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Nephrol. Dial. Transplant. · Aug 2012
ReviewFGF-23: the rise of a novel cardiovascular risk marker in CKD.
- Gunnar H Heine, Sarah Seiler, and Danilo Fliser.
- Department of Internal Medicine IV—Nephrology and Hypertension, Saarland University Medical Center, Homburg/Saar, Germany. Gunnar.Heine@uks.eu
- Nephrol. Dial. Transplant. 2012 Aug 1; 27 (8): 3072-81.
AbstractElevated 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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