This may mean different thresholds in different cohorts, such as for urinary Cystatin C [26] or NGAL [27], [28] in sepsis, as well as recognising that the kidney injury “signal” may be drowned out by other sources of the biomarker in some circumstances, thus rendering the biomarker not diagnostic of Structural-AKI. This evidence concerns the gene LCN2 and acute kidney injury.