In the general population, the Hepatitis C virus (HCV) infection is a leading public health problem worldwide; in patients on long-term hemodialysis the prognosis of HCV-infected patients is significantly worse than in patients without HCV infection; in renal transplant recipients this infection is responsible for both hepatic (mainly hepatocellular carcinoma and chronic hepatitis) and extra-hepatic complications (transplant glomerulopathy, HCV-related glomerular disease, acute rejection, new onset diabetes after transplant, cardiovascular disease, infections).1 HCV-positive patients with kidney transplant have increased risk of graft loss, increased morbidity and mortality rate compared to HCV-negative recipients. The interferon and ribavirin treatment for HCV infection in kidney transplant recipients is limited, because of the risk for allograft rejection and poor tolerability. In 2011 the U.S. Food and Drug Administration approved the introduction of direct-acting antiviral agents (DAAs) for the treatment of chronic HCV infection. Since 2014, in the European Union, Sofosbuvir (SOF) 400mg/Ledipasvir (LDV) 90mg (Harvoni®) is licensed for chronic HCV infection therapy. According to the EASL Guidelines, no dose adjustment of SOF/LDV is required for patients with mild or moderate renal impairment (estimated glomerular filtration rate [eGFR]>30ml/min/1.73m2) and a full-dose SOF is recommended in patients with stage 5 chronic kidney disease (CKD) on dialysis; however, the safety has not been assessed in patients with stage 4 or 5 CKD not on dialysis.2 In the experience of Saxena et al., a progressive deterioration of renal function and renal symptoms was reported in patients with eGFR ≤45ml/min/1.73m2 receiving an SOF-based regimen, although efficacy was comparable to that observed in patients without renal impairment.3 The experience of DAA therapy for HCV in the post kidney transplant setting is poor and limited than in liver transplant recipients.4 There has been a concern that HCV-positive recipients of HCV-positive kidneys have worse clinical outcomes compared to HCV-positive recipients of HCV-negative grafts.5 Here we report our experience. In September 2015 a 54-year-old female, suffering from ADPKD, on long-term hemodialysis, became HCV-positive (genotype 1b, viral load 1,260,000UI/ml), without abnormal liver laboratory investigations. In November 2015 she successfully received a renal transplant from HCV-positive (genotype 1b, viral load 960,000UI/ml) deceased donor, with early functioning graft (creatinine 0.66mg/dl). From March to May 2016 she received anti-HCV therapy. She was taking prednisone, everolimus and tacrolimus. She was treated with SOF/LDV 1 tablet/day for 12 weeks. At the baseline (January 2016), the viral load was 18,770,000UI/ml. The patient had a Sustained Virological Response at 12 and 24 weeks after treatment. In this period, she did not suffer from any of the most common adverse events of SOF/LDV treatment (fatigue, headache, anemia requiring blood transfusion, nausea), and we did not observe any abnormalities of the common laboratory parameters. At follow-up (February 2018), the HCV-RNA detection was negative.
Our experience confirms the positive results by Gallegos-Orozco JF et al.,5 We highlight the efficacy of antiviral therapy in a HCV-positive (with active HCV-RNA replication) renal transplant recipient from HCV-positive donor, without severe adverse events or drug–drug interactions with her immunosuppressive therapy.
