Treatment of Hepatitis C Virus Infection (HCV) After Renal Transplantation: Implications for HCV-Positive Dialysis Patients Awaiting a Kidney Transplant

Multiorgan Transplant Unit, CHU Rangueil, Toulouse, France.
Transplantation (Impact Factor: 3.83). 11/2006; 82(7):853-6. DOI: 10.1097/
Source: PubMed


Patient survival is significantly lower in hepatitis C virus (HCV)-positive compared to HCV-negative dialysis patients. After renal transplantation, immunosuppressive therapy can result in an increased burden of HCV viremia. Both patient and graft survivals are lower in HCV-positive compared to matched HCV-negative renal-transplant patients. Therefore, it is important to treat HCV infection. At present, after renal transplantation, there is no current safe and efficient therapy. Alpha-interferon (alpha-IFN) does not give a sustained virological response, and is associated with a high rate of renal failure. Ribavirin and amantadine monotherapies are associated with a significant improvement in liver enzymes, but have no impact upon HCV viremia. Ribavirin, however, may be indicated in cases of HCV-related glomerulopathy because it can significantly decrease proteinuria. The combined use of alpha-IFN and ribavirin should only be given to those patients who have developed posttransplant fibrosing cholestatic hepatitis. Therefore, HCV infection needs to be treated pretransplant. In dialysis patients, the only recommended therapy, as yet, is alpha-IFN monotherapy. Pegylated alpha-IFN is under evaluation and ribavirin is contraindicated because it results in severe hemolytic anemia. Twelve months of alpha-IFN therapy results in sustained virological clearance in approximately 40% of patients, regardless of their genotype. HCV RNA, after three months of alpha-IFN therapy, is a predictive factor for a long-term sustained response. Finally, when HCV-positive dialysis patients with a sustained virological response undergo successful renal transplantation, very few suffer a virological relapse, thus emphasizing that these patients were cured.

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    • "It leads to higher mortality in maintenance hemodialysis patients compared to noninfected patients and reduces the survival rates of patients undergoing kidney transplantation as well as their grafts [2]. It renders patients with a higher risk of developing diabetes mellitus, de novo or recurrent membranoproliferative glomerulonephritis, lymphoproliferative disorders, and fibrosing cholestatic hepatitis after kidney transplantation [3]. "
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    ABSTRACT: Background. There are few data on the combination of (pegylated-) interferon- (Peg-IFN-) α, ribavirin, and first-generation direct-acting antiviral agents (DAAs). Our aim was to describe the efficacy and safety of Peg-IFN-α, ribavirin, and boceprevir in hemodialysis patients. Patients. Six hemodialysis patients, chronically infected by genotype-1 HCV, were given Peg-IFN-α (135 µg/week), ribavirin (200 mg/d), and boceprevir (2400 mg/d) for 48 weeks. Results. At initiation of antiviral therapy, median viral concentration was 5.68 (3.78-6.55) log IU/mL. HCV RNA was undetectable in four of the six patients at week 4 and in all patients at week 24. A breakthrough was observed in two patients between weeks 24 and 48, and a third patient stopped antiviral therapy between weeks 24 and 48 because of severe peripheral neuropathy. At week 48, HCV RNA was undetectable in three patients. Of these, two patients relapsed within a month after antiviral therapy was stopped. Hence, only one patient had a sustained virological response; he was a previous partial responder. Overall, anemia was the main side effect. Conclusion. A triple antiviral therapy based on Peg-IFN-α, ribavirin, and boceprevir is not optimal at treating hemodialysis patients with chronic HCV infection. Studies using new-generation drugs are required in this setting.
    Journal of Transplantation 08/2015; 2015(109):159795. DOI:10.1155/2015/159795
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    • "Pageaux et al. [132] showed that treatment of HCV with IFN after transplantation might not be as risky as initially shown. Posttransplant monotherapies with ribavirin and/or amantadine have no apparent impact on HCV viremia or liver histology [133]. So the best strategy is to treat HCV infection in patients on dialysis before transplantation after excluding cirrhosis by liver biopsy and if present patients should be considered for combined kidney-liver transplantation [128, 132, 133]. "
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    ABSTRACT: Viruses are among the most common causes of opportunistic infection after transplantation. The risk for viral infection is a function of the specific virus encountered, the intensity of immune suppression used to prevent graft rejection, and other host factors governing susceptibility. Although cytomegalovirus is the most common opportunistic pathogen seen in transplant recipients, numerous other viruses have also affected outcomes. In some cases, preventive measures such as pretransplant screening, prophylactic antiviral therapy, or posttransplant viral monitoring may limit the impact of these infections. Recent advances in laboratory monitoring and antiviral therapy have improved outcomes. Studies of viral latency, reactivation, and the cellular effects of viral infection will provide clues for future strategies in prevention and treatment of viral infections. This paper will summarize the major viral infections seen following transplant and discuss strategies for prevention and management of these potential pathogens.
    The Scientific World Journal 05/2012; 2012:820621. DOI:10.1100/2012/820621 · 1.73 Impact Factor
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    • "Although there are no published data on the outcome of lung transplant in HCV-positive recipients, one small series has shown that selected lung transplant candidates can safely and effectively be treated for HCV prior to transplant(Doucette, Weinkauf et al. 2007). Posttransplant: Generally, posttransplantation IFN therapy is contraindicated in recipients of SOT, other than liver allografts due to a high risk of precipitation of organ rejection from IFN therapy(Shu, Lan et al. 2004; Kamar, Ribes et al. 2006). There is well-documented evidence to support the theory that the liver allograft provides some level of immunologic protection to the kidney allograft(Calne, Davis et al. 1971; Rasmussen, Davies et al. 1995). "

    Viral Hepatitis - Selected Issues of Pathogenesis and Diagnostics, 11/2011; , ISBN: 978-953-307-760-4
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