Research Progress on the Relationship between Coronary Artery Calcification and Chronic Renal Failure Translated title: 冠状动脉钙化与慢性肾功能衰竭关系的研究进展

Abstract

Objective:

Coronary artery calcification (CAC) is thought to be a controlled metabolic process that is very similar to the formation of new bone. In patients with chronic renal failure (CRF), CAC is very common, and CAC severity correlates with the deterioration of renal function. We summarized the current understanding and emerging findings of the relationship between CAC and CRF.

Data Sources:

All studies were identified by systematically searching PubMed, Embase, and CNKI databases for the terms “coronary calcification”, “chronic renal failure”, “vascular smooth muscle cell”, and their synonyms until September 2017.

Study Selection:

We examined the titles and abstracts of all studies that met our search strategy thoroughly. The full text of relevant studies was evaluated. Reference lists of retrieved articles were also scrutinized for the additional relevant studies.

Results:

CRF can accelerate CAC progression. CRF increases the expression of pro-inflammatory factors, electrolyte imbalance (e.g., of calcium, phosphorus), parathyroid hormone, and uremic toxins and their ability to promote calcification. These factors, through the relevant signaling pathways, trigger vascular smooth muscle cells to transform into osteoblast-like cells while inhibiting the reduction of vascular calcification factors, thus inducing further CAC.

Conclusions:

Coronary heart disease in patients with CRF is due to multiple factors. Understanding the mechanism of CAC can help interventionists to protect the myocardium and reduce the prevalence of coronary heart disease and mortality.

摘要

目的:

目前认为冠脉钙化是一种与新骨形成极为相似的受调控的主动性代谢过程。而在慢性肾功能衰竭患者，冠状动脉钙化非常普遍，并且随着肾功能的恶化钙化病变越重。此综述总结了关于冠状动脉钙化和慢性肾功能衰竭之间关系的理解及新发现。

方法:

所有文献都是以“冠状动脉钙化”、“慢性肾衰”、“血管平滑肌细胞”及他们的同义词，通过PubMed, Embase, 和CNKI数据库系统检索的，且这些文献发表年限为2017年9月以前。对符合检索条件文献的标题、摘要及全文，我们都进行了仔细的审阅。为了进一步了解学习，对文章的参考文献也进行了详细解读。

结果:

慢性肾衰会加速冠脉钙化的进程。慢性肾衰使得炎症因子增加，钙磷、PTH等代谢紊乱，尿毒素分子及其促进钙化的因素增加，这些因素通过相关信号通路让血管平滑肌细胞向成骨样细胞转变，同时抑制血管钙化的因素减少这样就更加诱导冠脉钙化的形成。在各因素影响着血管病变的同时，实际上各自又在相互作用。

结论:

由此可见慢性患者发生冠脉钙化是有多因素共同影响。尽管目前冠脉钙化的机制并非十分明确，但了解清楚冠脉钙化机制有助于我们保护心肌并降低冠心病的发病率及死亡率。因此，需要进一步的学习及研究慢性肾衰患者发生冠脉钙化的精确机制。