Our results highlight the presence of abnormal lipid metabolism namely significantly lower concentrations of the protective ApoA1, HDL-C, HDL-2 cholesterol and significantly higher concentrations of the atherogenic IDL-TG, S-VLDL-C, XS-VLDL-TG, LDL-TG and ApoB/ApoA1 ratio in late compared to early stages of CKD as well as in every increment of CKD stage compared with the previous stage of disease. This evidence concerns the gene APOA1 and chronic kidney disease.