Volume 79, Pages S24-S27 (April 2011)

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Volume 79, Pages S24-S27 (April 2011) Phosphate and FGF-23  Harald Jüppner  Kidney International  Volume 79, Pages S24-S27 (April 2011) DOI: 10.1038/ki.2011.27 Copyright © 2011 International Society of Nephrology Terms and Conditions

Figure 1 Spectrum of serum fibroblast growth factor (FGF)-23 levels in early chronic kidney disease and end-stage renal disease (ESRD) as compared with the normal condition and with different disorders affecting FGF-23. ADHR, autosomal dominant hypophosphatemic rickets; ARHP, autosomal recessive hypophosphatemia; TIO, tumor-induced osteomalacia; XLH, X-link ed hypophosphatemia. Adapted with permission from Isakova et al.20 Kidney International 2011 79, S24-S27DOI: (10.1038/ki.2011.27) Copyright © 2011 International Society of Nephrology Terms and Conditions

Figure 2 Mortality in patients with end-stage renal disease (ESRD) receiving hemodialysis in relationship to quartiles of serum fibroblast growth factor (FGF)-23 concentration at initiation of dialysis. R, reference. Reproduced with permission from Gutiérrez et al.23 Copyright The Massachusetts Medical Society. Kidney International 2011 79, S24-S27DOI: (10.1038/ki.2011.27) Copyright © 2011 International Society of Nephrology Terms and Conditions

Figure 3 ‘Trade-off hypothesis’ revisited. Involvement of fibroblast growth factor (FGF)-23 in end-stage renal disease (ESRD) pathology, reflecting potentially adverse effects of increased secretion of this phosphaturic hormone, which helps normalize phosphate homeostasis but contributes to the development of secondary hyperparathyroidism. PTH, parathyroid hormone. Kidney International 2011 79, S24-S27DOI: (10.1038/ki.2011.27) Copyright © 2011 International Society of Nephrology Terms and Conditions