Abstract

Recently, a new view into the molecular mechanisms of phosphate homeostasis and secondary hyperparathyroidism pathogenesis has been proposed, with Fibroblast Growth Factor 23 (FGF-23) as a novel player in the field. Enhanced serum FGF-23 levels cause a reduction in serum phosphate, together with calcitriol suppression and consequent hyperparathyroidism. In contrast, reduced serum FGF-23 levels are associated with hyperphosphatemia, higher calcitriol levels and parathyroid hormone (PTH) suppression. In addition, there are different FGF-23 actions that need investigation. In clinical practice, increased knowledge of mineral metabolism disorders alterations in chronic kidney disease (CKD) may be used to improve diagnostics and select future treatments. The discovery of FGF23 represents a novel factor in the pathogenesis of phosphate handling and secondary hyperparathyroidism in cardiovascular, bone and renal disease.

Keywords: FGF-23, chronic kidney disease, secondary hyperparathyroidism, phosphatonins, vascular calcification, klotho