Honore Patrick M, Jacobs Rita, De Waele Elisabeth, Van Gorp Viola, De Regt Jouke, Joannes-Boyau Olivier, Boer Willem, Spapen Herbert D
Intensive Care Department, Universitair Ziekenhuis Brussel, Vrije Universiteit Brussel, Brussels, Belgium.
Intensive Care Unit, Haut Leveque University Hospital of Bordeaux, University of Bordeaux 2, Pessac, France.
Int J Nephrol Renovasc Dis. 2015 Mar 13;8:25-8. doi: 10.2147/IJNRD.S75960. eCollection 2015.
Recent case reports of acute esophageal necrosis in patients with chronic kidney disease (CKD) undergoing hemodialysis encouraged us to look beyond hypoperfusion/ischemia as a sole explanation for this dramatic complication. At least three intriguing pathways, ie, accumulation of protein-bound toxins, endotoxin translocation, and altered mucosal defense mechanisms, have been proposed to explain the inherent susceptibility of CKD patients to developing ischemia-related and cardiovascular events. Interestingly, all the proposed pathways can be potentially antagonized or attenuated. At present, however, it is not known whether one pathway predominates or if any interaction exists between these pathways. More solid experimental and clinical data are warranted to acquire a better insight into the complex pathogenesis of CKD-associated ischemia.
近期有关于接受血液透析的慢性肾脏病（CKD）患者发生急性食管坏死的病例报告，这促使我们不再将低灌注/缺血作为这一严重并发症的唯一解释。至少有三种引人关注的途径，即蛋白结合毒素的蓄积、内毒素移位和黏膜防御机制改变，被提出用以解释CKD患者发生缺血相关事件和心血管事件的内在易感性。有趣的是，所有提出的途径都可能被潜在地拮抗或减弱。然而，目前尚不清楚是一种途径占主导，还是这些途径之间存在相互作用。需要更确凿的实验和临床数据，以便更好地洞察CKD相关缺血的复杂发病机制。
