To the Editor:
Chronic hepatitis due to the hepatitis C virus (HCV) in patients with chronic renal failure (CRF) reduces survival in haemodialysis and kidney transplant and graft survival, as well as worsening liver disease, increasing the frequency of fibrosing cholestatic hepatitis and accelerating the progression to cirrhosis,1,2 particularly in kidney transplant patients or those with hepatocellular carcinoma.3
We report the case of a 67-year-old female, with a dry weight of 41.5kg and a history of CRF secondary to Alport syndrome. The patient underwent deceased donor renal transplantation in May 1995 after receiving peritoneal dialysis over a one-year period. The patient initially displayed acute vascular rejection and did not respond to corticosteroids, and as such, she was treated with muromonab (OKT3), and her creatinine levels remained stable. She subsequently presented with chronic allograft nephropathy with elevated levels of anti-HLA-2 antibodies and received immunosuppressive therapy with prednisone, mycophenolate mofetil and tacrolimus. In 2003, a liver biopsy was performed and the results were consistent with chronic periportal hepatitis due to HCV genotype 2, functional CPD8 and MEDE of 15-17. At this time, she had fluid retention with ascites and started haemodialysis due to a deterioration of her general condition, severe acidosis, resistant high blood pressure and symptomatic uraemia along with hepatic encephalopathy.
The patient initially displayed a viral load (VL) of 2,790,000 copies/ml. However, after 4 months on haemodialysis, this decreased (43,200 copies/ml). Treatment was started with 135μg/week peginterferon and 200mg/day ribavirin,4 although due to a haemoglobin decrease to 9.3g/dl in week 10, we decreased the ribavirin dose to 200mg/48h in non-dialysis days, with a break one day a week; we also increased the darbepoetin and erythropoietin dose. In week 16, we decreased the peginterferon dose to 135μg/14 days due to a decrease in platelets to 77,000μl.
The patient had a rapid viral response (negative VL in week 4), maintaining viral suppression until the end of the 38-week treatment.
After 3 weeks of treatment with combination therapy, we decreased the darbepoetin and erythropoietin dose to 30mg/week due to haematocrit of 41.2% and intravenous iron administration was discontinued; an improvement in residual renal function was also observed (glomerular filtration rate = 15ml/min, Kt/V: 1.8), with dialysis frequency being reduced to 2 days/week. However, although there was still acceptable residual clearance and diuresis, it was necessary to increase the frequency of dialysis to 3 times/week due to high blood pressure with hyperphosphataemia and acidosis.
Twenty-four days after the end of treatment, a sustained viral response was confirmed, with an improvement in liver disease and normalisation of transaminases, and the patient was included in the dual kidney and liver transplant waiting list. However, she died a sudden death secondary to acute myocardial infarction before receiving a transplant.
DISCUSSION
Currently, treatment with peginterferon and ribavirin in patients with kidney disease is limited by creatinine clearance.5,6 The Kidney Disease Improving Global Outcomes,7 the American Association for the Study of Liver Diseases8, the Japanese Society for Dialysis Therapy9 and the Spanish Society of Nephrology10 guidelines do not recommend treating HCV in kidney transplant patients with peginterferon because it may cause acute rejection and/or acute interstitial nephropathy, or peginterferon in combination with ribavirin due to the risk of anaemia. In light of our results, we believe that it is possible to achieve a sustained viral response with combination therapy by carrying out a strict clinical control on the patient and minimising potential adverse effects, and thus achieve retransplantation in this patient group.
Conflicts of interest
The authors declare that they have no conflicts of interest related to the contents of this article.
