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[Fibroblast growth factor 23 in chronic kidney disease in children]
Magdalena Okarska-Napierała1, Piotr Skrzypczyk2, Małgorzata Pańczyk-Tomaszewska2
1Medical University of Warsaw, Poland: Department of Pediatrics with Observational Ward.
Insights
Fibroblast growth factor 23 (FGF23) may drive cardiovascular risk in children with chronic kidney disease (CKD). FGF23 impacts calcium-phosphorus metabolism and may directly harm heart muscle, necessitating further research.
Area of Science:
- Nephrology
- Cardiology
- Biochemistry
Background:
- Children with chronic kidney disease (CKD) face significantly elevated cardiovascular risk.
- Fibroblast growth factor 23 (FGF23), discovered in 2000, is implicated in this risk.
- FGF23 and α-Klotho protein regulate calcium-phosphorus metabolism, crucial in CKD.
Purpose of the Study:
- To explore the role of FGF23 in cardiovascular complications in pediatric CKD.
- To investigate FGF23's direct effects on cardiac health in children with CKD.
- To assess FGF23's contribution to calcium-phosphorus imbalances in pediatric CKD.
Main Methods:
- Review of recent clinical trials and studies in pediatric CKD populations.
- Analysis of FGF23's interaction with its receptor on cardiomyocytes.
- Examination of FGF23's impact on calcium-phosphorus metabolism and cardiovascular alterations.
Main Results:
- FGF23 directly binds to cardiomyocyte receptors, promoting left ventricular hypertrophy.
- Studies suggest FGF23 is key in developing calcium-phosphorus disturbances in pediatric CKD.
- Evidence indicates FGF23's significance in cardiovascular damage pathogenesis in this group.
Conclusions:
- FGF23 plays a critical role in cardiovascular risk and damage in children with CKD.
- Further large-scale clinical trials are needed to confirm FGF23's role.
- Understanding FGF23's mechanisms may lead to novel therapeutic strategies for pediatric CKD patients.
Abstract:
Cardiovascular risk in children with chronic kidney disease (CKD) is many times higher compared to their healthy peers, and discovered in year 2000 fibroblast growth factor 23 (FGF23) may be one of the factors responsible. FGF23 together with its cofactor, α-Klotho protein, plays a pivotal role in calcium-phosphorus metabolism in patients with CKD by decreasing secretion of active metabolite of vitamin D and antagonizing phosphate resorption in renal tubules. Studies conducted in recent years revealed that FGF23 directly binds to its receptor on cardiomyocytes and promotes left ventricular hypertrophy. Clinical trials in children with CKD, similarly to adult studies, suggest a key role of this protein in development of calciumphosphorus disturbances. Single studies in small patient groups suggest also a significance of FGF23 in pathogenesis of cardiovascular alterations in this population. Further clinical trials investigating role of FGF23 in development of cardiovascular damage in larger groups of children are necessary, which may open new therapeutic options for these patients in future.
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