Arterial stiffness in dialysis patients: where are we now?

Patients with end-stage renal disease treated by chronic dialysis have an impressive mortality, which more than half of this mortality is attributable to cardiovascular disease. Despite stratification for sex, race, and the presence of diabetes, cardiovascular disease mortality is 10–30 times higher in dialysis patients compared to general population. In dialysis patients, both atherosclerosis (mainly affecting the intima of the arteries) and arteriosclerosis (affecting predominantly the media of large- and middle-sized arteries diffusely) are highly prominent. Arteriosclerosis characterized by reduced arterial compliance (i.e., reduced elasticity of the arteries) is due to increased fibrosis, loss of elastic fibers, and extensive vessel wall calcification. Arteriosclerosis is closely related to arterial stiffness. A generally accepted mechanistic view is that an increase in arterial stiffness causes a premature return of reflected waves in late systole, increasing central pulse pressure, thus systolic. An increased arterial stiffness can increase the risk of stroke through several mechanisms, including an increase in central pulse pressure, influencing arterial remodeling both at the site of the extracranial and intracranial arteries, increasing carotid wall thickness, and the development of stenosis and plaques, and the likelihood of plaque rupture. Very importantly, it was also suggested that arterial stiffness itself independently plays a role in exacerbating chronic kidney disease progression. This review deals briefly with the definition of arterial stiffness, methods of measuring arterial stiffness and pathophysiology of arterial stiffness, and factors related with arterial stiffness.