Sections of Nephrology and
Division of Nephrology and Dialysis, St. Bassiano Hospital, Bassano del Grappa, Italy.
J Am Soc Nephrol. 2019 Jun;30(6):918-928. doi: 10.1681/ASN.2019020117. Epub 2019 Apr 30.
CKD frequently leads to chronic cardiac dysfunction. This complex relationship has been termed as cardiorenal syndrome type 4 or cardio-renal link. Despite numerous studies and reviews focused on the pathophysiology and therapy of this syndrome, the role of arterial stiffness has been frequently overlooked. In this regard, several pathogenic factors, including uremic toxins (, uric acid, phosphates, endothelin-1, advanced glycation end-products, and asymmetric dimethylarginine), can be involved. Their effect on the arterial wall, direct or mediated by chronic inflammation and oxidative stress, results in arterial stiffening and decreased vascular compliance. The increase in aortic stiffness results in increased cardiac workload and reduced coronary artery perfusion pressure that, in turn, may lead to microvascular cardiac ischemia. Conversely, reduced arterial stiffness has been associated with increased survival. Several approaches can be considered to reduce vascular stiffness and improve vascular function in patients with CKD. This review primarily discusses current understanding of the mechanisms concerning uremic toxins, arterial stiffening, and impaired cardiac function, and the therapeutic options to reduce arterial stiffness in patients with CKD.
CKD 常导致慢性心脏功能障碍。这种复杂的关系被称为 4 型心肾综合征或心肾关联。尽管有许多研究和综述集中在该综合征的病理生理学和治疗上,但动脉僵硬的作用经常被忽视。在这方面,包括尿毒症毒素(、尿酸、磷酸盐、内皮素-1、晚期糖基化终产物和不对称二甲基精氨酸)在内的几个致病因素可能会涉及其中。它们通过慢性炎症和氧化应激的直接或间接作用,对动脉壁产生影响,导致动脉僵硬和血管顺应性降低。主动脉僵硬增加会导致心脏工作量增加和冠状动脉灌注压降低,进而可能导致微血管心肌缺血。相反,动脉僵硬降低与生存率增加相关。可以考虑几种方法来降低 CKD 患者的血管僵硬并改善血管功能。这篇综述主要讨论了关于尿毒症毒素、动脉僵硬和心脏功能障碍的机制的最新认识,以及降低 CKD 患者动脉僵硬的治疗选择。