Valdivielso J M
Hospital Universitari Arnau de Vilanova, Lleida.
Nefrologia. 2011;31(2):142-7. doi: 10.3265/Nefrologia.pre2010.Nov.10754.
Vascular calcification has traditionally been considered to be a passive process that was associated with advanced age, atherosclerosis, uncommon genetic diseases and some metabolic alterations such as diabetes mellitus and end-stage kidney failure. However, in the last years, vascular calcification has been proven to be an active and regulated process, similar to bone mineralisation, in which different bone-related proteins are involved. Recent results question the classic classification of vascular calcification into intimal and medial calcification, at least in capacitance arteries. Pro and anti-calcifying mechanisms play an active role in calcium deposition in vascular cells, making this area an active focus of research. The identification of therapeutic targets which can slow down the progression or even reverse vascular calcification could be an important step forward in the treatment of patients with chronic kidney disease.
传统上，血管钙化被认为是一个被动过程，与高龄、动脉粥样硬化、罕见的遗传性疾病以及一些代谢改变（如糖尿病和终末期肾衰竭）有关。然而，近年来，血管钙化已被证明是一个活跃且受调控的过程，类似于骨矿化，涉及不同的骨相关蛋白。最近的研究结果对血管钙化分为内膜钙化和中膜钙化的经典分类提出了质疑，至少在容量动脉中是如此。促钙化和抗钙化机制在血管细胞的钙沉积中发挥着积极作用，使该领域成为一个活跃的研究焦点。确定能够减缓血管钙化进展甚至逆转血管钙化的治疗靶点，可能是慢性肾脏病患者治疗向前迈出的重要一步。
