Remote ischemic preconditioning has a neutral effect on the incidence of kidney injury after coronary artery bypass graft surgery
Remote ischemic preconditioning has a neutral effect on the incidence of kidney injury after coronary artery bypass graft surgery
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DOI：
10.1038/ki.2014.259
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发表时间：
2015-02-01
影响因子：
19.6
通讯作者：
Yaqoob, Muhammad M.
中科院分区：
文献类型：
--
作者：
Gallagher, Sean M.;Jones, Dan A.;Yaqoob, Muhammad M.
急性肾损伤（AKI）是心脏手术的常见并发症，通常发生在既往存在慢性肾脏疾病（CKD）的患者中。远程缺血预处理（RIPC）可以减轻心脏手术相关的肾缺血再灌注损伤，可能是术后AKI的预防策略。我们对86例接受冠状动脉搭桥术（CABG）的CKD患者（估计肾小球滤过率低于60 ml/min / 1.73 m(2)）进行了RIPC预防AKI的随机对照试验。43名患者随机接受有或没有RIPC的标准治疗，包括3个5分钟周期的前臂缺血再灌注。主要终点是AKI的发展，定义为手术后48小时内血清肌酐浓度升高超过0.3 mg/di。次要终点包括研究组与对照组之间的肾损伤血清生物标志物的比较，包括胱他汀- c、中性粒细胞明胶酶相关脂钙素（NGAL）和白细胞介素-18 (IL-18)，以及在CABG后6、12和24小时测量的尿液生物标志物，包括NGAL、IL-18和肾损伤分子-1，以及曲线下72小时血清肌钙蛋白T浓度区域，作为心肌损伤的标志。预处理组和对照组的临床和手术特征相似。两组均有12例患者在冠脉搭桥后48小时内发生AKI。CABG术后两组患者血清或尿液中肾脏或心脏损伤生物标志物的浓度均无显著差异。因此，前臂缺血再灌注诱导的RIPC对CKD患者CABG后AKI的发生频率没有影响。
Acute kidney injury (AKI) is a frequent complication of cardiac surgery and usually occurs in patients with preexisting chronic kidney disease (CKD). Remote ischemic preconditioning (RIPC) may mitigate the renal ischemia-reperfusion injury associated with cardiac surgery and may be a preventive strategy for postsurgical AKI. We undertook a randomized controlled trial of RIPC to prevent AKI in 86 patients with CKD (estimated glomerular filtration rate under 60 ml/min per 1.73 m(2)) undergoing coronary artery bypass graft (CABG) surgery. Forty-three patients each were randomized to receive standard care with or without RIPC consisting of three 5-minute cycles of forearm ischemia followed by reperfusion. The primary end point was the development of AKI defined as an increase in serum creatinine concentration over 0.3 mg/di within 48 h of surgery. Secondary end points included a comparison between the study and control groups of several serum biomarkers of renal injury including cystatin-C, neutrophil gelatinase-associated lipocalin (NGAL), and interleukin-18 (IL-18), and urinary biomarkers including NGAL, IL-18, and kidney injury molecule-1 measured at 6, 12, and 24h after CABG, and the 72-h serum troponin T concentration area under the curve as a marker of myocardial injury. Clinical and operative characteristics were similar between the preconditioned and control groups. AKI developed in 12 patients in both groups within 48 h of CABG. There were no significant differences between the two groups in the concentrations of any of the serum or urinary biomarkers of renal or cardiac injury after CABG. Thus, RIPC induced by forearm ischemia-reperfusion had no effect on the frequency of AKI after CABG in patients with CKD.