Genetic diseases resulting from disordered FGF23/klotho biology

- XLH, ADHR, ARHR, and tumor induced osteomalacia result in elevated FGF23 concentrations, causing hypophosphatemia.
- Iron deficiency increases FGF23 expression, but normal individuals cleave excess intact FGF23.
- α Klotho is a necessary co-receptor for FGF23.
- Excess circulating α Klotho increases FGF23 concentrations, resulting in hypophosphatemia.
- Deficiency in either intact FGF23 or α Klotho results in hyperphosphatemia.