Palit Shyamal, Kendrick Jessica
Division of Renal Diseases and Hypertension, University of Colorado Denver, Denver Health Medical Center, 660 Bannock St Mail Code 4000, Denver, CO 80204.
Curr Pharm Des. 2014;20(37):5829-33. doi: 10.2174/1381612820666140212194926.
In patients with chronic kidney disease (CKD), vascular calcification is associated with significant morbidity and mortality. The prevalence of vascular calcification increases as glomerular filtration rate (GFR) declines and calcification occurs years earlier in CKD patients than in the general population. The mechanisms of vascular calcification in CKD patients are complex and not completely understood but likely involve non-traditional risk factors, which may be unique to patients with CKD. These unique risk factors may predispose patients to early and more accelerated calcification. Experimental and clinical studies show that disorders in mineral metabolisms including calcium and phosphorus homeostasis initiate and promote vascular calcification in patients with CKD. It is currently unknown if vascular calcification can be prevented or reversed with therapies aimed at maintaining calcium and phosphorus homeostasis. This review focuses on the potential mechanisms by which disordered mineral metabolism may promote vascular calcification in patients with CKD.
在慢性肾脏病（CKD）患者中，血管钙化与显著的发病率和死亡率相关。随着肾小球滤过率（GFR）下降，血管钙化的患病率增加，且CKD患者的钙化比普通人群早数年发生。CKD患者血管钙化的机制复杂，尚未完全明确，但可能涉及非传统风险因素，这可能是CKD患者所特有的。这些独特的风险因素可能使患者易发生早期且更快速的钙化。实验和临床研究表明，包括钙磷稳态在内的矿物质代谢紊乱会引发并促进CKD患者的血管钙化。目前尚不清楚针对维持钙磷稳态的治疗能否预防或逆转血管钙化。本综述重点关注矿物质代谢紊乱可能促进CKD患者血管钙化的潜在机制。
