Arterial structure and function in end-stage renal disease

Abstract

Summary Cardiovascular disease (CVD) is a major cause of morbidity and mortality in patients with end-stage renal disease (ESRD). The risk of CVD disease in these patients appears to be far greater than in the general population and even after the stratification for age, gender, race and the presence or absence of diabetes, cardiovascular mortality in dialysis patients is about 10 to 20 times higher than in the general population. As a diagnostic categorie, CVD includes two principal conditions, i.e., cardiac complications stricto sensu , and vascular complications. These two complications are interrelated and arterial alterations can be the primary reason for the development of cardiac complications. Macrovascular disease develops rapidly in ESRD patients and is responsible for the high incidence of congestive heart failure, left ventricular hypertrophy (LVH), ischemic heart disease, sudden death, cerebrovascular accidents and peripheral artery diseases. Although the most frequent cause of these complications is occlusive lesions due to atheromatous plaques, many complications arise in ESRD patients in the absence of clinically significant atherosclerotic disease. Atherosclerosis, disease characterized by the presence of plaques, represents only one form of structural response to metabolic and hemodynamic alterations which interfere with the “natural” process of aging. The spectrum of arterial alterations in ESRD is broader, including large artery remodeling and changes in viscoelastic properties of arterial walls. The consequences of these alterations are different from those attibuted to plaques. While atheromatous lesions alter principally the conduit function of arteries and perfusion of tissue and organs downstream the lesions, non-atheromatous remodelling result principally in changes in dampening function of arteries, characterized by stiffening of arterial walls and with deleterious effects on the left ventricle and coronary perfusion. Arterial stiffening in ESRD patients is multifactorial at origin with extensive arterial calcifications as an important covariate.