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肾损伤分子-1对于脓毒症相关肾损伤的早期预测价值 被引量:11

Predictive value of kidney injury molecule-1 testing for acute kidney injury in patients with sepsis
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摘要 目的观察脓毒症患者肾损伤分子-1(kidney injury molecule-1,KIM-1)的浓度,探讨KIM-1是否对脓毒症相关肾损伤具有早期预测价值。方法选取自2007年10月至2008年10月在首都医科大学附属北京朝阳医院急诊抢救室收治的脓毒症患者176例,另有50例健康者为对照组。分别检测KIM-1、血β2-微球蛋白(beta 2-microglobulin,β2-MG)。随访28天,记录急性肾损伤(acute kidney injury,AKI)的发生率及病死率。结果随访28天,51例患者出现AKI,AKI发生率29%。脓毒症患者KIM-1浓度显著高于对照组(P<0.05);全部患者按KIM-1浓度五分位分组,随着KIM-1浓度升高,AKI发病率升高;Logistic回归分析得到KIM-1是预测肌酐升高的独立危险因素,(OR:1.416,95%CI:1.155-1.737)。KIM-1是预测急性肾损伤的指标,ROC曲线下面积为0.879。结论 KIM-1在肾损伤早期浓度升高,并与急性肾损伤的严重程度有一定的关系,KIM-1是脓毒症相关肾损伤的预测因子。 Objective This study was to evaluate whether kidney injury molecule-1 ( KIM-1 ) had predictive value in the early stage of sepsis-induced renal injury. Methods Totally 176 patients with sepsis were included in the study in the emergency department of Beijing Chaoyang Hospital during Oct. 2007 to Oct. 2008, with 50 healthy volunteers as control group. The levels of KIM-1, beta 2- microglobulin (β2-MG) in serum were detected respectively. The incidence rate of acute kidney injury (AKI) and death rate were recorded after 28 days follow-up. Results In the following 28 days, 51 subjects(29% ) developed AKI. KIM-1 increased significantly ( P 〈 0.05 ) in septic patients compared with the control group. With the rising of KIM-1, the incidence of AKI increased. Logistic regression analyses showed that high urinary KIM-1 was an independent risk factor to predict creatinine increase( OR: 1. 416, 95% CI: 1. 155 - 1. 737). The area under the receiver operating characteristics curve was greater (AUC = 0. 879, P 〈 0. 05 ) for predicting AKI. Conclusion KIM-1 increases in the early stage of renal damage, which associates with the severity of acute kidney injury. KIM-1 is a potential predictive factor in sepsis-induced renal injury.
出处 《首都医科大学学报》 CAS 2012年第3期394-398,共5页 Journal of Capital Medical University
关键词 肾损伤分子-1 β2- 微球蛋白 脓毒症 急性肾损伤 kidney injury molecule-l beta 2-microglobulin sepsis acute kidney injury
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二级参考文献27

共引文献67

同被引文献128

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