Acute Kidney Injury in Severe Trauma
Condition: Acute Kidney Injury
MeSH terms: Acute Kidney Injury; Wounds and Injuries
Study type: Observational

Summary: 
      Acute kidney injury (AKI) represents a serious complication following severe injury
      associated with adverse outcome. Main goals of the presented study were to define the
      incidence of AKI and to evaluate the validity of AKI biomarker neutrophil
      gelatinase-associated lipocalin (NGAL) in AKI prediction in severely injured patients.
      Secondary goals were to determine the time-dependent role of injury-related tissue hypoxia,
      systemic inflammatory response, and rhabdomyolysis in the pathophysiology of AKI.
    

Detailed description: 
      The main goal of the presented study was to define the epidemiology of AKI and to evaluate
      the validity of AKI biomarker neutrophil gelatinase-associated lipocalin in AKI prediction in
      severely injured patients with Injury Severity Score (ISS) > 24. Secondary goals were to
      determine the time-dependent role of insults associated directly with the intensity of injury
      (tissue hypoxia, systemic inflammatory response and/or infection, rhabdomyolysis) in the
      pathophysiology of AKI.

      The study was performed in a single center at the University Hospital in Ostrava in the Czech
      Republic. The Ethics Committee of the University Hospital Ostrava approved the study, which
      conformed to the tenets of the Declaration of Helsinki. Each of the awake and conscious study
      subjects signed the Informed Consent Form approved by the Ethics Committee of the University
      Hospital Ostrava. For enrolment of unconscious study subjects who were unable to sign
      informed consent, approval of two independent (i.e. not involved in the study) physicians was
      needed.

      Patients and methods: All adult severely injured patients defined by Injury Severity Scale
      (ISS) > 24 admitted to the Department of Anaesthesiology and Intensive Care in University
      Hospital Ostrava between June 2013 and December 2015 were enrolled into the study. Subjects
      were screened for AKI presence defined by Kidney Disease: Improving Global Outcomes (KDIGO)
      criteria daily up to 8 days after injury. Arterial levels of neutrophil gelatinase-associated
      lipocalin (NGAL), lactate, interleukin-6 (IL-6), procalcitonin (PCT) and myoglobin were
      investigated at the time points 24 hours (T1), 48 hours (T2) and 96 hours (T3) after injury.

      Methods All consecutive severely injured patients (ISS > 24) older than 18 years of age were
      enrolled in this prospective observational study between June 2013 and December 2015. All
      participants were admitted to the Level 1 Trauma Centre (Department of Anaesthesiology and
      Critical Care) at the University Hospital of Ostrava. Exclusion criteria included age < 18
      years, history of kidney disease, pregnancy, death within 24 hours after injury, unsurvivable
      injury with an end of life decision (withhold or withdraw of therapy) pronounced within 24
      hours after injury and, finally, clinical signs of brain death within 24 hours after injury.

      Basic observed demographic parameters included age, ISS and mechanism of injury. The
      laboratory parameters included blood NGAL; arterial lactate level, IL-6, PCT and myoglobin at
      the 24 hours (T1), 48 hours (T2) and 96 hours (T3) after injury. Serum Creatinine level was
      assessed once daily at 6.00 a.m. and urine output collected hourly from admission (D0) to Day
      8 were the basis for evaluation of AKI presence. Because of the recent pre-injury values of
      Creatinine were unknown almost in all of the subjects, first serum Creatinine level (sCr)
      taken on admission to the emergency room was used as a baseline reference value.

      All diagnostic and therapeutic interventions were performed in accordance with guidelines and
      standards for the treatment of the critically injured patients. The study protocol does not
      contain any additional diagnostic or therapeutic intervention except the laboratory
      investigations mentioned above.

      Early AKI defined according to KDIGO criteria occurs in one-third of victims of severe
      injury. Blood NGAL levels during the first 96 hours after injury are significantly higher in
      patients who subsequently develop AKI. Prolonged tissue hypoxia, excessive and prolonged
      activation of inflammatory response and rhabdomyolysis are factors contributing the
      development of AKI.
    

Intervention name(s): Neutrophil gelatinase-associated lipocalin (NGAL); Arterial lactate; Interleukin-6 (IL-6); Procalcitonin (PCT); Myoglobin
Intervention type(s): Diagnostic Test; Diagnostic Test; Diagnostic Test; Diagnostic Test; Diagnostic Test
Intervention description(s): Blood neutrophil gelatinase-associated lipocalin (NGAL) test was performed in all patients.; Arterial lactate level was assessed in all patients.; The level of interleukin-6 was assessed in all patients.; The level of procalcitonin (PCT) was assessed in all patients.; The level of myoglobin was assessed in all patients.
Observational model: Case-Only
Time perspective: Prospective
Sampling method: Non-Probability Sample
Study population: 
        Severely injured patients (ISS > 24) older than 18 years.
      
Keywords: Acute Kidney Injury; Severe Trauma; NGAL; Tissue Hypoxia; Inflammatory Response; Rhabdomyolysis