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To the Editor:

Here we report a case of an HCV positive patient treated successfully with antiviral therapy who subsequently donated a kidney to an HCV negative recipient without viral transmission. The safety of this approach relies on the fact that sustained virological response (SVR) usually means lack of viral presence in the liver and other organs [1]. This rationale served to get approval from our Institution Ethics Committee as well as informed consent from both donor and recipient. The patient was a 49-year-old male diagnosed with IgA nephropathy. When glomerular filtration rate (GFR) was 20 mL/min, options for renal replacement therapy, including preemptive living-donor kidney transplantation, were given to him. His wife was candidate for living donation. She was a 49-year-old female with antecedent of blood transfusion in 1986 during open myomectomy. However, chronic hepatitis C virus infection was diagnosed. She had mild elevation of liver enzymes and normal ultrasound examination. The Fibroscan® liver ultrasound transient elastography value was 8.9 kPa (moderate fibrosis). HCV was genotype 3, and viral load was 65 610 UI/mL. A 24-week peginterferon alfa (180 g/week sc) and ribavirin (800 mg/day po) treatment was performed with negative viral load after 4 weeks. SVR as well as normalization of liver enzymes was achieved. Therefore, 1 year after antiviral treatment was finished we decided to proceed with laparoscopic nephrectomy and living donor kidney transplantation. At this time, recipient GFR was 10 mL/min.

Kidney transplantation was performed uneventfully for donor and recipient. The recipient received induction immunosuppression based on basiliximab, tacrolimus, mofetil mycophenolate and early steroid discontinuation. There was rapid and full recovery of renal function. Six-month protocol kidney allograft biopsy was normal. Liver enzymes remained within the normal range during the 2-year follow-up. HCV viral load monitoring at Days 7, 30, 60, 90, 120, 150 and 180 as well as 1 and 2 years after transplantation was always negative. At last follow-up, GFR was higher than 60 mL/min without proteinuria (0.05 g/day) and microhematuria. Likewise, donor follow-up showed SVR, normal liver enzymes and normal renal function without hypertension, proteinuria (0.07 g/day) or microhematuria.

Active HCV in the donor is considered a contraindication to living donation since the risk of HCV transmission approaches 100% if transplanted into a HCV negative recipient. In our kidney donor, HCV infection showed some predictors of treatment response (genotype 3 and low viral load) [2]. Therefore, after confirmation of achieving SVR we proceeded with donor nephrectomy and kidney transplantation assuming that, in this case, occult HCV infection was unlikely. Occult HCV infection is defined as the presence of HCV RNA in the liver or peripheral blood mononuclear cells of HCV RNA negative patients [3]. However, its clinical significance is rather controversial [4]. On the other hand, while one study reported 2% of detectable hepatic HCV RNA after SVR [5], there is strong evidence that liver HCV RNA remains negative in the long term [1]. Therefore, although the likelihood of HCV transmission in our case seems very low, we cannot completely exclude HCV transmission without having assessed HCV RNA in the donor kidney. This is the first case reported in the literature showing that chronic HCV infection does not preclude kidney living donation to a HCV negative recipient if viral clearance is achieved. Although our observation may increase the chances for candidates for living donor kidney transplantation, prospective studies that incorporate monitoring of all necessary virological donor and recipient parameters are needed to confirm the safety of this approach.

  • J. M. Cruzado1,*, S. Gil-Vernet1, J. Castellote2, O. Bestard1, E. Melilli1 and J. M. Grinyó1

  • 1Nephrology Department, Hospital Universitari de Bellvitge, University of Barcelona, L'Hospitalet de Llobregat, Spain

  • 2Hepatology Department, Hospital Universitari de Bellvitge, L'Hospitalet de Llobregat, Spain

  • *Corresponding author: Josep M. Cruzado, jmcruzado@bellvitgehospital.cat

Disclosure

The authors of this manuscript have no conflicts of interest to disclose as described by the American Journal of Transplantation.

References

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