Acute kidney injury after cardiac arrest

Abstract

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 24h; 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 24h in ICU, PRCS, and pre-CA renin-angiotensin-aldosterone-system blockade were independently associated with RIFLE-'I'/'F' AKI; while higher serum lactate 12h 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.