HCV is a significant cause of glomerulopathy in countries with a high prevalence of HCV infection[3]. Several studies have postulated a causal link between HCV infection and renal diseases through the induction of cryoglobulinemia[4]. The affinity for the http://www.selleckchem.com/products/CHIR-258.html kidney mesangium appears to be a major factor responsible for the precipitation of type-II mixed cryoglobulins in glomerular structures and the ensuing damage[5]. The principal clinical manifestations of glomerular disease in HCV-infected patients are the presence of proteinuria and microscopic hematuria with or without impaired kidney function[6]. Diabetes mellitus-mediated glomerulonephropathy in HCV patients may be considered, particularly with epidemiological studies showing a high occurrence of type 2 diabetes in patients with chronic HCV-G4[7].

Various approaches have been tried for the treatment of HCV-associated glomerulonephritis, including immunosuppressive therapy (corticosteroids and cytotoxic agents), plasma exchange and antiviral agents. Limited data exist regarding antiviral treatment of HCV-associated glomerulonephritis. We present a novel study reporting the prevalence of microalbuminuria, with other measures of renal insufficiency [albumin creatinine ratio (ACR), estimated glomerular filtration rate (GFR)] in HCV-G4 patients compared to HCV-negative controls, and the effect of viral load on liver histology, microalbuminuria, and renal insufficiency. Also, we investigated the effect of antiviral therapy with pegylated interferon and ribavirin on microalbuminuria, and other measures of renal insufficiency.

MATERIALS AND METHODS In this prospective study, 300 consecutive eligible subjects who attended the gastroenterology clinic in Hamad Hospital were recruited in the period between January 2006 and 2009. Of these, 233 were chronic HCV-G4 patients who fulfilled the inclusion criteria, and 77 were control subjects who were either non hepatic patients followed in the clinic during the same period or healthy volunteers who were referred to Hamad hospital when Dacomitinib they were ill. Controls were eligible if they did not have liver disease, evidenced by: persistently normal transaminases, negative serology for hepatitis serology, negative screening for auto-immune disease and no history of alcohol consumption, normal platelet count and �� fetoprotein, and normal ultrasound scans. All study participants were seen 2-3 times to provide repeated blood samples at baseline. Chronic HCV patients were also seen periodically to assess the response to treatment. All patients provided written informed consent as stated in the Declaration of Helsinki of 1979, and the ethics research committee of the Hamad Medical Corporation provided ethical approval.