Treatment of hepatitis C virus infection after kidney transplantation.
The prevalence of chronic hepatitis C virus (HCV) infection after kidney transplantation (KT) varies a lot from one country to another. In the setting of (powerful) immunosuppression, HCV replication can sharply increase, thereby leading to potential severe HCV-related liver damage such cirrhosis or fibrosing cholestatic hepatitis. In the setting of KT, α-interferon (α-IFN) therapy alone has been associated with a very low sustained virological response (SVR), and a poor tolerance, particularly with regard to the kidney allograft, i.e. it induces acute rejection. The combined use of α-IFN plus ribavirin leads to a greater rate of SVR, but randomized clinical trials are missing in order to evaluate its safety with respect to the allograft function. Ribavirin monotherapy, or ribavirin plus amantadine therapy are not able to induce SVR; ribavirin may have an effect upon HCV-related proteinuria. Finally, it seems advisable to try and eradicate HCV infection prior to KT, i.e. while the patient is on dialysis therapy. After KT, α-IFN plus ribavirin therapy could be attempted only in those patients developing rapid cirrhosis or in those developing fibrosing cholestatic hepatitis or in those having de novo cryoglobulinemic glomerulonephritis within the allograft.
Lionel
L
Rostaing
Hugo
H
Weclawiak
Jacques
J
Izopet
Nassim
N
Kamar
D000998:Antiviral Agents / Q000627:therapeutic use*; D004359:Drug Therapy, Combination; D006526:Hepatitis C / Q000188:drug therapy*; D006801:Humans; D007165:Immunosuppression Therapy / Q000009:adverse effects; D016898:Interferon-alpha / Q000627:therapeutic use*; D016030:Kidney Transplantation; D012254:Ribavirin / Q000627:therapeutic use*
D000998:Antiviral Agents; D016898:Interferon-alpha; D012254:Ribavirin