Arterial Interactions with Mineral and Bone Disorders

Associated with deleterious changes in the structure and function damage to large arteries is a major risk factor contributing to the cardiovascular complications in hypertension, diabetes, chronic kidney disease, and chronic inflammatory diseases [1–3]. In many circumstances, these changes are in many aspects similar to those occurring with aging, with this age-related process accelerated and intensified in diabetes and chronic kidney disease (CKD) [4, 5]. Although atherosclerosis and plaque-associated occlusive lesions are the frequent underlying causes of these complications, the spectrum of arterial alterations is broader, including remodeling of large arteries and stiffening of arterial walls, with consequences that differ from those due to atherosclerotic plaques burden [6, 7]. Arterial stiffening is related to intrinsic changes in biophysical and geometric characteristics of arteries with increased calcium content and arterial calcifications (AC) as one of the most frequent consequences of arterial damage associated with deleterious changes in the structure and function of the arterial system [7–10]. AC are frequently associated with mineral and bone disorders which play an important pathophysiological role in the pathogenesis and progression of arterial damage [11–16]. Many studies showed that the extents of calcifications are associated with subsequent cardiovascular mortality and morbidity beyond established conventional risk factors [17–20].