Why is diabetic nephropathy listed as a cause of nephrotic syndrome for patients with HCV?
In addition to the lymphotropic effect of HCV, this virus also binds to bb-islet cells.
The interaction of the virus surface antigens with bb-islet cells in the pancreas initiates a sequence of events that leads to islet dysfunction and secondary type II diabetes.
In addition, viral structural proteins interfere with the post-receptor response to insulin, leading to a combination of type I and type II diabetes in these patients.
Over years, the end-organ complications of diabetes can accrue, especially the development of diabetic nephropathy.
Therefore in a patient with HCV and diabetes who presents with nephrotic syndrome and kidney dysfunction, the differential diagnosis needs to include diabetic nephropathy. Clinically, the presence of low complement levels (C3 and C4) and an active urinary sediment possibly associated with systemic manifestations of vasculitis would all be supportive of HCV-related cryoglobulinemia as opposed to diabetes as the cause of kidney dysfunction.
The treatment of diabetic nephropathy in patients with HCV is similar to that of diabetic nephropathy in the general population and includes inhibition of the renin-angiotensin-aldosterone system (RAAS), blood pressure control, and glycemic control.
