Fibroblast growth factor 23 and adverse clinical outcomes in chronic kidney diseaseIsakova, TamaraCurrent Opinion in Nephrology and Hypertension: May 2012 - Volume 21 - Issue 3 - p 334–340 doi: 10.1097/MNH.0b013e328351a391 EPIDEMIOLOGY AND PREVENTION: Edited by Chi-yuan Hsu Buy Abstract Author InformationAuthors Article MetricsMetrics Purpose of review The aim is to review data on the epidemiology of fibroblast growth factor 23 (FGF23) and adverse clinical outcomes in chronic kidney disease (CKD) and introduce recent insights into the pathophysiology behind the observed relationships. Recent findings End-stage renal disease and cardiovascular disease are frequent events in patients with CKD, in whom cardiovascular disease is the leading cause of death. Elevated levels of FGF23, a phosphate and vitamin D-regulating hormone, have been associated with risks of end-stage renal disease, cardiovascular disease and mortality. FGF23 excess has also been linked with left-ventricular hypertrophy, and innovative translational experiments have recently established direct end-organ toxicity of FGF23, which induced left-ventricular hypertrophy in animals. Summary FGF23 is emerging as a novel risk factor in CKD. Future studies should determine whether interventions that lower FGF23 levels improve clinical outcomes in CKD. Division of Nephrology and Hypertension, Department of Medicine, University of Miami, Miller School of Medicine, Florida, USA Correspondence to Tamara Isakova, Division of Nephrology and Hypertension, Department of Medicine, University of Miami, Miller School of Medicine, 1120 NW 14th St., Suite 822, Miami, FL 33136, USA. Tel: +1 305 243 4374; fax: +1 305 243 8914; e-mail: firstname.lastname@example.org © 2012 Lippincott Williams & Wilkins, Inc.