血清乙型肝炎病毒阴性肾小球肾炎与乙型肝炎病毒感染关系的探讨

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

目的了解乙型肝炎病毒(HBV)感染与肾小球肾炎的相关性,探讨肾组织中HBV抗原的来源及其与病理变化的关系,以有助于进一步研究HBV相关性肾炎的发病机制。方法应用免疫组织化学(SP)法检测96例血清HBV感染标志阴性,5例血清HBV感染标志阳性肾炎肾组织中的HBV抗原[HBV表面抗原(HBsAg)、HBV核心抗原(HBcAg)],用原位杂交方法检测32例肾炎组织HBV抗原阳性的(包括5例血清HBV感染标志阳性者)中的HBV-DNA。5例肾组织中检出HBV抗原的膜性肾病(其中1例血清HBV感染标志阳性)作透射电镜观察。结果发现血清HBV感染标志阴性肾炎肾组织中HBV标志物沉积与在血清HBV标志阳性肾炎中一致:HBV抗原除在肾小球沉积外,肾小管常有阳性表达,并且肾小管HBcAg阳性率高于其在肾小球中的表达(43.6%vs23.8%)。肾小管HBcAg阳性组的肾组织病变程度明显严重于肾小管HBcAg阴性组,且差异有显著性(P<0.05)。27例血清学阴性肾炎中8例肾组织中HBV-DNA阳性,主要沉积于肾小管上皮细胞质。电镜观察显示,血清HBV标志阴性膜性肾病表现为基底膜弥漫增厚,电子致密物在上皮下沉积及上皮足状突细胞融合;血清HBV标志阳性膜性肾病表现为基底膜不均匀增厚,基膜内小而散在的高密度电子致密物沉积。结论血清HBV感染与肾炎[膜性肾小球肾炎(MGN)、膜增生性肾小球肾?

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 (P<0.05=. 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.