Arterial accelerated aging in dialysis patients: the clinical impact of vascular calcification.

Chronic Kidney Disease Mineral and Bone Disorder (CKD-MBD) is a systemic disorder of mineral and bone metabolism that occurs in Chronic Kidney Disease (CKD). In addition to abnormalities in serum calcium (Ca) and phosphate (P) profile, CKD-MBD is characterized by abnormalities of bone turnover, mineralization, volume and growth as well as vascular calcification (VC). Indeed, the co-localization of bone markers such as Osteopontin, Alkaline Phosphatase and Osteocalcin along with osteoblast-like cells in the contest of the arterial wall of uremic patients, indicate that VC is an active biological process with peculiar analogies with bone mineralization. Thus, VC represents a plausible link between Ca and P derangements and the increased mortality associated with CKD-MBD. The process of VC starts in early stages of CKD and patients with CKD-3, -4 and -5 not undergoing haemodialysis may present a significant burden of calcification in the coronaries. Considering that presence and extent of VC in CKD portend poor prognosis, many efforts have been made to shed light on this complicated phenomenon to prevent VC deposition and progression. Indeed, careful control of calcium load, serum P and parathyroid hormone along with the use of calcium-free P binders and vitamin D analogs represent our current armamentarium to improve quality of life and reduce mortality in CKD. We herein summarize the current understanding and evidence supporting strategies available for VC treatment.