Chinyere Ikeotunye Royal
Sarver Heart Center, University of Arizona, Tucson, AZ 85724, USA.
Division of Cardiology, Banner - University Medical Center, Tucson, AZ 85724, USA.
Rev Cardiovasc Med. 2025 Jul 30;26(7):37400. doi: 10.31083/RCM37400. eCollection 2025 Jul.
Many patients with chronic renal impairment experience cardiac comorbidities throughout their lives, and the incidence of electrophysiological demise for patients with terminal renal impairment requiring renal replacement therapy is higher than in patients with normal renal function. Thus, this relationship warrants continued examination, such that the risk of subsequent cardiac complications might eventually be mitigated. This review aims to outline the electrophysiology concepts, both basic and clinical, underlying the pathophysiology mediated by end-stage renal disease (ESRD). An evaluation of how chronic kidney disease may accelerate adverse cardiac remodeling, as well as the mechanisms through which hemodialysis may precipitate electrophysiological aberrations that impair the ability of the conduction system to maintain normal sinus rhythm, are provided. Furthermore, relevant animal models for this pathophysiology, with respect to their innate ability to recapitulate human renal and cardiac electrophysiology, are outlined. Specifically, the concepts of hyperkalemia, pericarditis, and arrhythmia are discussed in relation to ESRD. Furthermore, murine, porcine, and human species are compared and contrasted on all structural levels, from subcellular to clinical, illustrating which models best recapitulate this propensity to asystole.
许多慢性肾功能损害患者一生都会经历心脏合并症，需要肾脏替代治疗的终末期肾功能损害患者的电生理死亡发生率高于肾功能正常的患者。因此，这种关系值得持续研究，以便最终减轻后续心脏并发症的风险。本综述旨在概述终末期肾病（ESRD）介导的病理生理学基础的电生理概念，包括基础概念和临床概念。本文评估了慢性肾脏病如何加速不良心脏重塑，以及血液透析可能通过何种机制引发电生理异常，进而损害传导系统维持正常窦性心律的能力。此外，还概述了针对这种病理生理学的相关动物模型，及其重现人类肾脏和心脏电生理的固有能力。具体而言，讨论了与ESRD相关的高钾血症、心包炎和心律失常的概念。此外，还在从亚细胞到临床的所有结构层面上对小鼠、猪和人类物种进行了比较和对比，说明了哪种模型最能重现这种心搏停止的倾向。
