Cardiovascular complications are extremely frequent in patients with chronic kidney disease (CKD) and death from cardiac\ncauses is the most common cause of death in this particular population. Cardiovascular disease is approximately 3 times more\nfrequent in patients with CKD than in other known cardiovascular risk groups and cardiovascular mortality is approximately 10-\nfold more frequent in patients on dialysis compared to the age- and sex-matched segments of the nonrenal population. Among\nother structural and functional factors advanced calcification of atherosclerotic plaques as well as of the arterial and venous\nmedia has been described as potentially relevant for this high cardiovascular morbidity and mortality. One potential explanation\nfor this exceedingly high vascular calcification in animal models as well as in patients with CKD increased systemic and most\nimportantly local (micro)inflammation that has been shown to favor the development of calcifying particles by multiple ways. Of\nnote, local vascular up regulation of pro in flammatory and proosteogenic molecules is already present at early stages of CKD and\nmay thus be operative for vascular calcification. In addition, increased expression of costimulatory molecules and mast cells has\nalso been documented in patients with CKD pointing to a more inflammatory and potentially less stable phenotype of coronary\natherosclerotic plaques in CKD.
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