Fibroblast growth factor 23
Hormone · Phosphatonin alpha-Klotho needed
The principal phosphatonin. Using alpha-Klotho as an obligatory co-receptor for FGFR1 in the proximal tubule, FGF23 lowers serum phosphate by internalising the sodium-phosphate cotransporters, and lowers calcitriol by suppressing CYP27B1 while inducing CYP24A1.
Traced from the start
- Phosphate load and hyperphosphataemia
- Osteocyte phosphate sensing
- Fibroblast growth factor 23
Detail
- Co-receptor
- Alpha-Klotho is required for high-affinity binding to FGFR1; its expression is largely confined to kidney, parathyroid and choroid plexus, which is what gives FGF23 its tissue selectivity
- Phosphate
- Internalises and degrades NaPi-IIa (SLC34A1) and NaPi-IIc in the proximal tubule, producing phosphaturia
- Vitamin D
- Suppresses CYP27B1 (1-alpha-hydroxylase) and induces CYP24A1 (24-hydroxylase), so calcitriol falls
- Parathyroid
- Directly suppresses PTH secretion in health; in chronic kidney disease the gland loses Klotho and becomes FGF23-resistant, so PTH rises anyway
When it goes wrong
Chronic kidney disease
FGF23 rises earliest of all the mineral markers, before phosphate or PTH move; the calcitriol suppression it causes helps drive secondary hyperparathyroidism, and a high FGF23 tracks left ventricular hypertrophy and mortality
Burosumab, an anti-FGF23 antibody, in X-linked hypophosphataemia
Phosphate reabsorption and calcitriol production are restored and the rickets heals
Practise this structure
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