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FGF23: a mature renal and cardiovascular risk factor?
Blood Purif. 2013; 36(1):52-7.BP

Abstract

High FGF23 predicts renal function loss in chronic kidney disease (CKD) patients and graft failure in transplant patients. FGF23, parathyroid hormone and serum phosphate are all interrelated but among these CKD-MBD biomarkers only FGF23 is independently related with CKD progression. High FGF23 associates with endothelial dysfunction in CKD patients and in elderly individuals in the general population. Furthermore, independently of serum phosphate, high FGF23 associates with mortality and left ventricular hypertrophy in dialysis patients and with atherosclerosis in elderly individuals in the general population. FGF23 also predicts a high risk for death and cardiovascular events in predialysis CKD patients and in subjects with coronary artery disease. A recent trial in CKD patients showed that low phosphate intake associated with a phosphate binder produces a 35% decrease in plasma FGF23. Yet in this and in another trial testing several phosphate binders, FGF23 levels remained well beyond the upper limit of the normal range. Of note, in this latter study, calcification of the coronary arteries and abdominal aorta actually increased, rather than decreased, during treatment with these drugs in the face of evidence of negative phosphate balance and amelioration of hyperparathyroidism. Mechanistic studies are still needed before testing the hypothesis that FGF23 is implicated in a causal manner in cardiovascular and renal diseases. Given the modest effects of phosphate binders on serum FGF23 in CKD patients, pharmacologic interventions antagonizing the effects of this growth factor rather than phosphate-lowering interventions should be put in place to properly test this hypothesis in the clinical scenario in CKD.

Authors+Show Affiliations

Nephrology, Hypertension and Renal Transplantation Division and CNR-IBIM Clinical Epidemiology of Renal Diseases and Hypertension, Ospedali Riuniti, Reggio Calabria, Italy. carmine.zoccali@tin.itNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

23735695

Citation

Zoccali, Carmine, et al. "FGF23: a Mature Renal and Cardiovascular Risk Factor?" Blood Purification, vol. 36, no. 1, 2013, pp. 52-7.
Zoccali C, Yilmaz MI, Mallamaci F. FGF23: a mature renal and cardiovascular risk factor? Blood Purif. 2013;36(1):52-7.
Zoccali, C., Yilmaz, M. I., & Mallamaci, F. (2013). FGF23: a mature renal and cardiovascular risk factor? Blood Purification, 36(1), 52-7. https://doi.org/10.1159/000351001
Zoccali C, Yilmaz MI, Mallamaci F. FGF23: a Mature Renal and Cardiovascular Risk Factor. Blood Purif. 2013;36(1):52-7. PubMed PMID: 23735695.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - FGF23: a mature renal and cardiovascular risk factor? AU - Zoccali,Carmine, AU - Yilmaz,Mahmut Ilker, AU - Mallamaci,Francesca, Y1 - 2013/05/25/ PY - 2013/6/6/entrez PY - 2013/6/6/pubmed PY - 2014/1/25/medline SP - 52 EP - 7 JF - Blood purification JO - Blood Purif VL - 36 IS - 1 N2 - High FGF23 predicts renal function loss in chronic kidney disease (CKD) patients and graft failure in transplant patients. FGF23, parathyroid hormone and serum phosphate are all interrelated but among these CKD-MBD biomarkers only FGF23 is independently related with CKD progression. High FGF23 associates with endothelial dysfunction in CKD patients and in elderly individuals in the general population. Furthermore, independently of serum phosphate, high FGF23 associates with mortality and left ventricular hypertrophy in dialysis patients and with atherosclerosis in elderly individuals in the general population. FGF23 also predicts a high risk for death and cardiovascular events in predialysis CKD patients and in subjects with coronary artery disease. A recent trial in CKD patients showed that low phosphate intake associated with a phosphate binder produces a 35% decrease in plasma FGF23. Yet in this and in another trial testing several phosphate binders, FGF23 levels remained well beyond the upper limit of the normal range. Of note, in this latter study, calcification of the coronary arteries and abdominal aorta actually increased, rather than decreased, during treatment with these drugs in the face of evidence of negative phosphate balance and amelioration of hyperparathyroidism. Mechanistic studies are still needed before testing the hypothesis that FGF23 is implicated in a causal manner in cardiovascular and renal diseases. Given the modest effects of phosphate binders on serum FGF23 in CKD patients, pharmacologic interventions antagonizing the effects of this growth factor rather than phosphate-lowering interventions should be put in place to properly test this hypothesis in the clinical scenario in CKD. SN - 1421-9735 UR - https://www.unboundmedicine.com/medline/citation/23735695/FGF23:_a_mature_renal_and_cardiovascular_risk_factor L2 - https://www.karger.com?DOI=10.1159/000351001 DB - PRIME DP - Unbound Medicine ER -