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Long-term renal function in heart transplant children on cyclosporine treatment

Luca Dello Strologo1, Francesco Parisi, Antonia Legato

  • 1Division of Nephrology and Dialysis, Bambino Gesù Children's Hospital and Research Institute, Piazza S. Onofrio 4, 00165 Rome, Italy. dellostrologo@opbg.net

Pediatric Nephrology (Berlin, Germany)
|February 24, 2006
PubMed

Insights

Long-term renal function in heart transplant children often declines, with nearly a third developing renal insufficiency within three years. Cyclosporine

Area of Science:

  • Pediatric Nephrology
  • Cardiology
  • Transplantation Medicine

Background:

  • Renal function deterioration is a significant concern following pediatric heart transplantation.
  • Cyclosporine (CsA) is a common immunosuppressant, but its long-term effects on renal function in children are not fully understood.

Purpose of the Study:

  • To evaluate long-term renal function in pediatric heart transplant recipients treated with CsA.
  • To identify factors associated with renal function decline in this population.

Main Methods:

  • Retrospective review of creatinine clearances in 50 children post-heart transplant (median follow-up 99.7 months).
  • Analysis of variables including gender, age, body weight at transplant, rejection episodes, CsA cumulative dose, and trough levels.

Main Results:

  • After an initial increase, glomerular filtration rate (GFR) worsened in most patients.
  • 28% of children developed renal insufficiency (GFR <80 ml/min/1.73 m2) within the first three years.
  • No significant association was found between CsA dose, trough levels, or patient characteristics and renal function deterioration.

Conclusions:

  • A substantial proportion of pediatric heart transplant recipients experience long-term renal function decline.
  • The study did not find a direct correlation between CsA levels and renal insufficiency, suggesting potential patient predispositions.
  • Early identification of susceptible patients is crucial for considering calcineurin inhibitor-sparing strategies.

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