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Hepatitis C--associated glomerular disease in liver transplant recipients
C L Davis1, D R Gretch, J D Perkins
1Department of Medicine, University of Washington Medical Center, Seattle 98195, USA.
Insights
Hepatitis C virus (HCV) infection can cause kidney disease after liver transplants. Post-transplant, patients showed worsening kidney function and increased HCV viral load, suggesting a link between HCV recurrence and glomerulonephritis.
Area of Science:
- Nephrology
- Hepatology
- Virology
Background:
- Hepatitis C virus (HCV) infection is linked to extrahepatic manifestations, including renal disease.
- Liver transplantation is a treatment for end-stage liver disease due to HCV.
- The recurrence of HCV post-transplantation can lead to complications.
Observation:
- Three patients developed glomerulonephritis after liver transplantation for HCV.
- Patients experienced decreased renal function, proteinuria, and recurrent hepatitis C liver disease within a year.
- HCV viral load increased post-transplantation, while genotypes remained stable.
Findings:
- All patients had IgM deposits in glomerular capillary walls.
- One patient had cryoglobulinemia; others showed IgM against HCV core antigen with variable specificity.
- Interferon alfa-2b therapy showed a clinical response in one patient without hepatic rejection.
Implications:
- HCV-associated glomerulonephritis can complicate liver transplantation.
- Increased IgM production of variable specificity is associated with post-transplant HCV and kidney disease.
- The post-transplant setting offers a unique model to study HCV-induced renal disease mechanisms.
Abstract:
Hepatitis C virus (HCV) infection may be associated with extrahepatic illness including renal disease. We investigated the clinical and virological characteristics of three patients who developed a mesangial proliferative and sclerosing glomerulopathy alone or in association with membranoproliferative glomerulonephritis after liver transplantation for end-stage liver disease secondary to HCV infection. Using polymerase chain reaction technology and the IgM RIBA assay, viral load, genotype and IgM antibody response to HCV in the setting of glomerulonephritis was evaluated. Within 1 year of transplantation, the patients showed decreased renal function, proteinuria and recurrent hepatitis C liver disease. Likewise, HCV viral load increased following transplantation, whereas the viral genotypes remained unchanged. Although the first patient presented with classic type II cryoglobulinemia in association with glomerulonephritis, the second patient developed an IgM directed specifically against the hepatitis C core antigen. The third patient developed a low-titered IgM directed against the hepatitis C core antigen with rheumatoid factor activity but without cryoglobulinemia. All of the patients show IgM in glomerular capillary walls by biopsy. One patient has shown a clinical response to interferon (IFN) alfa-2b therapy without evidence of hepatic allograft rejection. The second and third patients have not responded to IFN or developed hepatic rejection. This study suggests that HCV-associated glomerulonephritis may complicate liver transplantation in conjunction with the production of increased amounts of IgM of variable specificity. The posttransplant setting may provide a unique situation in which to investigate the specific requirements for the onset of renal disease.