Chronic kidney disease (CKD) is a growing public health epidemic that is associated with a markedly increased risk of cardiovascular mortality. Disordered mineral metabolism and particularly, disordered phosphorus metabolism appears to be a contributing factor. Fibroblast growth factor 23 (FGF23) regulates phosphorus and vitamin D metabolism. Its levels increase progressively beginning in early CKD, presumably as a physiological adaptation to maintain normal serum phosphate levels or normal phosphorus balance. FGF23 promotes phosphaturia and decreases production of calcitriol. Recent studies suggest that increased FGF23 is associated with mortality, left ventricular hypertrophy, endothelial dysfunction and progression of CKD. These results were consistently independent of serum phosphate levels. At the very least, FGF23 is emerging as a novel biomarker that may help identify which CKD patients might benefit most from aggressive management of disordered phosphorus metabolism. It is also possible that markedly increased FGF23 levels in CKD could contribute directly to tissue injury in the heart, vessels and kidneys, an exciting question that is sure to be the topic of intense investigation in the near future.