A Predictive Model Based on Inflammatory and Coagulation Indicators for Sepsis-Induced Acute Kidney Injury.

Background: Sepsis-induced acute kidney injury (S-AKI) is associated with systemic inflammatory responses and coagulation system dysfunction, and it is associated with an increased risk of mortality. However, there was no study to explore the predictive value of inflammatory and coagulation indicators for S-AKI. Methods: In this retrospective study, 1051 sepsis patients were identified and divided into a training cohort (75%, n = 787) and a validation cohort (25%, n = 264) in chronological order according to the date they were admitted. Univariate analyses and multivariate logistic regression analyses were performed to identify the independent predictors of S-AKI. The logistic regression analyses (enter methods) were used to conducted the prediction models. The ROC curves were used to determine the predictive value of the constructed models on S-AKI. To test whether the increase in the AUC is significant, we used a two-sided test for ROC curves available online (http://vassarstats.net/roc_comp.html). The secondary outcome was different AKI stages and major adverse kidney events within 30 days (MAKE30). Stage 3B of S-AKI was defined as both meeting the stage 3 criteria [increase of Cr level by > 300% (≥ 4.0 mg/dL with an acute increase of ≥ 0.5 mg/dL) and/or UO < 0.3 mL/kg/h for > 24 h or anuria for > 12 h and/or acute kidney replacement therapy] and having cystatin C positive. MAKE30 were a composite of death, new renal replacement therapy (RRT), or persistent renal dysfunction (PRD). Results: We discovered that cardiovascular disease, white blood cell (WBC), mean arterial pressure (MAP), platelet (PLT), serum procalcitonin (PCT), prothrombin time activity (PTA), and thrombin time (TT) were independent predictors for S-AKI. The predictive value (AUC = 0.855) of the simplest model 3 (constructed with PLT, PCT, and PTA), with a sensitivity of 77.6% and a specificity of 82.4%, had a similar predictive value comparing with the model 1 (AUC = 0.872) and the model 2 (AUC = 0.864) in the training cohort (P > 0.05). Compared with the model 1 (AUC = 0.888) and the model 2 (AUC = 0.887), the model 3 (AUC = 0.887) had a similar predictive value in the validation cohort. Moreover, model 3 had the best predictive power for predicting S-AKI in the stage 3 (AUC = 0.777), especially in stage 3B (AUC = 0.771). Finally, the model 3 (AUC = 0.843) had perfect predictive power for predicting MAKE30 in sepsis patients. Conclusion: Within 24 hours after admission, the simplest model 3 (constructed with PLT, PCT, and PTA) might be a robust predictor of the S-AKI in sepsis patients, providing information for timely and efficient intervention.