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Nephrol Dial Transplant. 2016 Jan;31(1):31-9. doi: 10.1093/ndt/gfv111. Epub 2015 Apr 26.

Vascular calcification in chronic kidney disease: an update.

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Department of Nephrology, RWTH University of Aachen, Aachen, Germany.
Department of Biochemistry, Faculty of Medicine, Health and Life Science, Maastricht, The Netherlands.
Department of Cardiology, RWTH University of Aachen, Aachen, Germany.


Cardiovascular calcification is both a risk factor and contributor to morbidity and mortality. Patients with chronic kidney disease (and/or diabetes) exhibit accelerated calcification of the intima, media, heart valves and likely the myocardium as well as the rare condition of calcific uraemic arteriolopathy (calciphylaxis). Pathomechanistically, an imbalance of promoters (e.g. calcium and phosphate) and inhibitors (e.g. fetuin-A and matrix Gla protein) is central in the development of calcification. Next to biochemical and proteinacous alterations, cellular processes are also involved in the pathogenesis. Vascular smooth muscle cells undergo osteochondrogenesis, excrete vesicles and show signs of senescence. Therapeutically, measures to prevent the initiation of calcification by correcting the imbalance of promoters and inhibitors appear to be essential. In contrast to prevention, therapeutic regression of cardiovascular calcification in humans has been rarely reported. Measures to enhance secondary prevention in patients with established cardiovascular calcifications are currently being tested in clinical trials.


MGP; VSMC; cardiovascular diseases; phenotype switch; vitamin K

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