Endocrine Abstracts

The discovery that mutations in fibroblast growth factor 23 (FGF23) cause autosomal dominant hypophosphatemic rickets transformed our understanding of phosphate homeostasis in health and disease (White et al. Nat Genet 2000). Since then, the critical role of FGF23 in mineral metabolism in chronic kidney disease has been established (Larsson et al. Kidney Int 2003; Gutierrez et al. J Am Soc Nephrol 2005). Elevated FGF23 has emerged as the earliest alteration of disordered mineral metabolism in chronic kidney disease (Isakova et al. Kidney Int 2011). Several studies now demonstrate that elevated FGF23 is also a novel biomarker of risk for CKD progression, adverse cardiovascular outcomes and death among patients with chronic kidney disease (Fliser et al. J Am Soc Nephrol 2007; Gutierrez et al. N Engl J Med 2008; Isakova et al. JAMA 2011; Kendrick et al. J Am Soc Nephrol 2011; Jean et al. Nephrol Dial Transplant 2009). More recently, FGF23 was demonstrated to contribute mechanistically to development of left ventricular hypertrophy, which may underlie an important component of the association of elevated FGF23 levels with high risk of cardiovascular events (Faul et al. J Clin Invest 2011; Scialla et al. J Am Soc Nephrol 2013). These studies elevated FGF23 and disordered phosphate homeostasis from powerful biomarker to novel mechanism of cardiovascular disease in chronic kidney disease. This session will describe the latest data on FGF23 in chronic kidney disease with specific emphasis on the role of FGF23 in cardiovascular disease.