Fibroblast growth factor 23 and left ventricular hypertrophy in children on dialysis

Wacharee Seeherunvong1, Carolyn L Abitbol1, Jayanthi Chandar1

  • 1Division of Pediatric Nephrology, University of Miami Miller School of Medicine and Holtz Children's Hospital/Jackson Memorial Medical Center, PO Box 016960 (M-714), Miami, FL, 33101, USA.

Insights

Elevated fibroblast growth factor 23 (FGF-23) is linked to left ventricular hypertrophy (LVH) in pediatric hemodialysis patients. Higher FGF-23 levels correlate with increased LVMI, suggesting FGF-23’s role in cardiac hypertrophy.

Area of Science:

  • Pediatric Nephrology
  • Cardiology
  • Endocrinology

Background:

  • Elevated fibroblast growth factor 23 (FGF-23) is associated with left ventricular hypertrophy (LVH) in adults with chronic kidney disease.
  • The relationship between FGF-23 and cardiac structure in pediatric hemodialysis patients is not well-established.

Purpose of the Study:

  • To investigate the association between FGF-23 levels and left ventricular mass index (LVMI) and LVH in pediatric patients undergoing maintenance hemodialysis.
  • To test the hypothesis that FGF-23 is linked to cardiac hypertrophy in this population.

Main Methods:

  • Retrospective study of 26 pediatric patients (aged 6-21 years) on chronic hemodialysis.
  • Echocardiography was used to assess cardiac structure and geometry.
  • Circulating levels of FGF-23 and calciotropic hormones were measured.

Main Results:

  • FGF-23 levels were significantly elevated in all patients.
  • 55% of patients exhibited LVH, with an average LVMI of 43 ± 13 g/m(2.7).
  • Log-transformed FGF-23 concentrations correlated with LVMI (p=0.03) and were independently associated with interventricular septal thickness Z-score (p<0.001). Each 1 SD increase in log-FGF-23 was linked to a 17% increase in LVMI.

Conclusions:

  • FGF-23 levels are strongly associated with increased LVMI and prevalent LVH in pediatric hemodialysis patients.
  • These findings support the hypothesis linking FGF-23 to cardiac hypertrophy in pediatric chronic kidney disease patients.
Abstract

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