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Hepatitis C is reported to be associated with poorer renal survival in patients with diabetes. The mechanism for this observation has not been elucidated. Transforming growth factor β-1 is involved in signaling for human disease involving fi brosis and excess matrix deposition including diabetic nephropathy. Hepatitis C virus core protein is known to upregulate transcription of TGF β-1 in the liver and HCV patients have elevated levels of circulating TGF β-1 versus controls. There is evidence that elevated circulating TGF β-1 levels result in more rapid progression of nephropathy and that lowering circulating TGF β-1 levels with an angiotensin converting enzyme inhibitor correlates with treatment effi cacy in diabetic nephropathy. This paper outlines a hypothesis that the elevated level of circulating TGF β-1 which is associated with HCV is a mediator of more rapid progression of diabetic renal disease in persons with HCV.