Chen Nai-Ching, Hsu Chih-Yang, Chen Chien-Liang
Department of Neurology, Kaohsiung Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Kaohsiung, Taiwan; School of Medicine, Chung Shan Medical University, Taichung City, Taiwan.
Division of Nephrology, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan; Department of Medicine, National Yang-Ming University School of Medicine, Taipei, Taiwan.
Biomed Res Int. 2017;2017:9035193. doi: 10.1155/2017/9035193. Epub 2017 Feb 14.
The high prevalence of arterial calcification in end-stage renal disease (ESRD) is far beyond the explanation by common cardiovascular risk factors such as aging, diabetes, hypertension, and dyslipidemia. The finding relies on the fact that vascular and valvular calcifications are predictors of cardiovascular diseases and mortality in persons with chronic renal failure. In addition to traditional cardiovascular risk factors such as diabetes mellitus and blood pressure control, other ESRD-related risks such as phosphate retention, excess calcium, and prolonged dialysis time also contribute to the development of vascular calcification. The strategies are to reverse "calcium paradox" and lower vascular calcification by decreasing procalcific factors including minimization of inflammation (through adequate dialysis and by avoiding malnutrition, intravenous labile iron, and positive calcium and phosphate balance), correction of high and low bone turnover, and restoration of anticalcification factor balance such as correction of vitamin D and K deficiency; parathyroid intervention is reserved for severe hyperparathyroidism. The role of bone antiresorption therapy such as bisphosphonates and denosumab in vascular calcification in high-bone-turnover disease remains unclear. The limited data on sodium thiosulfate are promising. However, if calcification is to be targeted, ensure that bone health is not compromised by the treatments.
终末期肾病（ESRD）中动脉钙化的高患病率远远超出了诸如衰老、糖尿病、高血压和血脂异常等常见心血管危险因素所能解释的范围。这一发现基于以下事实：血管和瓣膜钙化是慢性肾衰竭患者心血管疾病和死亡率的预测指标。除了糖尿病和血压控制等传统心血管危险因素外，其他与ESRD相关的风险，如磷潴留、钙过量和透析时间延长，也会导致血管钙化的发生。策略是通过减少促钙化因素来逆转“钙悖论”并降低血管钙化，包括将炎症降至最低（通过充分透析以及避免营养不良、静脉不稳定铁剂以及钙和磷的正平衡）、纠正高和低骨转换以及恢复抗钙化因子平衡，如纠正维生素D和K缺乏；甲状旁腺干预仅适用于严重甲状旁腺功能亢进。双膦酸盐和地诺单抗等骨吸收抑制疗法在高骨转换疾病的血管钙化中的作用仍不明确。关于硫代硫酸钠的有限数据很有前景。然而，如果要针对钙化进行治疗，要确保治疗不会损害骨骼健康。
