LCN2 and acute kidney injury: These conclusions are supported by the role of serum and urine NGAL as biomarkers of tubular hypoperfusion and renal ischemia in experimental (eg, acute hemorrhage) and spontaneous (eg, cardiorenal syndrome) models of hypoxic AKI in dogs, regardless variations of sCr in I‐AKI.22, 25 Such findings emphasize the concept that VR‐AKI (prerenal) and I‐AKI (renal) represent a continuum of renal injury of increasing severity.16 Indeed, even mild VR‐AKI seems to increase mortality rates in dogs.7