The Arginine-Creatine Pathway is Disturbed in Children and Adolescents With Renal Transplants

Cardiovascular disease is an important cause of morbidity in recipients of renal transplants. The aim of the present study was to analyze the status of the arginine-creatine pathway in such patients, given the relationship between the arginine metabolism and both renal function and the methionine-ho...

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Bibliographic Details
Published inPediatric research Vol. 64; no. 2; pp. 218 - 222
Main Authors Andrade, Fernando, Rodríguez-Soriano, Juan, Prieto, José Angel, Elorz, Javier, Aguirre, Mireia, Ariceta, Gema, Martin, Sergio, Sanjurjo, Pablo, Aldámiz-Echevarría, Luis
Format Journal Article
LanguageEnglish
Published New York Nature Publishing Group US 01.08.2008
Lippincott Williams & Wilkins
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Summary:Cardiovascular disease is an important cause of morbidity in recipients of renal transplants. The aim of the present study was to analyze the status of the arginine-creatine pathway in such patients, given the relationship between the arginine metabolism and both renal function and the methionine-homocysteine cycle. Twenty-nine children and adolescents (median age 13, range 6–18 years), who had received a renal allograft 14.5–82.0 months before, were recruited for the study. On immunosuppressive therapy, all patients evidenced an adequate level of renal function. Plasma concentrations of homocysteine and glycine were significantly higher, whereas urinary excretions of guanidinoacetate and creatine were significantly lower than controls. Urinary excretions of guanidinoacetate and creatine correlated positively with creatinine clearance. Urinary excretion of creatine was negatively correlated with plasma concentration of homocysteine. The demonstration of disturbances in the arginine-creatine pathway in patients with well-functioning renal transplants and in absence of chronic renal failure represents a novel finding. We speculate that the low urinary excretion of guanidinoacetate and creatine is probably related to the nephrotoxic effect of immunosuppressive therapy and to defective methylation associated with the presence of hyperhomocysteinemia.
ISSN:0031-3998
1530-0447
DOI:10.1203/PDR.0b013e318176180e