[Arterial media calcification: from pathogenesis to diagnosis]

Patients with chronic kidneyl disease (CKD) have a higher cardiovascular mortality than the general population, in partly due to the development of arterial media calcification (AMC). It is still a matter of discussion as to whether arterial intimal calcification (AIC) and AMC should be considered as distinct entities with different pathogenesis or as a single nosological entity. The pathogenesis of mediocalcinosis is multifactorial. It consists of several stages which overlap; oxidative stress, endothelial dysfunction, shear stress, neoangiogenesis, degradation of the extracellular matrix. Endothelial cells stimulate angiogenesis both by passage of inflammatory cytokines and by migration of osteoprogenitor cells through the tunica media. VSMCs and pericytes are transformed into osteoclast-like cells with production of calcifying matrix vesicles through an active process regulated by promoters and inhibitors factors. Currently, radiology modalities are the only imaging methods that can be used to detect AMC in non-overlapping areas of vessels but X-ray imaging only allows us to identify this lesion when the vessel is widely calcified. Recently, ultrasonography and RX mammography has also been used as an alternative tool for the diagnosis of AMC in patients affected by CKD and they can be used to recognize it earlier than X-ray imaging, which will aid in the treatment of high-risk patients Calcium-sensing receptor (CaSR) and vitamin D receptor (VDR) have been identified in vascular smooth muscle cells (VSMC). Considering the essential role of VSMC in the pathogenesis of AMC, it could be important to identify in an early stage patients who develop this shape of arterial calcification to start drugs as cinacalcet or paricalcitol when possible.