• Catherine J Morgan, Peter J Gill, Simon Lam, and Ari R Joffe.
• Department of Pediatrics, University of Alberta, Edmonton, Canada. cmorgan@ualberta.ca
• Intensive Care Med. 2013 May 1;39(5):934-41.

PurposeCardiopulmonary bypass (CPB)-related inflammatory response might be one mechanism by which cardiac surgery associated acute kidney injury (CS-AKI) occurs. Interventions that may attenuate inflammation, including glucocorticoids or phosphodiesterase inhibitors, could therefore have a role in its prevention. We aimed to determine the role of inflammatory mediators in CS-AKI in children and the efficacy of commonly used peri-operative interventions to reduce CS-AKI risk.MethodsWe prospectively studied 109 children undergoing heart surgery. Using regression modeling (adjusting for covariates), we (1) evaluated the association between inflammatory mediators [interleukin (IL)-6, IL-8, C-reactive protein, and tumor necrosis factor-α levels] and CS-AKI, and (2) evaluated risk/prevention factors for CS-AKI including glucocorticoid and milrinone administration. CS-AKI was defined based on pRIFLE methods.ResultsCS-AKI occurred in 68% of children. No inflammatory mediator measured had an independent association with CS-AKI. Higher pre-operative glomerular filtration rate (GFR), sustained decrease in mean arterial pressure during CPB, post-operative single ventricle physiology, deep hypothermic circulatory arrest, and milrinone use at 24 h post-operatively were significant independent predictors of CS-AKI. Intra-operative steroid administration had no effect on the rate of CS-AKI.ConclusionsAlthough inflammatory mediators are up-regulated following CPB, we found no association between levels of inflammatory cytokines and CS-AKI. CS-AKI has complex pathophysiology and the observation that milrinone was associated with increased AKI risk (and that higher GFR predicts more injury) suggests that mechanisms beyond inflammation play a significant role. Intra-operative administration of glucocorticoid does not appear to be an effective intervention for reducing the risk of CS-AKI.

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