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Coronary artery calcification and cardiovascular disease in children with chronic kidney disease

Sara Paoli1, Mark M Mitsnefes

  • 1aDepartment of Pediatrics, University 'SAPIENZA', Pediatric Nephrology Policlinico Umberto I, Rome, Italy bDivision of Nephrology and Hypertension, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, USA.

Current Opinion in Pediatrics
|March 18, 2014
PubMed

Insights

Fibroblast growth factor 23 (FGF23) and Klotho factor are key in coronary artery calcification for children with chronic kidney disease (CKD). Early CKD shows reduced Klotho and increased FGF23, linked to calcification.

Area of Science:

  • Pediatric Nephrology
  • Cardiovascular Research
  • Mineral Metabolism

Background:

  • Cardiovascular disease is a leading cause of death in pediatric end-stage renal disease (ESRD).
  • Children with advanced chronic kidney disease (CKD) exhibit high cardiovascular risk factors.
  • Coronary artery calcification (CAC) is an early marker in pediatric ESRD.

Purpose of the Study:

  • To review new developments in the pathogenesis of CAC.
  • To describe recent studies on CAC in pediatric CKD.

Main Methods:

  • Review of recent scientific literature.
  • Analysis of studies on FGF23 and Klotho in pediatric CKD and CAC.

Main Results:

  • Growing evidence implicates fibroblast growth factor 23 (FGF23) and Klotho factor in CAC development in ESRD.
  • Vascular calcification begins in early normophosphatemic CKD with reduced Klotho and increased FGF23.
  • Pediatric studies confirm abnormal FGF23/Klotho metabolism and its association with CAC in children with CKD.

Conclusions:

  • New insights into vascular calcification mechanisms in early CKD warrant further investigation.
  • Future research should explore if controlling FGF23/Klotho metabolism can prevent or delay CAC and cardiovascular outcomes.
Abstract

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