4 mortality,” Nephrology Dialysis Transplantation, vol. 18, no. 9, pp. 1731–1740, 2003. [4] F. Tentori, M. J. Blayney, J. M. Albert et al., “Mortality risk for dialysis patients With diﬀerent levels of serum calcium, phosphorus, and PTH: the dialysis outcomes and practice patterns study (DOPPS),” American Journal of Kidney Diseases, vol. 52, no. 3, pp. 519–530, 2008. [5] R. Wald, M. J. Sarnak, H. Tighiouart et al., “Disordered mineral metabolism in hemodialysis patients: an analysis of cumulative eﬀects in the hemodialysis (HEMO) study,” American Journal of Kidney Diseases, vol. 52, no. 3, pp. 531– 540, 2008. [6] R. Goetz, A. Beenken, O. A. Ibrahimi et al., “Molecular insights into the Klotho-dependent, endocrine mode of action of ﬁbroblast growth factor 19 subfamily members,” Molecular and Cellular Biology, vol. 27, no. 9, pp. 3417–3428, 2007. [7] T. Yamashita, “Structural and biochemical properties of ﬁbroblast growth factor 23,” Therapeutic Apheresis and Dial- ysis, vol. 9, no. 4, pp. 313–318, 2005. [8] M. Crestani, A. Sadeghpour, D. Stroup, G. Galli, and J. Y. L. Chiang, “Transcriptional activation of the cholesterol 7α- hydroxylase gene (CYP7A) by nuclear hormone receptors,” Journal of Lipid Research, vol. 39, no. 11, pp. 2192–2200, 1998. [9] A. Kharitonenkov, T. L. Shiyanova, A. Koester et al., “FGF-21 as a novel metabolic regulator,” Journal of Clinical Investiga- tion, vol. 115, no. 6, pp. 1627–1635, 2005. [10] M. Riminucci, M. T. Collins, N. S. Fedarko et al., “FGF- 23 in ﬁbrous dysplasia of bone and its relationship to renal phosphate wasting,” Journal of Clinical Investigation, vol. 112, no. 5, pp. 683–692, 2003. [11] A. Khosravi, C. M. Cutler, M. H. Kelly et al., “Determination of the elimination half-life of ﬁbroblast growth factor-23,” Journal of Clinical Endocrinology and Metabolism, vol. 92, no. 6, pp. 2374–2377, 2007. [12] H. Kurosu, Y. Ogawa, M. Miyoshi et al., “Regulation of ﬁbroblast growth factor-23 signaling by Klotho,” The Journal of Biological Chemistry, vol. 281, no. 10, pp. 6120–6123, 2006. [13] T. Nakatani, B. Sarraj, M. Ohnishi et al., “In vivo genetic evidence for klotho-dependent, ﬁbroblast growth factor 23 (Fgf23) -mediated regulation of systemic phosphate home- ostasis,” The FASEB Journal, vol. 23, no. 2, pp. 433–441, 2009. [14] M. S. Razzaque, D. Sitara, T. Taguchi, R. St-Arnaud, and B. Lanske, “Premature aging-like phenotype in ﬁbroblast growth factor 23 mice is a vitamin D-mediated process,” The FASEB Journal, vol. 20, no. 6, pp. 720–722, 2006. [15] S. Liu, L. Vierthaler, W. Tang, J. Zhou, and L. D. Quarles, “FGFR3 and FGFR4 do not mediate renal eﬀects of FGF23,” Journal of the American Society of Nephrology, vol. 19, no. 12, pp. 2342–2350, 2008. [16] E. G. Farrow, S. I. Davis, L. J. Summers, and K. E. White, “Ini- tial FGF23-mediated signaling occurs in the distal convoluted tubule,” Journal of the American Society of Nephrology, vol. 20, no. 5, pp. 955–960, 2009. [17] K. I. Miyamoto, H. Segawa, M. Ito, and M. Kuwahata, “Phys- iological regulation of renal sodium-dependent phosphate cotransporters,” Japanese Journal of Physiology, vol. 54, no. 2, pp. 93–102, 2004. [18] K. I. Miyamoto, M. Ito, M. Kuwahata, S. Kato, and H. Segawa, “Inhibition of intestinal sodium-dependent inorganic phos- phate transport by ﬁbroblast growth factor 23,” Therapeutic Apheresis and Dialysis, vol. 9, no. 4, pp. 331–335, 2005. [19] M. Ito, Y. Sakai, M. Furumoto et al., “Vitamin D and phosphate regulate ﬁbroblast growth factor-23 in K-562 cells,” International Journal of Nephrology American Journal of Physiology, vol. 288, no. 6, pp. E1101– E1109, 2005. [20] O. I. Kolek, E. R. Hines, M. D. Jones et al., “1α,25-dihydrox- yvitamin D upregulates FGF23 gene expression in bone: the ﬁnal link in a renal-gastrointestinal-skeletal axis that controls phosphate transport,” American Journal of Physiology, vol. 289, no. 6, pp. G1036–G1042, 2005. [21] D. M. Antoniucci, T. Yamashita, and A. A. Portale, “Dietary phosphorus regulates serum ﬁbroblast growth factor-23 con- centrations in healthy men,” Journal of Clinical Endocrinology and Metabolism, vol. 91, no. 8, pp. 3144–3149, 2006. [22] S. A. M. Burnett, S. C. Gunawardene, F. R. Bringhurst, H. J u¨ppner, H. Lee, and J. S. Finkelstein, “Regulation of C- terminal and intact FGF-23 by dietary phosphate in men and women,” Journal of Bone and Mineral Research, vol. 21, no. 8, pp. 1187–1196, 2006. [23] N. Ito, S. Fukumoto, Y. Takeuchi et al., “Eﬀect of acute changes of serum phosphate on ﬁbroblast growth factor (FGF)23 levels in humans,” Journal of Bone and Mineral Metabolism, vol. 25, no. 6, pp. 419–422, 2007. [24] T. Krajisnik, P. Bjo¨rklund, R. Marsell et al., “Fibroblast growth factor-23 regulates parathyroid hormone and 1α-hydroxylase expression in cultured bovine parathyroid cells,” Journal of Endocrinology, vol. 195, no. 1, pp. 125–131, 2007. [25] T. Shimada, H. Hasegawa, Y. Yamazaki et al., “FGF-23 is a potent regulator of vitamin D metabolism and phosphate homeostasis,” Journal of Bone and Mineral Research, vol. 19, no. 3, pp. 429–435, 2004. [26] T. Kawata, Y. Imanishi, K. Kobayashi et al., “Parathyroid hor- mone regulates ﬁbroblast growth factor-23 in a mouse model of primary hyperparathyroidism,” Journal of the American Society of Nephrology, vol. 18, no. 10, pp. 2683–2688, 2007. [27] S. Liu, W. Tang, J. Zhou et al., “Fibroblast growth factor 23 is a counter-regulatory phosphaturic hormone for vitamin D,” Journal of the American Society of Nephrology, vol. 17, no. 5, pp. 1305–1315, 2006. [28] R. Marsell, E. Grundberg, T. Krajisnik et al., “Fibroblast growth factor-23 is associated with parathyroid hormone and renal function in a population-based cohort of elderly men,” European Journal of Endocrinology, vol. 158, no. 1, pp. 125– 129, 2008. [29] M. Roos, J. Lutz, H. Salmhofer et al., “Relation between plasma ﬁbroblast growth factor-23, serum fetuin-A levels and coronary artery calciﬁcation evaluated by multislice computed tomography in patients with normal kidney function,” Clinical Endocrinology, vol. 68, no. 4, pp. 660–665, 2008. [30] O. Gutierrez, T. Isakova, E. Rhee et al., “Fibroblast growth factor-23 mitigates hyperphosphatemia but accentuates cal- citriol deﬁciency in chronic kidney disease,” Journal of the American Society of Nephrology, vol. 16, no. 7, pp. 2205–2215, 2005. [31] T. Larsson, U. Nisbeth, O¨ . Ljunggren, H. J u¨ppner, and K. B. Jonsson, “Circulating concentration of FGF-23 increases as renal function declines in patients with chronic kidney disease, but does not change in response to variation in phosphate intake in healthy volunteers,” Kidney International, vol. 64, no. 6, pp. 2272–2279, 2003. [32] D. Fliser, B. Kollerits, U. Neyer et al., “Fibroblast Growth Factor 23 (FGF23) predicts progression of chronic kidney disease: the mild to moderate kidney disease (MMKD) study,” Journal of the American Society of Nephrology, vol. 18, no. 9, pp. 2600–2608, 2007.