Renal hemodynamic effects of L-arginine and sodium nitroprusside in heart transplant recipients

Background. Long-term treatment with cyclosporine A (CsA) induces vasoconst riction in the kidney and causes renal impairment. An altered L-arginine (L -Arg)/nitric oxide (NO) pathway may play a key role in CsA nephrotoxicity. Methods. We studied the effect of L-Arg (dosage, 17 mg/kg/min over 30 min), the precursor of NO synthesis, and sodium nitroprusside (SNP; dosage, 1.0 mu g/kg/min over 30 min) on renal hemodynamics in a double-blind, placebo-c ontrolled, randomized, three-way cross-over study comprising 12 stable card iac transplant recipients on long-term CsA treatment, 10 patients with chro nic nephropathy not receiving CsA, and 13 healthy controls. Renal plasma fl ow (RPF) and glomerular filtration rate (GFR) were measured by paraaminohip purate (PAH) and the inulin clearance method, respectively. Results. In healthy subjects, L-Arg induced an increase in RPF (P = 0.009) and GFR (P = 0.001). By contrast, L-Arg did not induce renal hemodynamic ef fects in heart transplant patients or patients with chronic nephropathy. SN P reduced RPF (P = 0.050) and GFR (P = 0.005) in patients with chronic neph ropathy but did not affect renal hemodynamics in heart transplant recipient s or in healthy subjects. Conclusions These data indicate that L-Arg cannot be used to reverse CsA-in duced renal vasoconstriction in heart transplant recipients under long-term CsA treatment, although these patients have a normal renal response to SNP .