Specifically, mildly increased but clinically relevant urinary NGAL concentrations have been detected during the course of VR‐AKI in people, whereas higher concentrations indicating severe tubular injury have been found during I‐AKI.13, 14, 15, 16 Moreover, an increase in NGAL concentration has been repeatedly associated with worse outcomes.17 Despite the high sensitivity of NGAL for AKI detection, its specificity is hampered by the strong impact of systemic inflammation, because nonrenal sources of NGAL markedly increase the concentration of this biomarker under such conditions.18, 19. This evidence concerns the gene LCN2 and acute kidney injury.