Reslerova Martina, Moe Sharon M
Department of Medicine, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
Am J Kidney Dis. 2003 Mar;41(3 Suppl 1):S96-9. doi: 10.1053/ajkd.2003.50094.
Vascular calcification is believed to have a crucial role in the excess cardiovascular mortality and morbidity in patients with end-stage renal disease (ESRD).
Recent evidence suggests that uremic vascular calcification is an active cell-mediated process resembling osteogenesis in bone, rather than passive precipitation of calcium and phosphorus in the setting of deranged mineral metabolism. To date, several bone-associated proteins (osteopontin, bone sialoprotein, alkaline phosphatase, and type I collagen) have been shown in histological sections of vessels obtained from patients with ESRD or calcific uremic arteriolopathy. In in vitro experiments, the addition of uremic serum upregulates osteopontin expression by cultured vascular smooth muscle cells (VSMCs).
We are only beginning to understand the process by which VSMCs transform into osteoblast-like cells, although phosphorus may have a key role. Additional factors mediating or modulating the development of vascular calcification in patients with ESRD remain to be identified. Further understanding of the pathophysiological state of uremic vascular calcification is needed to design effective therapeutic strategies to intervene with this devastating condition in the ESRD population.
血管钙化被认为在终末期肾病（ESRD）患者心血管疾病死亡率和发病率过高方面起着关键作用。
最近的证据表明，尿毒症血管钙化是一个活跃的细胞介导过程，类似于骨中的骨生成，而非在矿物质代谢紊乱情况下钙和磷的被动沉淀。迄今为止，在从ESRD患者或钙化性尿毒症小动脉病患者获取的血管组织切片中已发现几种与骨相关的蛋白质（骨桥蛋白、骨唾液蛋白、碱性磷酸酶和I型胶原）。在体外实验中，添加尿毒症血清可上调培养的血管平滑肌细胞（VSMC）中骨桥蛋白的表达。
尽管磷可能起关键作用，但我们才刚刚开始了解VSMC转化为成骨样细胞的过程。介导或调节ESRD患者血管钙化发展的其他因素仍有待确定。需要进一步了解尿毒症血管钙化的病理生理状态，以设计有效的治疗策略来干预ESRD人群中的这种破坏性疾病。
