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Clinical consequences of arterial calcifications and soft-tissue calcifications in chronic kidney disease 

Clinical consequences of arterial calcifications and soft-tissue calcifications in chronic kidney disease
Chapter:
Clinical consequences of arterial calcifications and soft-tissue calcifications in chronic kidney disease
Author(s):

Gérard M. London

, Bruno Pannier

, Alain P. Guerin

, and Sylvain J. Marchais

DOI:
10.1093/med/9780199559176.003.018
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date: 28 February 2020

The arterial calcifications from an active process implicating the interaction of promoters and inhibitors of calcifications that are responsible for phenotype transdiferentiation of vascular smooth muscle cells into ostoblast-like osteogenic cells. This process is influenced by mechanical factors including pulsatile and shear stresses. The two types of calcifications, i.e. intimal and medial have a different impact on arterial functions. The intimal calcification as a part of advanced atherosclerosis results in the development of plaques, arterial lumen decrease or occlusion, and ischemic lesions downstream. Medial calcifications result in the stiffening of arterial walls with an increased systolic and decreased diastolic pressures. This leads to cardiac pressure overload, left ventricular hypertrophy and decreased myocardial perfusion. The two types of calcifications are associated with increased mortality.

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