On the other hand, oxidative stress and inflammatory reactions, uremic toxins, etc. in CKD patients cause denaturation, oxidation, and carbamylation of ApoA-I and other protein components of HDL particles, which affects the binding of HDL to cell surface cholesterol transporters, resulting in a decrease in HDL's ability to promote cholesterol efflux (37, 38). This evidence concerns the gene APOA1 and chronic kidney disease.