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.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
