These results are consistent with the available human medical literature: plasma NGAL concentrations are overexpressed by circulating neutrophils during both infection‐triggered and sterile inflammatory states, and NGAL itself is able to alter the inflammatory response.18, 43, 44, 45 There are also positive correlations between NGAL and inflammatory cytokines, markers of systemic inflammation and endothelial activation, as well as sepsis severity scores.46, 47, 48 Moreover, systemic inflammation itself contributes to the development of AKI in critically ill patients. This evidence concerns the gene LCN2 and acute kidney injury.