This suggests that structural alterations in renal cells caused by fluid overload (e.g., interstitial edema), hemodynamic changes induced by high CVP (increased afterload and reduced renal perfusion pressure), and host immune response (increased levels of pro-inflammatory IL-8) are factors clinically relevant for the association between CETP genotype and risk of sepsis-associated AKI. This evidence concerns the gene CETP and Sepsis.