Department of Internal Medicine, Division of Nephrology, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands.
Department of Cardiology, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands.
Am J Kidney Dis. 2014 Aug;64(2):265-73. doi: 10.1053/j.ajkd.2013.11.010. Epub 2013 Dec 21.
Hemodialysis may acutely induce regional left ventricular (LV) systolic dysfunction, which is associated with increased mortality and progressive heart failure. We tested the hypothesis that hemodialysis-induced regional LV systolic dysfunction is associated with inflammation and endothelial injury. Additionally, we studied whether hemodialysis-induced LV systolic dysfunction is associated with an exaggerated bioincompatibility reaction to hemodialysis.
Cross-sectional study.
SETTING & PARTICIPANTS: 105 hemodialysis patients on a thrice-weekly dialysis schedule were studied between March 2009 and March 2010.
Plasma indexes of inflammation (high-sensitivity C-reactive protein, pentraxin 3 [PTX3], interleukin 6 [IL-6], and IL-6:IL-10 ratio), bioincompatibility (leukocytes, neutrophils, complement C3, and myeloperoxidase), and endothelial function (soluble intercellular adhesion molecule 1 [ICAM-1], von Willebrand factor, proendothelin, and endothelin) were measured just before dialysis and at 60, 180, and 240 minutes intradialysis.
Hemodialysis-induced regional LV systolic function. Wall motion score was measured by echocardiography at 30 minutes predialysis, 60 and 180 minutes intradialysis, and 30 minutes postdialysis. We defined hemodialysis-induced regional LV systolic dysfunction as an increase in wall motion score in 2 or more segments.
Patients with hemodialysis-induced regional LV systolic dysfunction (n=29 [27%]) had significantly higher predialysis high-sensitivity C-reactive protein, PTX3, IL-6, and lL-6:IL-10 ratio values. Predialysis levels of bioincompatibility and endothelial markers did not differ between groups. Intradialysis courses of markers of inflammation, bioincompatibility, and endothelial function did not differ in patients with versus without hemodialysis-induced regional LV systolic dysfunction.
Coronary angiography or computed tomography for quantification of coronary calcifications in our patients was not performed; therefore, we could not relate markers of inflammation to the extent of atherosclerosis.
Patients with hemodialysis-induced regional LV systolic dysfunction have a proinflammatory cytokine profile. There was no indication of an association with an exaggerated bioincompatibility reaction to hemodialysis.
血液透析可能会急性引发局部左心室(LV)收缩功能障碍,这与死亡率增加和心力衰竭进展有关。我们检验了这样一个假设,即血液透析引起的局部 LV 收缩功能障碍与炎症和内皮损伤有关。此外,我们还研究了血液透析引起的 LV 收缩功能障碍是否与血液透析引起的生物不相容性反应过度有关。
横断面研究。
2009 年 3 月至 2010 年 3 月期间,我们研究了 105 名每周三次血液透析的血液透析患者。
血液透析前和血液透析 60、180 和 240 分钟时,测量炎症(高敏 C 反应蛋白、五聚素 3[PTX3]、白细胞介素 6[IL-6]和 IL-6:IL-10 比值)、生物不相容性(白细胞、中性粒细胞、补体 C3 和髓过氧化物酶)和内皮功能(可溶性细胞间黏附分子 1[ICAM-1]、血管性血友病因子、前内皮素和内皮素)的血浆指标。
29 名(27%)患者出现血液透析引起的局部 LV 收缩功能障碍。在血液透析前 30 分钟、血液透析 60 和 180 分钟以及血液透析后 30 分钟,通过超声心动图测量壁运动评分。我们将血液透析引起的局部 LV 收缩功能障碍定义为 2 个或更多节段壁运动评分增加。
与没有血液透析引起的局部 LV 收缩功能障碍的患者相比,有血液透析引起的局部 LV 收缩功能障碍的患者在血液透析前具有更高的高敏 C 反应蛋白、PTX3、IL-6 和 IL-6:IL-10 比值。两组患者的生物不相容性和内皮标志物的血液透析前水平没有差异。有血液透析引起的局部 LV 收缩功能障碍的患者与没有血液透析引起的局部 LV 收缩功能障碍的患者相比,炎症、生物不相容性和内皮功能标志物的血液透析过程没有差异。
由于我们的患者未进行冠状动脉造影或计算机断层扫描来量化冠状动脉钙化,因此我们无法将炎症标志物与动脉粥样硬化程度联系起来。
血液透析引起的局部 LV 收缩功能障碍的患者具有促炎细胞因子谱。没有迹象表明与血液透析引起的生物不相容性反应过度有关。