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FGF23 – Hormone, Function & Related Disorders

FGF23 is a hormone produced by bone cells that regulates phosphate and vitamin D balance. It plays a key role in kidney and bone disorders.

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Things worth knowing about "FGF23"

FGF23 is a hormone produced by bone cells that regulates phosphate and vitamin D balance. It plays a key role in kidney and bone disorders.

What is FGF23?

FGF23 (Fibroblast Growth Factor 23) is a hormone primarily produced by osteoblasts and osteocytes – the cells responsible for forming and maintaining bone. It belongs to the family of fibroblast growth factors and functions as a key phosphaturic hormone, meaning it controls how much phosphate the kidneys excrete in the urine.

Mechanism of Action

FGF23 acts mainly on the kidneys, where it works together with its essential co-receptor Klotho to regulate two major processes:

Inhibition of phosphate reabsorption: FGF23 reduces the reuptake of phosphate from urine back into the bloodstream, resulting in increased phosphate excretion (phosphaturia).
Inhibition of vitamin D activation: FGF23 suppresses the enzyme 1-alpha-hydroxylase, which converts the inactive form of vitamin D (calcidiol) into its biologically active form (calcitriol). It also promotes the breakdown of active vitamin D.

Through these mechanisms, FGF23 lowers blood phosphate levels and indirectly reduces calcium absorption, since less active vitamin D is available.

Biological Role and Regulation

Several factors regulate the release of FGF23:

Elevated blood phosphate levels (hyperphosphatemia) stimulate FGF23 production.
Active vitamin D (calcitriol) also increases FGF23 secretion.
Parathyroid hormone (PTH) can modulate FGF23 secretion.
Iron deficiency can impair FGF23 cleavage, leading to elevated FGF23 levels in the blood.

FGF23 is therefore a central element of the hormonal feedback system that keeps phosphate, calcium, and vitamin D in balance.

Clinical Relevance – Disorders Associated with FGF23

Elevated FGF23 Levels (FGF23 Excess)

Excessively high FGF23 levels lead to abnormal phosphate loss through the kidneys and impaired vitamin D activation, causing:

X-linked Hypophosphatemia (XLH): The most common hereditary form of hypophosphatemia, caused by mutations in the PHEX gene leading to uncontrolled FGF23 overproduction. Affected individuals develop rickets in childhood and osteomalacia in adulthood.
Tumor-induced Osteomalacia (TIO): Certain tumors produce excessive FGF23, leading to severe bone pain, fractures, and muscle weakness.
Chronic Kidney Disease (CKD): As kidney function declines, FGF23 rises dramatically as a compensatory mechanism. Elevated FGF23 in CKD is strongly associated with an increased risk of cardiovascular disease, left ventricular hypertrophy, and mortality.

Low FGF23 Levels (FGF23 Deficiency)

Low FGF23 levels are rare but can result in excessive phosphate retention and hyperphosphatemia, as seen in familial tumoral calcinosis (FTC) – a rare condition characterized by calcium deposits in soft tissues.

Diagnosis – Measuring FGF23

FGF23 is measured in the blood using specialized immunoassays. Two main types of assays exist:

Intact FGF23 assay: Measures only the complete, biologically active FGF23 molecule.
C-terminal FGF23 assay: Detects both intact and cleaved FGF23 fragments.

FGF23 measurement is particularly relevant in cases of unexplained hypophosphatemia, suspected osteomalacia, kidney disease, and for monitoring treatment response in FGF23-related disorders.

Therapeutic Approaches

Several treatment strategies are available for FGF23-related conditions:

Burosumab (Crysvita®): A monoclonal antibody that directly targets and inhibits FGF23. It is approved for the treatment of X-linked hypophosphatemia (XLH) in children and adults.
Phosphate and vitamin D supplementation: The traditional treatment for hypophosphatemia; however, it does not directly address elevated FGF23 levels.
Management in chronic kidney disease: Dietary phosphate restriction and the use of phosphate binders help to reduce the compensatory rise in FGF23 levels.

References

Shimada T et al. - Cloning and characterization of FGF23 as a causative factor of tumor-induced osteomalacia. Proceedings of the National Academy of Sciences, 2001.
Ketteler M et al. - Executive summary of the 2017 KDIGO Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD) Guideline Update. Kidney International, 2017.
Insogna KL et al. - A Randomized, Double-Blind, Placebo-Controlled, Phase 3 Trial Evaluating the Efficacy of Burosumab in Adults with X-Linked Hypophosphatemia. Journal of Bone and Mineral Research, 2018.

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