Introduction: Acute kidney injury (AKI) after cardiac arrest (CA) results from hypoperfusion/ischemia. Previous studies have shown an AKI incidence of up to 50% post CA. The impact of targeted temperature management (TTM) on the development of post-arrest AKI remains unclear.
Aim: We aimed to compare the incidence of AKI after non-traumatic CA in a post-arrest cohort who received TTM vs those who did not receive TTM.
Methods: Using a multicenter national US registry of post-arrest care at 38 hospitals (The Penn Alliance for Therapeutic Hypothermia, or PATH), we performed a retrospective analysis of this cohort from 2005-2017 to identify AKI in patients who had three or more creatinine values available post CA. Using the Kidney Disease: Improving Global Outcomes (KDIGO) criteria, AKI was defined as an increase in creatinine by > 0.3 mg/dL. Time 0 was defined as the first creatinine value within 6 hours of return of spontaneous circulation (ROSC); subsequent daily creatinine values were analyzed for three days (closest value ± 12 hours).
Results: Of 6480 patients in the registry, 3390 (53%) attained ROSC. 445 patients had serial creatinine values available and met the inclusion criteria of no previously documented renal insufficiency. Mean age was 59.4±16 y; 58.2% were male; 63.6% received TTM. 24.7 % of the patients who received TTM developed AKI compared to 27.2 % of patients who did not receive TTM (P=0.57). The difference in median creatinine values between the TTM vs non TTM group was highest on Day1.
Conclusion: In post-arrest patients, the use of TTM was not associated with the frequency of AKI. Concern for renal dysfunction should not be a deterrent for use of TTM. Further research is needed to assess the factors that influence AKI in CA.