Acute kidney injury (AKI) and multiple organ failure (MOF) are leading causes of mortality in trauma injuries. Early diagnosis of AKI and MOF is vital to improve outcomes, but current diagnostic criteria rely on laboratory markers that are delayed or unreliable. In this study, we investigated whether damage associated molecular patterns such as high-mobility group box 1 (HMGB1), syndecan-1 (SDC-1) and C3a correlate with the development of trauma-induced AKI and MOF.
Thirty-nine swine underwent smoke inhalation and severe burns, then received critical care for 72 hours or until death. AKI was defined by the KDIGO (Kidney Disease: Improving Global Outcomes) criteria, which labels AKI when a 1.5-fold increase in blood creatinine levels from baseline or a urine output < 0.5 mL/kg/h for 6 hours or more occurs. MOF was defined by the presence of both AKI and acute respiratory distress syndrome (PaO2/FiO2<300 for 4 hours).
Eight of 39 pigs developed AKI and seven of those developed MOF. Pathological analysis revealed that polytrauma induces significantly higher kidney injury scores compared to sham controls. The average time from injury to KDIGO AKI was 24 hours (interquartile range: 22.50-32.25). Twelve hours after injury, HMGB1 levels were significantly increased in animals that went on to develop AKI compared to those that did not (73.07 ± 18.66 ng/mL vs. 31.64 ± 4.15 ng/mL,
Twelve-hour post-injury HMGB1 levels predict AKI and MOF in a smoke inhalation and burn swine model. Further research is needed to validate this result in other polytrauma models and in critical combat causalities.