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Recently in Critical Care, Sugita et al. confirmed the previously reported positive association between high HMGB-1 (high-mobility group box-1) levels and a poor neurological outcome in post–cardiac arrest (post-CA) patients [1]. Although we applaud this excellent study, we would like to make some comments. Brain damage after out-of-hospital CA is a leading cause of mortality and long-term neurological disability in survivors. Primary injury is caused by an immediate shutdown of cerebral blood flow. In the hours and days following CA, systemic ischemia/reperfusion (I/R)-induced processes may culminate in secondary neuronal cell death [2]. HMGB-1, a typical damage-associated molecular pattern protein, is crucial in inflammation and is critically involved in thrombosis and also mediates systemic organ I/R. Interestingly, almost half of the patients resuscitated after CA may develop acute kidney injury (AKI). More than 75% of AKI episodes occurred within 3 days after CA and about one third of these patients eventually needed continuous renal replacement therapy (CRRT) [3]. Sugita et al. did not mention the incidence of

Validity of the relationship between mobility group box-1 protein and poor post–cardiac arrest neurological outcome during renal replacement therapy