Management of hepatitis C virus infection in kidney transplant patients pre- and post-transplantation

Background: Prevalence of HCV infection varies throughout the world with the highest number of infection reported in Egypt. The risk factors for HCV transmission that specifically sets Egypt a part from other countries is history of parenteral antischistosomal therapy. Other routes of transmission and risk factors include intravenous drug users and blood transfusion. HCV has hepatic manifestations including acute hepatitis, chronic hepatitis, fulminant hepatitis, liver cirrhosis and hepatocellular carcinoma. There are several extrahepatic manifestations of HCV as hemolytic anemia, thrombocytopenia, thyroid disease, peripheral neuropathy, lymphoma, polyartritis nodosa and dermatological diseases. Kidney disease associated with HCV infection including membranopliferative glomerulonephritis and membranous nephropathy. Focal segmental glomulosclerosis and IgA nephropathy. Cryoglobulinemia types II and III and diabetes mellitus are common in renal transplant patients. HCV infection is the main cause of chronic liver disease after renal transplantation. It is considered to be a risk factor for graft loss and patient death. In dialysis patients with chronic HCV infection, serum aminotransferase levels are not reliable in determining disease activity and fibrosis severity. Liver biopsy remains the gold standard for assessment of disease severity. Because of the current shortage of cadaveric kidneys, grafting kidneys from anti-HCV positive donors into anti-HCV positive recipients. Transplantation of kidneys from anti-HCV positive donors only into HCV RNA viremic patients may be a new option. It is important to kidney transplant patients to be examined before transplantation not only to diagnose the infection but also to identify patients whom became clinically free. Kidney transplant patients who are positive for HCV antibodies (anti-HCV) have higher rates of liver complications and lower survival rates after transplantation than anti-HCV negative patients. eradication of HCV infection before transplantation seems to reduce the risk for HCV-associated renal dysfunction after transplantation and may reduce the risk of HCV progression. Standard treatment of HCV in dialysis patients is IFN monotherapy as thrice weekly administration of non-pegylated-IFNα2b was more efficacious and associated with a shorter duration of treatment-related adverse effects than once-weekly administration of pegylated IFN. For renal transplant patients, standard treatment as ribavirin in a dose of 600 mg/day for 48 weeks with ultra low dosage of IFN-α (1 Mu thrice weekly). Associated hemolytic anemia may require large dose of rHu EPO or ribavirin dosage modifications. The most pressing reasons to consider HCV therapy are recurrent and progressive HCV-associated glomerulopathy in the transplanted kidney, severe cholestatic hepatitis, and advanced histologic stages of liver disease. Risk of acute rejection with IFN remains a concern. Antiviral therapy may be safer if given years after transplantation and patients with stable graft function and no history of rejection. In addition, patients should be on a stable immunosuppressive regimen and have therapeutic drug levels of immunoisuppressive drugs at the time of IFN treatment. The use of ribavirin a drug with immunomodulatory potential, may positively modulate the risk of acute rejection. HCV mediated glomulonephritis may be effectively managed with IFN-based therapy.Objectives: The aim of this work is to study the recent advances in management of kidney transplant patients with hepatitis C virus infection in pre- and post-transplantation period.