Phosphate, pyrophosphate, and vascular calcification: a question of balance.

Abstract

Vascular calcification (VC), the pathological calcification of cardiovascular structures, is one of the most important factors determining patients' mortality around the world. Although different mechanisms on pathogenesis of vascular calcification have been proposed,1 our understanding of the calcification pathogenesis is far from complete. However, in recent years, some risk factors are emerging, including elevated serum phosphorus and defective synthesis of pyrophosphate.2 The presence of calcium phosphate crystals (CPCs) in blood vessels ( Figure 1 ), myocardium, cardiac valves, and others soft tissues is considered a pathological or ectopic calcification.1 However, the accumulation of CPC in hard tissues (such as bone and teeth) is considered a physiological process. In blood vessels, calcified deposits are found in distinct layers of the aortic wall. Intimal calcification occurs in atherosclerotic lesions, whereas medial calcification (so-called Monckeberg's medial sclerosis) occurs in medial layer of the aortic wall and is associated with elastic lamin.2 Figure 1 Representative images of typical vascular calcifications. ( A ) Computerized tomography (CT) angiography: 3D volume-rendered image shows calcification in the aortic-iliac axis (white) in a haemodialysis patient. ( B – D ) Curved MIP (maximum intensity projection) views. Cardiac-CT scan shows calcification in the right coronary artery ( B ) and in the Cx and LAD ( C ) (arrows). ( D ) Supra-aortic CT scan shows calcification in the internal and common carotid arteries (arrows). Ao, Aorta; RCA, right coronary artery; LAD, left anterior descending artery; Cx, circumflex artery; LM, left main artery; SA, subclavian artery; CCA, common carotid artery; ICA, internal carotid artery; ECA, external carotid artery. The physicochemical process of CPC formation is similar both in hard (bone) and soft tissues (vessels). However, in physiological conditions, CPC deposition is enhanced or inhibited …