Related Experiment Video
Updated: Oct 23, 2025

Identification of the Source of Secreted Proteins in the Kidney by Brefeldin A Injection
Published on: November 10, 2021
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.
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.
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.
More Related Videos
08:38Author Spotlight: A Neonatal Heterotopic Rat Heart Transplantation Model for the Study of Endothelial-to-Mesenchymal Transition
Published on: July 21, 2023
08:505/6th Nephrectomy in Combination with High Salt Diet and Nitric Oxide Synthase Inhibition to Induce Chronic Kidney Disease in the Lewis Rat
Published on: July 3, 2013
Related Concept Videos
Chronic Kidney Disease I: Introduction
Chronic Kidney Disease III: Interprofessional Care
Chronic Kidney Disease II: Clinical Manifestations
Heart Failure II: Pathophysiology
Chronic Kidney Disease IV: Nursing Management
Drug Dosing in Renal Diseases: Estimation of Glomerular Filtration Rate Based on Serum Creatinine Concentration