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Rundgren et al. studied the evolution of renal function in postcardiac arrest as a function of hypothermia and timing of angiography (early vs. late). They have concluded that early coronary angiography (CA) does not increase the risk of developing acute kidney injury (AKI). They also showed a significant difference in survival at 6 months [1]. The authors also noted that lactate at admission was statistically significantly higher in the AKI group [1]. This leads us to question whether these patients had more severe shock or hemodynamic instability and in turn consider whether there was a potential selection bias, with these patients receiving delayed CA due to the need to be stabilized before proceeding. A recent study has shown that an increased number of incompletely revascularized lesions was associated with a greater risk of intra-hospital mortality and poorer neurological outcome in patients after cardiac arrest [2]. The result of the CA and the success of the revascularization procedure should be potential confounders to consider in the AKI risk assessment. It is indeed very elegant to postulate that early CA is accompanied by a recovery of cardiac function that results in improved renal function despite concurrent contrast administration. Renal function strongly depends on renal interstitial pressure and arteriovenous pressure difference. The combination of significant vasodilation from postarrest ischemiareperfusion with venous congestion, low cardiac output, and activation of a systemic inflammatory response leads to multiple organ dysfunction where AKI is prominent. Increased central venous pressure has been shown to be the most important hemodynamic factor driving

Early vs. late coronary angiography in cardiac arrest improves survival and preserves renal function: some confounding factors to consider