Epidemiological and clinical studies have shown that damage to large arteries contributes to the high cardiovascular mortality in patients with end-stage renal disease (ESRD). Atherosclerosis is the most frequent cause of arterial damage. Occlusive lesions from atherosclerotic plaques (calcification) decrease the conduit function of arteries and reduce the elasticity of capacitance arteries (stiffening), affecting their dampening function. Arterial calcification and aortic stiffness are independent predictors of cardiovascular risk in the general population, and independent predictors of all-cause and cardiovascular mortality in ESRD patients. Successful treatment to reduce blood pressure (BP) and reverse aortic stiffness has a significant, BP-independent effect on survival in ESRD patients. However, response to such treatment may be limited in patients with microinflammation and raised levels of C-reactive protein.