Serum antithrombin III level predicts acute kidney injury in patients with traumatic brain injury

血清抗凝血酶III水平可预测创伤性脑损伤患者的急性肾损伤。

阅读:1

Abstract

As an important anticoagulant molecule, antithrombin III (ATIII) has been confirmed to inhibit inflammation and to alleviate renal ischemia-reperfusion injury. The present study aimed to explore the relationship between serum ATIII level and acute kidney injury (AKI) in patients with traumatic brain injury (TBI). The clinical data of patients diagnosed with TBI and hospitalized in the West China Hospital (Chengdu, China) between January 2015 and June 2019 were collected. Logistic regression analysis was performed to analyze the relationship between ATIII and AKI and to construct predictive models. The area under the receiver operating characteristic curve (AUC) was calculated to evaluate the predictive value of ATIII and models were constructed. As a result, 203 patients with TBI were included in the present study. A total of 43 (19.7%) patients developed AKI at 24 h after admission. Compared with the non-AKI group, the AKI group had a lower Glasgow Coma Scale, injury severity score and ATIII, but had a higher glucose level, prothrombin time, levels of blood urea nitrogen and serum creatinine (SCr) and higher transfusion rate of fresh frozen plasma (FFP), red blood cell and hydroxyethyl starch. The mortality of the AKI group was 65.1%, which was higher compared with the 30.0% of the non-AKI group. SCr, ATIII and transfusion of FFP were independently associated with development of AKI after TBI. The AUC of the constructed three-factors predictive model was 0.850, which was higher compared with the AUC of 0.759 of only ATIII. Overall, ATIII was an effective predictive marker of AKI after TBI. Evaluating serum ATIII level and maintaining normal ATIII level may be beneficial for physicians to reduce the occurrence of AKI in patients with TBI.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。