Fibroblast Growth Factor 23 and Left Ventricular Hypertrophy in Chronic Kidney Disease-A Pediatric Perspective

Andrea Grund1,2, Manish D Sinha3, Dieter Haffner1,2

  • 1Department of Paediatric Kidney, Liver and Metabolic Diseases, Hannover Medical School Children's Hospital, Hanover, Germany.

Frontiers in Pediatrics
|August 23, 2021
PubMed

Insights

Fibroblast growth factor (FGF) 23 may drive left ventricular hypertrophy (LVH) in children with chronic kidney disease (CKD). This hormone increases with declining kidney function, posing a cardiovascular disease risk.

Area of Science:

  • Nephrology
  • Cardiology
  • Pediatrics

Background:

  • Cardiovascular diseases (CVD) are a major concern in pediatric chronic kidney disease (CKD).
  • Fibroblast growth factor (FGF) 23, a phosphaturic hormone, rises with kidney dysfunction.
  • Elevated FGF23 is linked to left ventricular hypertrophy (LVH) and CVD risk in CKD.

Purpose of the Study:

  • To review current data on FGF23 in pediatric CKD.
  • To discuss the role of FGF23 in causing LVH in this population.
  • To explore FGF23 excess prevalence and determinants in children with CKD.

Main Methods:

  • Literature review of existing studies on FGF23, CKD, and LVH in pediatric patients.
  • Analysis of experimental data on FGF23's direct effects on cardiac myocytes.
  • Synthesis of clinical findings from adult CKD studies.

Main Results:

  • FGF23 levels increase significantly with declining kidney function in CKD.
  • Experimental evidence shows FGF23 directly induces cardiac myocyte hypertrophy.
  • Clinical data in adults suggests FGF23 cardiotoxicity.

Conclusions:

  • FGF23 is a potential key driver of LVH in pediatric CKD.
  • Further research is needed to confirm FGF23's role and determinants in children.
  • Understanding FGF23's impact is crucial for managing CVD risk in pediatric CKD.

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