Detection of the hepatitis C virus antigen in kidney tissue from infected patients with various glomerulonephritis

Several studies have postulated a causal link between hepatitis C virus (HCV) infection and renal diseases through the induction of cryoglobulinaemia. However, the detection of viral antigens within kidneys of HCV-infected patients has proved to be difficult. We studied a cohort of Chinese HCV-infected patients with various glomerulonephritis (GN) in an attempt to detect HCV antigens within their kidneys.

Twenty-one patients with various GN were found to be serum HCV-antibody positive (seven serum HCV-RNA positive simultaneously), at the time of renal biopsy, from January 2005 to April 2008 in our hospital. A murine monoclonal antibody against the HCV-NS3 protein was employed to detect the HCV antigen using immunohistochemistry and immunogold labelling. Their clinical and pathological data were collected and further analysed.

The HCV-NS3 antigen was detected in six (6/21, 28.6%) HCV-antibody-positive patients by immunohistochemistry and four out of the six were serum HCV-RNA positive (4/7 in HCV-RNA positive, 57.1%). The HCV antigen mainly displayed a linear or granular deposition along glomerular capillary walls and/or mesangial region. Immunoelectron microscopy showed that the labelling of HCV-NS3 was localized mainly in electronic dense deposits. In the HCV-NS3 detectable patients, three patients were with membranoproliferative glomerulonephritis (MPGN), one with membranous nephropathy, one with IgA nephropathy and one with amyloid nephropathy. The age and urinary protein were significantly greater in HCV-NS3-positive patients than those in HCV-NS3 negative, while serum C3 level was significantly lower in the former group. No significant difference was found in serum ALT, albumin and creatinine level between the two groups.

HCV-NS3 antigens could be detected in kidney tissue of HCV-infected patients with various GN, but mainly in those with MPGN and HCV-RNA positive. HCV itself might be involved directly in the pathogenesis of HCV-associated GN.