 Existing evidence and our preliminary data indicate that impairment of vasodilatory response mediated by nitric oxide NO plays an important role in the pathogenesis of calcineurin inhibitor nephrotoxicity. Our overall hypothesis is that L-arginine supplement provides protection against calcineurin inhibitor nephrotoxicity. L-arginine, a naturally occurring amino acid, is the main substrate of the NO synthase enzyme and exogenous supplementation of L-arginine may improve renal perfusion by inducing renal vasodilation via increased NO production. Although L-arginine has been shown to prevent renal damage from calcineurin inhibitors in experimental animals, its efficacy in preserving renal function has not been studied in human LTx recipients. 