Role of fibroblast growth factor 23 in health and in chronic kidney disease.
PURPOSE OF REVIEW: This review summarizes the molecular properties and biological roles of a new phosphaturic factor, fibroblast growth factor 23 (FGF23). Significant roles of FGF23 are discussed, especially in terms of its effects on the kidney, the main target organ. RECENT FINDINGS: FGF 23 is a recently discovered phosphaturic factor. Several animal experiments including overexpression or ablation of the FGF23 gene have recently revealed the significant effects of this factor on phosphate excretion and on vitamin D synthesis in the kidney. Although FGF23 was originally identified as a factor responsible for several hypophosphatemic disorders, recent data indicate its role in the physiological regulation of phosphate homeostasis. In chronic kidney disease, FGF23 plays a crucial role in the pathogenesis of secondary hyperparathyroidism. Effects of FGF23 on other organs including bone and intestine remain to be elucidated. SUMMARY: FGF23 is a physiological regulator of phosphate homeostasis. Excessive activity of FGF23 with normal renal function results in hypophosphatemia, low 1,25-dihydroxyvitamin D levels, and rickets/osteomalacia. By contrast, excessive FGF23 activity suppresses 1,25-dihydroxyvitamin D synthesis, but may not be sufficient to excrete the phosphate load appropriately with deteriorating renal function, both of which contribute to the development of hyperparathyroidism.[1]References
- Role of fibroblast growth factor 23 in health and in chronic kidney disease. Fukagawa, M., Nii-Kono, T., Kazama, J.J. Curr. Opin. Nephrol. Hypertens. (2005) [Pubmed]
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