Arterial calcification: cardiovascular function and clinical outcome.

G M London

Journal: Nefrologia : publicacion oficial de la Sociedad Espanola Nefrologia 2012;31(6):644-7

PMID: 22130278

Free Full Text on Ediciones Doyma, S.L. View on PubMed

Abstract

Arterial calcification (AC) is a common complication of CKD and ESRD, and the extents of AC are predictive of subsequent cardiovascular mortality beyond established conventional risk factors. AC develop in two distinct sites: the intima and media layers of the large and medium-sized arterial wall. These two forms are frequently associated. AC is tightly associated with aging and arterial remodeling, including intima-media thickening, but also changes of the geometry and function of aortic valves. Evidence has accumulated pointing to the active and regulated nature of the calcification process. Elevated phosphate and calcium may stimulate sodium–dependent phosphate cotransport involving osteoblast–like changes in cellular gene expression. AC is responsible for stiffening of the arteries with increased left ventricular afterload and abnormal coronary perfusion as the principal clinical consequences.

Address: INSERM U970, Paris and Hopital F.H. Manhès, Fleury-Mérogis, France. [email protected]

DOI: 10.3265/Nefrologia.pre2011.Oct.11175

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MeSH Terms: Arterial Occlusive Diseases, Atherosclerosis, Calcinosis, Calcium, Cell Differentiation, Chronic Disease, Core Binding Factor Alpha 1 Subunit, Gene Expression Regulation, Humans, Kidney Diseases, Kidney Failure, Chronic, Muscle, Smooth, Vascular, Osteoblasts, Phosphates, Sp7 Transcription Factor, Transcription Factors, Tunica Intima, Tunica Media, Vascular Resistance, Ventricular Dysfunction, Left