Both vascular calcification and inflammation are common in patients with chronic kidney disease (CKD). In patients on dialysis, there is increased coronary artery and peripheral artery calcification compared to the general population. Both intimal (atherosclerotic) and medial calcification in CKD patients are associated with increased morbidity and mortality. Vascular calcification is an active cell-mediated process, and likely reflects a transformation of vascular smooth muscle cells to osteoblast-like cells. Pooled uremic serum can induce this transformation, but the mechanism by which it does so is not yet clear. Several mediators of inflammation such as oxidation, carbonyl stress, C-reactive protein, and cytokines may directly stimulate vascular calcification. In addition, inflammation itself reduces fetuin-A, a naturally occurring inhibitor of vascular calcification which binds excess mineral in serum. The combination of the acceleration of vascular calcification together with impaired defense mechanisms creates a uremic milieu primed for extra-osseous calcification.