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The role of fibroblast growth factor 23 in renal disease
Department of Surgical Sciences, Unit of Orthopedic Surgery, Uppsala University, Uppsala, Sweden
Correspondence and offprint requests to: Kenneth B. Jonsson, Department of Surgical Sciences, Unit of Orthopedic Surgery, Uppsala University, SE-751 85 Uppsala, Sweden. E-mail: Kenneth.jonsson@surgsci.uu.se
Keywords: CKD; ESRD; FGF23; hyperparathyroidism; hyperphosphataemia; phosphate; renal failure; vitamin D
| The first 150 words of the full text of this article appear below. |
| FGF23 is a phosphate regulator in physiology and pathology |
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Activating mutations in the fibroblast growth factor 23 (FGF23) gene were identified as the cause of autosomal dominant hypophosphataemic rickets (ADHR) [1]. This secreted protein was later shown to play a role in both physiological and pathological phosphate handling.
FGF23 may be the key pathogenetic molecule in three different diseases with hypophosphataemia and inappropriate regulation of vitamin D metabolism. In ADHR, the mutations stabilize the FGF23 protein, which leads to increased circulating levels [2]. In X-linked hypophosphataemia (XLH), a disease caused by inactivating mutations of the PHEX gene, the loss of a membrane-bound protease results in increased circulating levels of FGF23 [3]. Also, in the paraneoplastic syndrome of tumour-induced osteomalacia (TIO), tumours secrete large amounts of FGF23 [35]. Thus, in three disorders of inorganic phosphate (Pi) wasting, FGF23 circulates in increased amounts, suggesting a pathological role for the molecule.
Evidence for
| Phosphate homeostasis and vitamin D metabolism in renal disease |
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| The role of FGF23 in the dysregluation of phosphate/calcium/vitamin D homeostasis in CKD |
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FGF23 levels are increased in renal disease
So its up, does it matter?
Are FGF23 measurements clinically useful in CKD patients?
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