Fibroblast Growth Factor 23 and CKD Prognosis Navdeep Tangri, MD, FRCPC, Andrew S. Levey, MD  American Journal of Kidney Diseases  Volume 59, Issue 5, Pages 607-610 (May 2012) DOI: 10.1053/j.ajkd.2011.11.017 Copyright © 2012 National Kidney Foundation, Inc. Terms and Conditions

Figure 1 Endocrine regulation of phosphate homeostasis. Ten years ago, 2 principal calcium-regulating hormones, 1,25 dihydroxyvitamin D3 (vitamin D) and parathyroid hormone (PTH), were thought to regulate phosphate metabolism. PTH increases vitamin D synthesis in the kidney ①. Vitamin D in turn decreases PTH ②, thereby closing a negative feedback loop. Now the fibroblast growth factor 23 (FGF-23)–klotho system has emerged as the principal phosphate-regulating endocrine axis. FGF-23 is secreted from bone and acts on kidney to decrease vitamin D synthesis ③. Because vitamin D increases FGF-23 expression in bone ④, a negative-feedback loop exists between FGF-23 and vitamin D. FGF-23 also acts on parathyroid to decrease PTH ⑤. Because PTH increases FGF-23 expression ⑥, another negative-feedback loop exists between PTH and FGF-23. Reproduced and adapted from Kuro-o8 and John et al9 with permission of Macmillan Publishers Ltd and the National Kidney Foundation, respectively. American Journal of Kidney Diseases 2012 59, 607-610DOI: (10.1053/j.ajkd.2011.11.017) Copyright © 2012 National Kidney Foundation, Inc. Terms and Conditions