Vascular calcifications constitute an important risk factor for mortality in chronic kidney disease patients. A better knowledge of physiopathologic phenomena responsible for vascular mineralization leads to emerging biological markers of vascular calcifications. In calcified arteries, presence of bone matrix as well as osteoblast and osteoclast cells suggests that vascular calcification is an active and highly regulated process. In uremic environment, vascular smooth muscle cells can transdifferentiate into osteoblast like cells. The OPG/RANK/RANKL system is clearly of central significance in controlling vascular calcifications as in bone metabolism. Converging results suggest that circulating OPG determination should be a relevant marker of calcifications. Impairment in inhibitory system such as Matrix Gla Protein and fetuin-A promotes bone matrix calcification. Finally, FGF23, an early and sensitive marker of bone and mineral disorders in chronic kidney disease patients appears as a promising marker.
Keywords: Vascular calcification, fetuin A, FGF-23
