The arginine-creatine pathway is disturbed in children and adolescents with renal transplants

Fernando Andrade1, Juan Rodríguez-Soriano, José Angel Prieto

  • 1Department of Pediatrics, Division of Metabolism, Cruces Hospital, Bilbao, Basque Country, Spain.

Pediatric Research
|April 9, 2008
PubMed

Insights

Renal transplant recipients show altered arginine-creatine pathway function, with lower creatine excretion and higher homocysteine levels. These changes occur despite adequate kidney function and may stem from immunosuppressants and hyperhomocysteinemia.

Area of Science:

  • Nephrology
  • Biochemistry
  • Transplantation

Background:

  • Cardiovascular disease is a significant complication in renal transplant recipients.
  • The arginine-creatine pathway is linked to renal function and the methionine-homocysteine cycle.
  • Understanding metabolic alterations in transplant patients is crucial for managing long-term health.

Purpose of the Study:

  • To investigate the arginine-creatine pathway status in pediatric and adolescent renal transplant recipients.
  • To explore the relationship between this pathway, renal function, and homocysteine levels.

Main Methods:

  • Study included 29 children and adolescents post-renal transplant on immunosuppressive therapy.
  • Measured plasma homocysteine and glycine concentrations.
  • Assessed urinary guanidinoacetate and creatine excretion.
  • Correlated metabolic markers with creatinine clearance and homocysteine levels.

Main Results:

  • Patients exhibited significantly higher plasma homocysteine and glycine levels compared to controls.
  • Urinary excretion of guanidinoacetate and creatine was significantly lower in transplant recipients.
  • Lower creatine excretion correlated negatively with plasma homocysteine levels.
  • Urinary guanidinoacetate and creatine excretion positively correlated with creatinine clearance.

Conclusions:

  • Disturbances in the arginine-creatine pathway are present in renal transplant patients even with adequate renal function.
  • Low urinary guanidinoacetate and creatine may be linked to immunosuppressive therapy's nephrotoxic effects.
  • Hyperhomocysteinemia and defective methylation might contribute to these observed metabolic changes.

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