Thrombomodulin: a potential biomarker for sepsis-associated acute kidney injury resulting from bacterial infections

Sepsis-associated acute kidney injury (SA-AKI) is a common complication of sepsis. Serum creatinine is a delayed AKI marker influenced by multiple confounders and cannot reflect endothelial injury central to SA-AKI. Thrombomodulin (TM) is an endothelial biomarker linked to coagulation and inflammation, but its predictive value for SA-AKI in bacterial infection remains undefined. We aimed to evaluate the independent predictive performance of TM for SA-AKI in bacterial sepsis.

This was a single-center retrospective observational study enrolling 81 patients with bacterial sepsis (37 with SA-AKI, 44 without SA-AKI) admitted to the intensive care unit of the First Affiliated Hospital of Soochow University. Blood samples were collected within 24 hours of sepsis diagnosis for TM measurement. For comparisons between two independent groups, Student's t-test was used for normally distributed variables, while Mann-Whitney U test was utilized for non-normally distributed variables. For multi-group comparisons involving normal distribution with homogeneous variance data, One-way analysis of variance with Bonferroni post-hoc test was applied, whereas Mann-Whitney U test was utilized for non-normally distributed variables. Categorical variables were compared using the Chi-square test. Spearman's correlation analysis was performed to assess relationships. Binary logistic regression analysis was conducted to evaluate the independent relationships with SA-AKI. A receiver operating characteristic (ROC) curve was employed to determine diagnostic accuracy. Subgroup analyses were performed stratified by vasoactive drug use and continuous renal replacement therapy (CRRT) status.

Thrombomodulin was significantly elevated in patients with AKI compared to that in non-AKI patients, and the odds ratio for thrombomodulin was 1.17 in a multivariable logistic regression analysis. The Area under curve (AUC) value for thrombomodulin in SA-AKI was 0.81. In subgroup analysis, thrombomodulin expression was significantly higher in the vasoactive drug group. The AUC of thrombomodulin with vasopressor use was 0.70. In the group that did not utilize vasoactive drugs, the AUC of thrombomodulin in SA-AKI was 0.81. Thrombomodulin expression was significantly higher in the Continuous Renal Replacement Therapy (CRRT) group. The AUC of Thrombomodulin (TM) when CRRT was used was 0.80. In the group that did not receive CRRT, the AUC of thrombomodulin predicted by SA-AKI was 0.75.

Thrombomodulin may be valuable in independently predicting SA-AKI.