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NDT Advance Access originally published online on July 2, 2009
Nephrology Dialysis Transplantation 2009 24(9):2618-2620; doi:10.1093/ndt/gfp323
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© The Author [2009]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org


As nature did not predict dialysis—what we can learn from FGF23 in end-stage renal disease?

Markus Ketteler and Patrick H. Biggar

Division of Nephrology, Klinikum Coburg, Coburg, Germany

Correspondence and offprint requests to: Markus Ketteler; E-mail: markus.ketteler@klinikum-coburg-de

Keywords: calcification; dialysis; FGF23; hyperphosphataemia; mortality

The first 10% of the full text of this article appears below.

The fibroblast growth factor 23 (FGF23)/klotho system has raised a lot of attention in the past 10 years. Genetic knockout models demonstrated that failure of this system produces a phenotype of premature ageing and especially a failure to excrete phosphate resulting in significant hyperphosphataemia and vascular calcification [1,2]. FGF23 is synthesized in the bone, and osteocytes increase FGF23 production in response to elevated phosphate and calcitriol [3]. Therefore, FGF23 may be a key adaptive factor preventing early hyperphosphataemia in progressive chronic kidney disease (CKD). In the preterminal phases of CKD, FGF23 may become a valuable biomarker of phosphate load and phosphate exposure, perhaps analogous to the predictive value of HbA1C in the evaluation of diabetes control.

The central target organ of FGF23 appears to be the kidney, where tubular phosphate reabsorption and 1-alpha-hydroxylase expression are suppressed. These features raised the . . . [Full Text of this Article]


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