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FGF-23: the rise of a novel cardiovascular risk marker in CKD
Author(s) -
Gunnar H. Heine,
Sarah Seiler,
Danilo Fliser
Publication year - 2012
Publication title -
nephrology dialysis transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.654
H-Index - 168
eISSN - 1460-2385
pISSN - 0931-0509
DOI - 10.1093/ndt/gfs259
Subject(s) - medicine , fibroblast growth factor 23 , kidney disease , dialysis , hemodialysis , intensive care medicine , epidemiology , risk factor , pathogenesis , disease , endocrinology , parathyroid hormone , calcium
Elevated plasma levels of the phosphaturic hormone fibroblast growth factor 23 (FGF-23) are a hallmark of chronic kidney disease (CKD)-mineral and bone disorder. FGF-23 allows serum phosphate levels within physiological limits to be maintained in progressive CKD until end-stage renal disease is reached. Despite its seemingly beneficial role in phosphate homeostasis, several prospective studies in dialysis patients and in patients with less advanced CKD associated elevated FGF-23 with poor cardiovascular and renal outcome. Moreover, very recent evidence suggests an adverse prognostic impact of elevated FGF-23 even in subjects without manifest CKD. These epidemiological data are supplemented by laboratory findings that reveal a pathophysiological role of FGF-23 in the pathogenesis of myocardial injury. In aggregate, these clinical and experimental data identify FGF-23 as a promising target of novel therapeutic interventions in CKD and beyond, which should be tested in future clinical trials.

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