The insulin-like growth factor system is intimately involved in renal development, growth, function and the pathophysiology of several disease states. Exogenous IGF-I increases GFR and RPF, perhaps mediated by nitric oxide (NO). In chronic renal failure, IGF-I, the binding proteins and their fragments decrease bioavailability. After transplantation, the levels of bioactive IGF-I increase likely due to better nutrition and increased clearance of the binding proteins and their fragments. In the nephritic syndrome, a similar mechanism may be active, in that the binding proteins and their fragments may inhibit IGF-I action.