FGF23 Actions in CKD-MBD and other Organs During CKD
Related Experiment Video
Updated: Sep 6, 2025
Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway
Published on: August 23, 2024
1Laboratory of Endocrinology and Metabolism, Department of Endocrinology and Metabolism, Rare Disease Center, National Clinical Research Center for Geriatrics, West China Hospital, Sichuan University, Chengdu 610041, China.
Abstract:
Fibroblast growth factor 23 (FGF23) is a new endocrine product discovered in the past decade. In addition to being related to bone diseases, it has also been found to be related to kidney metabolism and parathyroid metabolism, especially as a biomarker and a key factor to be used in kidney diseases. FGF23 is upregulated as early as the second and third stages of chronic kidney disease (CKD) in response to relative phosphorus overload. The early rise of FGF23 has a protective effect on the body and is essential for maintaining phosphate balance. However, with the decline in renal function, eGFR (estimated glomerular filtration rate) declines, and the phosphorus excretion effect caused by FGF23 is weakened. It eventually leads to a variety of complications, such as bone disease (Chronic Kidney Disease-Mineral and Bone Metabolism Disorder), vascular calcification (VC), and more. Monoclonal antibodies against FGF23 are currently used to treat genetic diseases with increased FGF23. CKD is also a state of increased FGF23. This article reviews the current role of FGF23 in CKD and discusses the crosstalk between various organs under CKD conditions and FGF23. Studying the effect of hyperphosphatemia on different organs of CKD is important. The prospect of FGF23 for therapy is also discussed.
Insights
Fibroblast growth factor 23 (FGF23) initially protects against phosphorus overload in early chronic kidney disease (CKD). However, declining kidney function impairs FGF23’s effectiveness, leading to complications.
Area of Science:
- Endocrinology
- Nephrology
- Mineral Metabolism
Background:
- Fibroblast growth factor 23 (FGF23) is a key hormone regulating phosphate and vitamin D metabolism.
- FGF23 plays a critical role in mineral and bone disorders, particularly in chronic kidney disease (CKD).
- Early-stage CKD involves elevated FGF23, offering a protective effect against phosphorus imbalance.
Approach:
- This review examines the multifaceted role of FGF23 in CKD progression.
- It explores the intricate crosstalk between FGF23 and various organs affected by CKD.
- The article discusses the therapeutic potential of targeting FGF23 in CKD management.
Key Points:
- FGF23 is upregulated in early CKD stages (II-III) to manage phosphorus overload.
- Reduced kidney function in advanced CKD diminishes FGF23 efficacy, causing complications like bone disease and vascular calcification.
- Current FGF23-targeting therapies are used for genetic disorders and show promise for CKD.
Conclusions:
- FGF23 is a crucial biomarker and factor in CKD, influencing mineral metabolism and disease progression.
- Understanding FGF23's interactions is vital for developing effective CKD therapies.
- Targeting FGF23 presents a promising therapeutic avenue for managing CKD complications.
Related Concept Videos
01:28Chronic Kidney Disease III: Interprofessional Care
01:25Chronic Kidney Disease I: Introduction
01:24Chronic Kidney Disease II: Clinical Manifestations