Lipocalin-2 deficient mice demonstrated a higher susceptibility for bacterial infections, and in wild type animals undergoing sepsis, a strong correlation between plasma-NGAL, interleukin 6 (IL-6) and interleukin 10 (IL-10), but also with TNF alpha was found [15, 16], which raised the question whether plasma-NGAL might be stronger related to inflammation than to AKI itself. This evidence concerns the gene LCN2 and acute kidney injury.