Vascular calcification contributes to the high risk of cardiovascular mortality in CKD patients. Dysregulation of mineral metabolism, in particular elevated serum phosphate levels with associated abnormalities in phosphate-regulating hormones, is common in CKD patients, and is thought to drive vascular calcification. In this talk, I will review current concepts in the pathogenesis of vascular calcification in CKD, and highlight our recent experimental findings directed at understanding the mechanisms by which elevated phosphate promotes vascular calcification. The effects of elevated phosphate on vascular cell differentiation, apoptosis, and matrix degradation will be reviewed. We have identified sodium-dependent phosphate cotransporters as important mediators of vascular smooth muscle cell calcification in response to elevated phosphate, and data on their roles in these processes, including phosphate uptake-dependent and -independent pathways, will be presented. Unravelling the complex pathways involved in vascular calcification will ultimately provide novel targets and therapies to limit the deleterious effects of vascular calcification in CKD patients.