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Abstract
HCV is a leading cause of liver cancer and cirrhosis, and Egypt possibly has the highest HCV prevalence worldwide. The effective number of HCV infections in Egypt underwent rapid exponential growth between 1930 and 1955. The timing and speed of this spread provides quantitative genetic evidence that the Egyptian HCV epidemic was initiated and propagated by extensive antischistosomiasis injection campaigns. Although the results show that HCV transmission has since decreased, HCV is likely to remain prevalent in Egypt for several decades (Pybus et al.,2003).
Mixed cryoglobulinemia, renal syndromes, lymphoproliferative disorders, Sjogren syndrome, porphyria cutanea tarda, and neuropathies are all strongly associated with HCV infection. Diabetes, thyroid disease, and the presence of autoantibodies in the serum are also linked to HCV, but less strongly. The pathophysiologic basis for most of these syndromes seems immunologic. Cirrhosis and chronic HCV infection seem to be risk factors (Ali and Zein ,2005).
HCV can cause membranoproliferative glomerulonephritis (MPGN) ,membranous GN, cryoglobulinemic GN (MPGN) and there is also some reports of IgA nephropathy, fibrillary and immunotactoid glomerulopathy (Warren ,2003).
RT recipients with anti-HCV antibody have an increased risk of mortality and graft failure compared with HCV antibody negative patients (Fabrizi et al.,2005).