Atherosclerosis, once present, in the intimal and medial spaces of the blood vessel wall becomes calcified due to a variety of cellular and metabolic processes. Patients with chronic kidney disease (CKD) appear to have both accelerated and amplified vascular calcification compared with the general population. Calcium deposition within vascular tissue in the form of calcium hydroxyapatite crystals appears to be a permanent step in the mature atherosclerotic plaque, and to date has not been found to be reversible or modifiable with common treatments for atherosclerosis or dialysis management strategies. Densely calcified lesions with a circumferential arc of calcium around the vessel wall may be severely stenotic, however, are unlikely to develop symptomatic plaque rupture with an acute coronary syndrome. For that reason, the expected outcomes of atherosclerotic therapies in patients with CKD bone and mineral disorder have not followed the same rules of evidence. This paper will review the differences between the CKD and general population with respect to vascular calcification and the observed natural history in observational and interventional studies.