Fibroblast Growth Factor-23 Fans the Flames of Heart and Kidney Failure.

SEE PAGE 829 C hronic kidney disease (CKD) promotes cardiac injury, and heart failure begets kidney injury. Although shared risk factors such as diabetes, hypertension, and atherosclerosis are wellknown igniters of the combustible interaction between chronic heart and kidney diseases, identification of the accelerants that drive the full-fledged public health conflagration of “cardiorenal” disease is a hot area of investigation. At the nexus of heart and kidney diseases, elevated levels of the bone-derived, phosphate-regulating hormone fibroblast growth factor (FGF)-23 has emerged as a novel candidate accelerant. FGF-23 levels increase early in the course of CKD and are strongly predictive of cardiovascular events and death, independently of traditional and CKD-specific risk factors (1,2). As a putative underlying molecular mechanism, laboratory data suggest that elevated FGF-23 can injure cardiac myocytes through a novel aKlotho–independent pathway that results in left ventricular hypertrophy (3). Reflecting the bidirectional role of FGF-23 in cardiovascular and kidney diseases, pre-existing heart disease is now increasingly recognized as another leading cause of chronically elevated FGF-23. Although it is currently