@article {10.3844/amjsp.2013.105.109,
article_type = {journal},
title = {Chronic Kidney Disease-Mineral Bone Disoder: Fibroblast Growth Factor-23 and Phosphate Metabolism},
author = {Cheungpasitporn, Wisit and Kue-A-Pai, Pongsathorn and Ungprasert, Patompong and Kittanamongkolchai, Wonngarm and Srivali, Narat and Ratanapo, Supawat and Jirajariyavej, Teeranun and Chongnarungsin, Daych and Kangwanpornsiri, Atipon},
volume = {4},
year = {2013},
month = {May},
pages = {105-109},
doi = {10.3844/amjsp.2013.105.109},
url = {https://thescipub.com/abstract/amjsp.2013.105.109},
abstract = {Chronic Kidney Disease (CKD) is a growing epidemic in the United States. There are hormonal changes that develop long before the mineral changes in patients with CKD occur. Increased Parathyroid Hormone (PTH) levels first become evident when the estimated Glomerular Filtration Rate (eGFR) is below 60 mL/min/1.73m2. High serum phosphate stimulates the secretion of the Fibroblast Growth Factor 23 (FGF-23) predominantly by bone osteocytes. Recent finding shows that chronically elevated FGF-23 levels in CKD patients are important for the high rates of LVH and the high rates of mortality. Managing phosphorus disorders with phosphate binders and secondary hyperparathyroidism with vitamin D analog and calcimimetics may theoretically reduce cardiovascular morbidity and mortality. We still need more studies on managing phosphorus disorders with phosphate binders, secondary hyperparathyroidism with vitamin D analog and calcimimetics and the outcome data on mortality and fractures in CKD patients.},
journal = {Current Research in Medicine},
publisher = {Science Publications}
}