclusion The results suggested that the HBV infection in serum is not identical with that in renal tissue of certain cases of glomerulonephritis (MGN, MPGN, MsPGN, IgAN ) ; HBV antigen-antibody immunocomplex deposited in renal tissue may develop in situ, aside from originating from the circulation; HBcAg deposition in renal tubules may be related to the severity of nephritides above-mentioned and their pathological changes.

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Available abstract

Objective To study the relationship between hepatitis B virus(HBV) infection and glomerulonephritis, to probe into the origin of renal HBV antigens and its with the relation that pathology change, and to make further research of pathologic mechanism of hepatitis B virus associated glomerulonephritis (HBV-GN) . Method HBV antigens (HBsAg, HBcAg) in 101 cases of renal biopsy specimens with various types of glomerulonephritis were examined by immunohistochemical techniques(S-P). There were 96 patients with negative serum HBV, and 5 patients with positive serum HBV in this study. In situ hybridization was used to detect HBV-DNA in 32 cases, which had erough renal tissues and had received the detection of HBV antigens (HBsAg and/or HBcAg) through immunohistochemical method. Electron microscopy examined 5 patients with membranous nephropathy, who all had received the detection of HBV antigens (HBsAg and/or HBcAg), and only 1 case had HBV antigenemia. Results The deposits of HBV marker in the renal tissue of the serun HBV-negative glomerulonephritis were coincident with those in HBV antigenemia. HBV antigens were frequently found in the tubular cells in addition to the appearance of HBV antigens on the glomeruli in certain glomerulonephritis. The positive rate of HBcAg in the tubular cells was 43.6%, higher than that in glomeruli (23.8%). Pathological change degree of the renal tissue in the group with positive HBcAg in their tubular cells was statistically, significantly, more serious than that in the group with negative HBcAg (P0.05=. Renal HBV-DNA was positive in 8 cases among 27 patients with negative serum HBsAg and/or HBcAg, which mainly deposited in cytoplasm of tubular cells. Electron microscopy revealed that serum HBV-negative MGN (membranous glomerulonephritis) showed a diffuse-thichened glomerular basement membrane (GBM) some electro-dense material deposited in subepithelium, and a fusion occurred in epithelial podocytes; while serum HBV-positive MGN showed an uneven-thickened GBM, and a deposition of small, sporadic electro-dense material (with high density) in the basilemma. Conclusion The results suggested that the HBV infection in serum is not identical with that in renal tissue of certain cases of glomerulonephritis (MGN, MPGN, MsPGN, IgAN ) ; HBV antigen-antibody immunocomplex deposited in renal tissue may develop in situ, aside from originating from the circulation; HBcAg deposition in renal tubules may be related to the severity of nephritides above-mentioned and their pathological changes.

Key concepts: HBcAg, HBsAg, Hepatitis B virus, Glomerulonephritis, Medicine, Antigen, Hepatitis B, Hepatitis

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