Acute kidney injury (AKI) occurs in approximately 20–40% of critically injured patients and is linked to worse outcomes. In sepsis and critical illness, dysregulated coagulation and fibrinolysis have been implicated in microangiopathic kidney dysfunction. The relationship between early coagulation changes and AKI after trauma is less well characterized. The present work is a secondary analysis of a single‑center randomized controlled trial (ClinicalTrials.gov NCT02535949) that investigated whether early postinjury coagulation and fibrinolysis biomarkers predict development of AKI in severely injured adult trauma patients.
Plasma levels of three biomarkers were assayed: thrombin‑antithrombin (TAT) complexes, plasmin‑α2‑antiplasmin (PAP) complexes, and fibrinogen. Samples were obtained within 2 hours of injury and again at 6 hours after injury. These measurements were selected to capture early activation of coagulation (TAT), fibrinolytic activity (PAP), and substrate availability (fibrinogen) in the immediate postinjury period.
The analysis included 149 severely injured adult trauma patients enrolled in the parent randomized controlled trial. The primary outcome for this secondary analysis was development of AKI defined by the RIFLE (Risk, Injury, Failure, Loss, End‑stage kidney disease) criteria. Thirty patients (20.1% of the cohort) met RIFLE criteria for AKI during the observation period.
Patients who developed AKI had distinct biomarker profiles compared with those who did not. Specifically, AKI cases demonstrated higher plasma concentrations of TAT and PAP and lower fibrinogen levels at both the early (≤2 hour) and 6‑hour time points. These group differences indicate early coagulation activation and relative fibrinogen depletion among patients who went on to develop AKI.
Adjusted logistic regression models were used to evaluate biomarker associations with AKI. The 6‑hour TAT‑to‑fibrinogen ratio remained independently associated with AKI after adjustment (adjusted odds ratio 7.17; 95% CI 2.34–21.9; p = 0.001). Discrimination of the 6‑hour TAT‑to‑fibrinogen ratio was strong, with an area under the receiver operating characteristic curve (AUC) of 0.88. Supplemental analyses reported consistent independent associations for TAT and fibrinogen individually, whereas PAP was not independently predictive of AKI in adjusted models.
Receiver operating characteristic analyses identified thresholds with clinical performance characteristics. A 6‑hour TAT level below 99 pg/mL identified patients unlikely to develop AKI, with a negative predictive value (NPV) of 93.9%. Similarly, a 6‑hour fibrinogen level greater than 173 mg/dL was associated with low likelihood of subsequent AKI (NPV 88.2%). These thresholds suggest potential utility for ruling out high near‑term AKI risk in injured patients when measured at 6 hours postinjury.
The study’s results indicate that early postinjury coagulation imbalance—characterized by elevated TAT and reduced fibrinogen—is associated with subsequent development of AKI in trauma patients. The strong independent association and discrimination of the 6‑hour TAT‑to‑fibrinogen ratio support its consideration as an early biomarker of evolving microvascular kidney dysfunction after severe injury. If validated prospectively, these measures or their combination could inform early risk stratification and prompt closer renal monitoring or targeted interventions in high‑risk trauma patients.
This report is based on the abstract of a secondary analysis; the source provides limited methodological detail in the abstract. Specifics such as the parent trial intervention, full inclusion and exclusion criteria, the covariates included in adjusted models, timing of AKI onset, severity staging breakdown, and broader demographic or clinical characteristics beyond those summarized were not reported in the abstract. The abstract also does not provide detailed number‑needed‑to‑test metrics or prospective validation data. Further information from the full manuscript would be required to fully appraise applicability, potential confounding, and operational implementation of the biomarkers in clinical practice.