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Erythropoietin in traumatic brain injury associated acute kidney injury: A randomized controlled trial.

Australian and New Zealand Intensive Care Research Centre, School of Public Health and Preventive Medicine, Monash University, Melbourne, Victoria, Australia. Division of Intensive Care, Department of Anaesthesiology, Intensive Care and Pain Medicine, Helsinki University Hospital and University of Helsinki, Helsinki, Finland. Department of Emergency Medicine and Services, Helsinki University Hospital and University of Helsinki, Helsinki, Finland. Department of Physiology and Pharmacology, Section of Anaesthesia and Intensive Care, Karolinska Institutet, Stockholm, Sweden. Department of Intensive Care, Western Health, Melbourne, Victoria, Australia. Department of Intensive Care, Royal Melbourne Hospital, Melbourne, Victoria, Australia. School of Medicine and Medical Sciences, University College Dublin, Dublin, Ireland. St Vincent's University Hospital, Dublin, Ireland. Department of Intensive Care and Hyperbaric Medicine, The Alfred, Melbourne, Victoria, Australia. Department of Anaesthesia and Intensive Care, Hôpitaux universitaires Paris Sud (HUPS), Université Paris Sud XI, Orsay, France. Departement d'anesthésie-réanimation, Hopital de la Cavale Blanche, Boulevard Tanguy Prigent, CHRU de Brest, Univeristé de Bretagne Occidental, Brest, France. King Saud Bin Abdulaziz University for Health Sciences and King Abdullah International Medical Research Center, Riyadh, Saudi Arabia. G&S Medical Associates, Urgent Care, Paterson, New Jersey. Department of Critical Care Medicine, Auckland City Hospital, Auckland, New Zealand. Department of Intensive Care, Austin Health, Melbourne, Victoria, Australia.

Acta anaesthesiologica Scandinavica. 2019;(2):200-207
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Abstract

BACKGROUND Acute kidney injury (AKI) in traumatic brain injury (TBI) is poorly understood and it is unknown if it can be attenuated using erythropoietin (EPO). METHODS Pre-planned analysis of patients included in the EPO-TBI (ClinicalTrials.gov NCT00987454) trial who were randomized to weekly EPO (40 000 units) or placebo (0.9% sodium chloride) subcutaneously up to three doses or until intensive care unit (ICU) discharge. Creatinine levels and urinary output (up to 7 days) were categorized according to the Kidney Disease Improving Global Outcome (KDIGO) classification. Severity of TBI was categorized with the International Mission for Prognosis and Analysis of Clinical Trials in TBI. RESULTS Of 3348 screened patients, 606 were randomized and 603 were analyzed. Of these, 82 (14%) patients developed AKI according to KDIGO (60 [10%] with KDIGO 1, 11 [2%] patients with KDIGO 2, and 11 [2%] patients with KDIGO 3). Male gender (hazard ratio [HR] 4.0 95% confidence interval [CI] 1.4-11.2, P = 0.008) and severity of TBI (HR 1.3 95% CI 1.1-1.4, P < 0.001 for each 10% increase in risk of poor 6 month outcome) predicted time to AKI. KDIGO stage 1 (HR 8.8 95% CI 4.5-17, P < 0.001), KDIGO stage 2 (HR 13.2 95% CI 3.9-45.2, P < 0.001) and KDIGO stage 3 (HR 11.7 95% CI 3.5-39.7, P < 0.005) predicted time to mortality. EPO did not influence time to AKI (HR 1.08 95% CI 0.7-1.67, P = 0.73) or creatinine levels during ICU stay (P = 0.09). CONCLUSIONS Acute kidney injury is more common in male patients and those with severe compared to moderate TBI and appears associated with worse outcome. EPO does not prevent AKI after TBI.

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