Fibroblast Growth Factor - 23 (FGF-23) e Cardiorenal Syndrome

Abstract

Several abnormalities in chronic kidney disease-related mineral and bone disease (CKD-MBD) have emerged as novel risk factors in excess cardiovascular mortality in patients with CKD and end-stage renal disease (ESRD). Hyperphosphatemia, vascular calcifications development, and decreased active vitamin D production, leading to activation of the renin angiotensin system (RAS), have been identified as the primary cause of CKD-MBD-associated mortality in CKD. Recently, the fibroblast growth factor-23 (FGF-23), a newly discovered hormone produced in the bone that regulates phosphate and vitamin D metabolism by the kidney, has been reported as a strong predictor of adverse cardiovascular outcomes in patients with CKD and ESRD. The main physiological functions of FGF-23 are mediated by the activation of the FGF receptor/α-klotho co-receptor complexes in target tissues. Elevated FGF-23 has been associated with left ventricular hypertrophy (LVH), and it has been suggested that FGF-23 may induce myocardial hypertrophy through a direct effect on cardiac myocytes. Understanding of FGF-23's pathophysiology and mechanisms of action responsible for its negative effects will be necessary to develop therapeutic strategies to treat CKD-MBD. (Cardionephrology)