Serum alpha 1-antitrypsin predicts severe acute kidney injury after cardiac surgery

血清 α1-抗胰蛋白酶可预测心脏手术后严重急性肾损伤

阅读:20
作者:Songlin Du, Jianwei Tian, Zhiwen Xiao, Zhiwen Luo, Tong Lin, Shaoyi Zheng, Jun Ai

Background

Human alpha 1-antitrypsin (A1AT) is involved in the pathophysiological process underlying ischemic acute kidney injury (AKI). To test the hypothesis that serum A1AT (sA1AT) is a predictor for severe AKI after cardiopulmonary bypass (CPB), we conducted a prospective cohort study in 201 patients undergoing cardiac surgery.

Conclusions

In summary, sA1AT is a valuable predictor of severe AKI development and prolonged ICU and hospital stays in patients after cardiac surgery.

Methods

We collected blood and urine samples, and analyzed the sA1AT and other injury biomarkers during the perioperative period. Severe AKI is defined as Kidney Disease Improving Global Outcomes (KDIGO) stage 2 or 3, and overall AKI is defined as KDIGO stage 1, 2, or 3.

Results

Ninety-one (45.3%) patients developed overall AKI, and 22 (10.9%) among them developed severe AKI after operation. sA1AT level spiked 2 hours after surgery in patients who subsequently developed severe AKI, while serum creatinine peaked 12 hours after operation. Higher postoperative sA1AT independently correlated to the development of severe AKI [OR, 1.54 (1.17-2.03); P=0.002]. The highest quartile of postoperative sA1AT level was associated with 6-fold higher hazards of severe AKI compared to the lowest quartile. Higher sA1AT levels were correlated with longer stays in the intensive care unit and the hospital. For predicting severe AKI, the AUC of sA1AT 2 hours after CPB reached 0.814. After combining with urine T cell immunoglobulin mucin-1 and clinical model, the AUC improved to 0.923. Conclusions: In summary, sA1AT is a valuable predictor of severe AKI development and prolonged ICU and hospital stays in patients after cardiac surgery.

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。