Center for Health and Biological Sciences, Pontifícia Universidade Católica do Paraná, Curitiba, Brazil.
Blood Purif. 2010;29(2):114-20. doi: 10.1159/000245636. Epub 2010 Jan 8.
A sustained status of chronic inflammation is closely linked to several complications of chronic kidney disease (CKD), such as vascular degeneration, myocardial fibrosis, loss of appetite, insulin resistance, increased muscle catabolism and anemia. These consequences of a chronically activated immune system impact on the acceleration of atherosclerosis, vascular calcification and development of heart dysfunction. Recent evidence suggests that these immune-mediated consequences of uremic toxicity are not only important to stratify the risk and understand the mechanisms of disease, but also represent an important area for intervention. Thus, the aim of this brief review is to discuss the immune mechanisms behind atherosclerosis and myocardiopathy in CKD. We also display the emerging evidence that strategies focusing on modulating the immune response or reducing the generation of triggers of inflammation may represent an important tool to reduce mortality in this group of patients. Ongoing studies may generate the evidence that will translate these strategies to definitive changes in clinical practice.
慢性炎症的持续状态与慢性肾脏病(CKD)的几种并发症密切相关,如血管退化、心肌纤维化、食欲不振、胰岛素抵抗、肌肉分解代谢增加和贫血。这些慢性激活的免疫系统的后果会加速动脉粥样硬化、血管钙化和心脏功能障碍的发展。最近的证据表明,尿毒症毒性的这些免疫介导的后果不仅对分层风险和了解疾病机制很重要,而且代表了一个重要的干预领域。因此,本综述的目的是讨论 CKD 中动脉粥样硬化和心肌病的免疫机制。我们还展示了新出现的证据,即专注于调节免疫反应或减少炎症触发因素生成的策略可能代表降低这群患者死亡率的一个重要工具。正在进行的研究可能会产生证据,将这些策略转化为临床实践中的明确改变。