Ogawa Tetsuya, Nitta Kosaku
Contrib Nephrol. 2018;196:71-77. doi: 10.1159/000485702. Epub 2018 Jul 24.
Vascular calcification is common in patients with end-stage renal disease (ESRD). In addition to traditional cardiovascular risk factors, ESRD patients also have a number of nontraditional cardiovascular risk factors that may play an important role in the pathogenesis of vascular calcification. The transformation of vascular smooth muscle cells into osteoblast-like cells may be a key element in the pathogenesis of vascular calcification in the presence of calcium and phosphate deposition due to abnormal bone metabolism and impaired renal excretion. Vascular calcification causes increased arterial stiffness, left ventricular hypertrophy, decreased coronary artery perfusion, myocardial ischemia, and increased cardiovascular morbidity and mortality. Although current treatment strategies focus on correcting abnormal calcium, phosphate, parathyroid hormone, or vitamin D levels in ESRD patients, a better understanding of the mechanisms of abnormal tissue calcification may lead to the development of new therapeutic agents that are capable of reducing vascular calcification and improving the cardiovascular outcome of ESRD patients. This review summarizes the pathogenesis and management of vascular calcification in ESRD patients.
血管钙化在终末期肾病（ESRD）患者中很常见。除了传统的心血管危险因素外，ESRD患者还存在许多非传统的心血管危险因素，这些因素可能在血管钙化的发病机制中起重要作用。在由于骨代谢异常和肾脏排泄受损导致钙和磷沉积的情况下，血管平滑肌细胞向成骨样细胞的转变可能是血管钙化发病机制中的关键因素。血管钙化会导致动脉僵硬度增加、左心室肥厚、冠状动脉灌注减少、心肌缺血以及心血管发病率和死亡率增加。尽管目前的治疗策略侧重于纠正ESRD患者异常的钙、磷、甲状旁腺激素或维生素D水平，但更好地了解组织异常钙化的机制可能会促使开发出能够减少血管钙化并改善ESRD患者心血管结局的新型治疗药物。本综述总结了ESRD患者血管钙化的发病机制和管理。
