Abstract
Cardiovascular complications are extremely frequent in patients with chronic kidney disease (CKD) and death from cardiac causes is the most common cause of death in this particular population. Cardiovascular disease is approximately 3 times more frequent in patients with CKD than in other known cardiovascular risk groups and cardiovascular mortality is approximately 10-fold more frequent in patients on dialysis compared to the age- and sex-matched segments of the nonrenal population. Among other structural and functional factors advanced calcification of atherosclerotic plaques as well as of the arterial and venous media has been described as potentially relevant for this high cardiovascular morbidity and mortality. One potential explanation for this exceedingly high vascular calcification in animal models as well as in patients with CKD increased systemic and most importantly local (micro)inflammation that has been shown to favor the development of calcifying particles by multiple ways. Of note, local vascular upregulation of proinflammatory and proosteogenic molecules is already present at early stages of CKD and may thus be operative for vascular calcification. In addition, increased expression of costimulatory molecules and mast cells has also been documented in patients with CKD pointing to a more inflammatory and potentially less stable phenotype of coronary atherosclerotic plaques in CKD.
Highlights
Patients with chronic kidney disease (CKD) and chronic renal failure (CRF) develop early on in the course of the disease structural and functional alterations of the heart and the vascular tree that represent a major clinical problem in these patients
It is speculated that dendritic cells (DCs) activation by nicotine, stress, hypoxia, or C-reactive protein (CRP) may stimulate the local immune response [61]. This might be of interest in view of our previous finding of an increased in situ expression of CRP in atherosclerotic plaques of CKD patients compared to controls [46]
Advanced stages of atherosclerotic plaques with plaque and vessel calcification are specific features in patients with CKD that might contribute to the high cardiovascular morbidity and mortality in these patients
Summary
Patients with chronic kidney disease (CKD) and chronic renal failure (CRF) develop early on in the course of the disease structural and functional alterations of the heart and the vascular tree that represent a major clinical problem in these patients. In addition to the cardiac alterations specific structural changes of the extracardiac arteries and veins are present which consist of vessel thickening (Figures 1(a) and 1(b)) but more importantly of marked calcification of the arterial intima and media as well as of venous walls and atherosclerotic coronary plaques giving rise to complications such as coronary artery thrombosis and myocardial infarction [14,15,16,17,18] Based on their clinical experience the group of Lindner and coworkers in 1974 [19] were the first to show that atherosclerosis in CKD patients is different from that of nonrenal patients.
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