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      Role of Ribavirin in Membranoproliferative Glomerulonephritis Associated with Hepatitis C Virus Infection Refractory to Alpha-Interferon

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          Chronic hepatitis C virus (HCV) has been associated with several extrahepatic diseases, such as membranoproliferative glomerulonephritis (MPGN). α-Interferon is currently the treatment of choice for this association. When this therapy fails clinicians face a difficult challenge due to the lack of useful information in these particularly difficult patients. We report the case of a severe nephrotic syndrome due to MPGN associated HCV infection, in which a triple association – interferon plus ribavirin and cyclophosphamide – was needed to control the disease.

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          Membranoproliferative glomerulonephritis associated with hepatitis C virus infection.

          Hepatitis C virus (HCV) infection causes both acute and chronic liver disease and is also associated with mixed cryoglobulinemia. Whether HCV is also associated with renal disease, as is the hepatitis B virus, is not known. We describe the clinical, pathologic, virologic, and immunologic features of eight patients with HCV infection who were referred to nephrologists for glomerulonephritis. Four patients were treated with interferon alfa. All eight patients had proteinuria, and seven had decreased renal function. Renal biopsy in all patients revealed membranoproliferative glomerulonephritis, characterized by the deposition of IgG, IgM, and C3 in glomeruli. Electron microscopy of the biopsy specimens showed cryoglobulin-like structures in three of four patients. All eight patients had HCV RNA detected in their serum, elevated serum aminotransferase concentrations, and hypocomplementemia, and the majority had cryoglobulins and circulating immune complexes in their serum. Cryoprecipitates from the three patients who were tested contained HCV RNA and IgG anti-HCV antibodies to the nucleocapsid core antigen (HCVc or c22-3). IgM rheumatoid factors, present in all patients, bound anti-HCV IgG in all six patients tested. Four patients received interferon alfa for 2 to 12 months; all had evidence of decreased HCV replication and improvement of their renal and liver disease. Chronic HCV infection is associated with cryoglobulinemia and membranoproliferative glomerulonephritis. The pathogenesis is unknown, but may relate to deposition within glomeruli of immune complexes containing HCV, anti-HCV IgG, and IgM rheumatoid factors.
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            Effects of ribavirin on hepatitis C-associated nephrotic syndrome in four liver transplant recipients.

            Hepatitis C virus infection (HCV) is associated with a variety of extrahepatic disorders such as membranoproliferative glomerulonephritis (MPGN), which is generally due to cryoglobulinemia. After liver transplantation for HCV cirrhosis, alpha-interferon treatment against the recurrence of HCV in the liver graft is poorly effective and may induce intractable graft rejection. We describe the cases of four liver transplant recipients treated with ribavirin for HCV-related glomerulopathy and nephrotic syndrome. The nephrotic syndrome was attenuated or disappeared during ribavirin therapy, and patients showed a marked decrease in proteinuria and an increase in albuminemia. The syndrome relapsed in two patients when ribavirin therapy was stopped, and a favorable response was again obtained in both cases when the treatment was resumed. The main adverse effect of ribavirin was anemia in two patients with renal impairment. No graft rejection occurred. These findings suggest that continuous therapy with low doses of oral ribavirin may improve the proteinuria of hepatitis C-related glomerulonephritis, at least in liver transplant recipients.
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              Appearance of Nephrotic Syndrome following Interferon-α Therapy in a Patient with Hepatitis B Virus and Hepatitis C Virus Coinfection

              A 59-year-old woman with hepatitis B surface antigen (HBsAg) and hepatitis C viral (HCV) antibody presented with proteinuria and hematuria. The patient was treated with interferon-alpha (INF-α) because plasma aminotransferase levels had been elevated and a liver biopsy had showed chronic active hepatitis. Her urinary protein excretion decreased as liver function normalized and her serum HCV-RNA was negative during treatment. Eleven weeks after completion of INF-α treatment, she suddenly presented with nephrotic-range proteinuria, although an improvement in the hepatic function was maintained. Renal pathologic findings were consistent with membranous glomerulonephritis (MGN), and HBsAg was detected in the glomeruli but not HCV. After treatment with prednisolone, her 24-hour protein excretion was below 0.7 g/day. To our knowledge this is the first report on hepatitis B virus MGN with nephrotic syndrome following IFN-α therapy for HCV. This suggests that treatment with INF-α might affect the immune processes and may be associated with the pathogenic mechanism in this patient.

                Author and article information

                S. Karger AG
                October 2002
                02 September 2002
                : 92
                : 2
                : 459-462
                Departments of aInternal Medicine, bImmunology and cPathology, Hospital Clínico Universitario ‘Lozano Blesa’, Zaragoza; dDepartment of Nephrology, Hospital Clinic, Barcelona, Spain
                63289 Nephron 2002;92:459–462
                © 2002 S. Karger AG, Basel

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