While we may be able to use some of the constructs outlined above to make therapeutic decisions (for example, a patient with NGAL elevation, who has FO and is not responsive to loop diuretics, may be an appropriate candidate for consideration of early KRT), less is known about the biological underpinnings of AKI phenotypes, which limits our ability to provide individualized, biology-informed treatments. This evidence concerns the gene LCN2 and acute kidney injury.