Arterial alterations in end-stage renal disease include large artery remodeling and stiffening, driven by multifactorial causes including extensive arterial calcifications.
Cardiovascular morbidity in ESRD is driven not only by atherosclerosis but also by nonatheromatous arterial remodeling and stiffening.
Cardiovascular disease is a major cause of morbidity and mortality in patients with end-stage renal disease (ESRD). Macrovascular disease develops rapidly in ESRD patients and is responsible for the high incidence of left ventricular hypertrophy, ischemic heart disease, cerebrovascular accidents, and peripheral artery diseases. Occlusive lesions due to atheromatous plaques frequently cause these complications; however, atherosclerosis represents only one form of structural response to metabolic and hemodynamic alterations interfering with the “natural” process of aging. The spectrum of arterial alterations in ESRD is broader, including large artery remodeling, changes in viscoelastic properties, and stiffening of arterial walls. Nonatheromatous remodeling principally changes the dampening function of arteries, characterized by stiffening of arterial walls and with deleterious effects on the left ventricle and coronary perfusion. The origin of arterial stiffening in ESRD patients is multifactorial, with extensive arterial calcifications as an important covariate.
G. London (Tue,) conducted a review in End-stage renal disease (ESRD). Arterial alterations in end-stage renal disease include large artery remodeling and stiffening, driven by multifactorial causes including extensive arterial calcifications.