Fibroblast growth factor 23: a potential cause of cardiovascular diseases in chronic kidney disease patients

Abstract

Fibroblast growth factor 23 (FGF-23) has been identified as one of the risk factors for the development of cardiovascular diseases (CVDs) in chronic kidney disease (CKD) patients. Although FGF-23 is necessary for the maintenance of phosphate balance, it has been implicated in the pathogenesis of left ventricular hypertrophy, vascular dysfunction, and hypertension in CKD patients. FGF-23 induced alterations in intracellular calcium is hypothesized to be a key mechanism in the development of these CVDs. In addition, increased angiotensin II levels, upregulation of the renal Na⁺Cl^- co-transporter and inhibition of endothelium-dependent vasorelaxation are among the potential mechanisms by which elevated FGF-23 levels cause hypertension in CKD. This review discusses these mechanisms and how these mechanistic pathways may be targeted in future experiments aimed at generating preventive and management therapies for CVDs in CKD patients.

Keywords: Fibroblast growth factor 23, Chronic Kidney Disease and Cardiovascular Disease