An analysis conducted by Boutin et al. of the urinary peptides NGAL, CysC, PENK, and liver fatty acid-binding protein (LFABP) in an extensive study of 1154 patients revealed similar pathological pathways in both sAKI and AKI, primarily involving inflammation, hemolysis, and endothelial dysfunction [50]. The gene discussed is LCN2; the disease is acute kidney injury.