Original Article
Serum alpha 1-antitrypsin predicts severe acute kidney injury after cardiac surgery
Abstract
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.
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.
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.
