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Analysis of Minerals Produced by hFOB 1.19 and Saos-2 Cells Using Transmission Electron Microscopy with Energy Dispersive X-ray Microanalysis
Published on: June 24, 2018
FGF23: a key player in mineral and bone disorder in CKD
1Division of Nephrology and Kidney Center, Kobe University School of Medicine, Kobe, Japan.
Abstract:
FGF23 is a recently identified hormone regulating mineral and vitamin D metabolism. In patients with chronic kidney disease (CKD), circulating FGF23 levels are progressively elevated to compensate for persistent phosphate retention, which result in reduced renal production of 1,25-dihydroxyvitamin D and thereby stimulate secretion of parathyroid hormone, suggesting its critical role in the pathogenesis of altered mineral homeostasis in CKD. Furthermore, it has recently been shown that FGF23 directly acts on parathyroid gland and mediate secretion of parathyroid hormone in the presence of Klotho as a cofactor, although such effects are not yet confirmed in patients with CKD. FGF23 can also be used as a predictor of mortality as well as future development of refractory hyperparathyroidism in patients undergoing dialysis therapy, where FGF23 levels are markedly elevated in response to hyperphosphatemia and active vitamin D treatment. This brief review summarizes recent insights into the role of FGF23 in the pathogenesis of mineral and bone disorders in CKD.
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