| 2007 JASN IMPACT FACTOR 7.111 | HOME AUTHOR INFO EDITORIAL BOARD SUBSCRIBE FEEDBACK ALERTS HELP | |||
| CURRENT ISSUE | ARCHIVES | JASN Express | ONLINE SUBMISSION | |



*
Department of Nephrology and Hypertension, University Medical Center,
Utrecht, the Netherlands
Department of Vascular Medicine, University Medical Center, Utrecht, the
Netherlands
Department of Laboratory of Metabolic Diseases, Wilhelmina Children's
Hospital, Utrecht, the Netherlands
§
Department of Department of Cellular and Molecular Pathology, German
Cancer Research Center, Heidelberg, Germany.
Correspondence to Dr. Ton J. Rabelink, Department of Vascular Medicine, University Medical Center, Utrecht, F02-126, Heidelberglaan 100, 3584 CX Utrecht, The Netherlands. Phone: 31-30-2537399; Fax: 31-30-2523741; E-mail: T.Rabelink{at}digd.azu.nl
Abstract. Recovery from ischemia/reperfusion and immune-mediated injury in the renal transplant is associated with reduced renal hemodynamics and increased leukocyte infiltration. In diverse models of renal failure, L-arginine supplementation improved hemodynamics and reduced inflammation. However in a proinflammatory environment, L-arginine can worsen renal injury. This study investigated the therapeutic potential of L-arginine supplementation in allogeneic renal transplantation: Brown Norway rat kidneys were transplanted into Lewis rat recipients, with one native kidney remaining. Recipients received low-dose cyclosporin A (2.5 mg/kg per d subcutaneously) to obtain moderate vascular and interstitial rejection, with or without 1% L-arginine in drinking water for 7 d posttransplantation. Transplantation increased renal vasoconstriction (from 16.9 ± 1.33 to 35.1 ± 8.6 units; P < 0.01), thereby reducing GFR (from 0.96 ± 0.09 to 0.48 ± 0.10 ml/min; P < 0.05). Treatment with L-arginine restored renal graft function to levels found in normal donors (renal vascular resistance, 15.7 ± 1.69 units; GFR, 0.80 ± 0.06 ml/min). L-arginine significantly reduced vascular occlusion because of less inflammation, endothelial disruption, and thrombosis. L-arginine also decreased tubulitis, interstitial injury, and macrophage infiltration. These protective effects suggest that L-arginine might be useful as additive therapy to conventional immune suppression.
This article has been cited by other articles:
![]() |
T. M.C. Brunini, A. C. Mendes-Ribeiro, J. C. Ellory, and G. E. Mann Platelet nitric oxide synthesis in uremia and malnutrition: A role for L-arginine supplementation in vascular protection? Cardiovasc Res, January 15, 2007; 73(2): 359 - 367. [Abstract] [Full Text] [PDF] |
||||
![]() |
K. M. Park, J. I. Kim, Y. Ahn, A. J. Bonventre, and J. V. Bonventre Testosterone Is Responsible for Enhanced Susceptibility of Males to Ischemic Renal Injury J. Biol. Chem., December 10, 2004; 279(50): 52282 - 52292. [Abstract] [Full Text] [PDF] |
||||
![]() |
K. M. Park, J.-Y. Byun, C. Kramers, J. I. Kim, P. L. Huang, and J. V. Bonventre Inducible Nitric-oxide Synthase Is an Important Contributor to Prolonged Protective Effects of Ischemic Preconditioning in the Mouse Kidney J. Biol. Chem., July 11, 2003; 278(29): 27256 - 27266. [Abstract] [Full Text] [PDF] |
||||
|
HOME
CURRENT ISSUE
ARCHIVES
JASN Express
ONLINE SUBMISSION
AUTHOR INFO
EDITORIAL BOARD SUBSCRIBE FEEDBACK ALERTS HELP |
Copyright © 2008 by the American Society of Nephrology. Online ISSN: 1533-3450 Print ISSN: 1046-6673