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International Journal of Nephrology
Volume 2018, Article ID 4310379, 7 pages
Review Article

Vascular Calcification in Chronic Kidney Disease: The Role of Inflammation

1Department of Nephropathology, Friedrich-Alexander University (FAU) Erlangen-Nürnberg, Germany
2Department of Nephrology and Hypertension, Friedrich-Alexander University (FAU) Erlangen-Nürnberg, Germany

Correspondence should be addressed to Kerstin Amann; ed.negnalre-ku@nnama.nitsrek

Received 18 April 2018; Accepted 24 July 2018; Published 13 August 2018

Academic Editor: Nicolas Verheyen

Copyright © 2018 Kerstin Benz et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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.