Acute kidney injury after cardiac arrest

Aim Cardiac arrest (CA) in humans causes warm renal ischemia-reperfusion injury, similar to animal models of ischemic acute kidney injury (AKI). We aimed to investigate the incidence and risk associations of AKI after CA, with or without post-resuscitation cardiogenic shock (PRCS). Methods We examined the renal outcomes of adult patients admitted to the intensive care unit (ICU), who survived for more than 48 h following successful resuscitation after CA. Results Of 105 patients (median age 65 years; 69% male), 58 (55.2%) had PRCS and were on vasoactive drugs beyond 24 h; and 9 (8.6%) (all of whom had PRCS) received renal replacement therapy. Only 3 (6.4%) of 47 patients without PRCS had RIFLE-‘I’/‘F’ AKI, compared to 30 (51.7%) of 58 patients with PRCS (p < 0.001). Median peak serum creatinine in the non-PRCS group was 102 μmol/L (interquartile range 85–115), compared to 155 μmol/L (interquartile range 112–267) (p < 0.001) in the PRCS group. On multivariate analysis, cumulative noradrenaline dose during the first 24 h in ICU, PRCS, and pre-CA renin–angiotensin–aldosterone-system blockade were independently associated with RIFLE-‘I’/‘F’ AKI; while higher serum lactate 12 h after CA, baseline creatinine, and PRCS were independently associated with greater rise in creatinine from pre-CA levels. Estimated time without spontaneous circulation, total adrenaline dose and initial cardiac rhythm during CA, had no independent associations with renal outcomes. Conclusions In the absence of PRCS, CA in isolation is uncommonly associated with significant AKI. The human kidney may be more resistant to warm ischemia-reperfusion injury than previously thought.