Cardiovascular (CV) morbidity and mortality is greatly enhanced in patients with chronic kidney disease, compared to the non-renal population. One key element of this high CV burden appears to be arterial stiffness, as an expression of premature vascular aging. Increased arterial stiffness in renal patients may be a consequence of vascular calcification, chronic volume overload, inflammation, endothelial dysfunction, oxidative stress and several other factors. The authors review briefly the main pathophysiological mechanisms leading to reduced arterial compliance. Increased arterial stiffness has significant clinical consequences: isolated systolic hypertension, left ventricular hypertrophy (and failure), and reduced myocardial perfusion. Better knowledge of the mechanisms of arterial functional and morphologic alteration may help in developing more refined therapeutic strategies aimed to reduce the high CV burden in chronic kidney disease. The potential therapeutic interventions - mainly the use of certain antihypertensive drugs and reduction of vascular calcification - are finally discussed.