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

Andrea Grund; Manish D Sinha; Dieter Haffner; Maren Leifheit-Nestler

doi:10.3389/fped.2021.702719

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

Front Pediatr. 2021 Aug 4:9:702719. doi: 10.3389/fped.2021.702719. eCollection 2021.

Authors

Andrea Grund^{1

2}, Manish D Sinha³, Dieter Haffner^{1

2}, Maren Leifheit-Nestler^{1

2}

Affiliations

¹ Department of Paediatric Kidney, Liver and Metabolic Diseases, Hannover Medical School Children's Hospital, Hanover, Germany.
² Paediatric Research Centre, Hannover Medical School, Hanover, Germany.
³ Department of Paediatric Nephrology, King's College London, Evelina London Children's Hospital, London, United Kingdom.

Abstract

Cardiovascular diseases (CVD) are a hallmark in pediatric patients with chronic kidney disease (CKD) contributing to an enhanced risk of all-cause and CV morbidity and mortality in these patients. The bone-derived phosphaturic hormone fibroblast growth factor (FGF) 23 progressively rises with declining kidney function to maintain phosphate homeostasis, with up to 1,000-fold increase in patients with kidney failure requiring dialysis. FGF23 is associated with the development of left ventricular hypertrophy (LVH) and thereby accounts to be a CVD risk factor in CKD. Experimentally, FGF23 directly induces hypertrophic growth of cardiac myocytes in vitro and LVH in vivo. Further, clinical studies in adult CKD have observed cardiotoxicity associated with FGF23. Data regarding prevalence and determinants of FGF23 excess in children with CKD are limited. This review summarizes current data and discusses whether FGF23 may be a key driver of LVH in pediatric CKD.

Keywords: children; chronic kidney disease; chronic kidney disease - mineral and bone disease; fibroblast growth factor 23; left ventricular hypertrophy.

Publication types

Review