Previous studies have suggested that a hyperglycemic environment enhanced the renal toxicity of LDL by promoting LDL glycosylation modification and oxidative stress: AGE-modified LDL could be more readily taken up by glomerular mesangial cells, activating the NF-κB pathway and inducing the expression of pro-fibrotic factors, thereby accelerating glomerulosclerosis (40). This evidence concerns the gene NFKB1 and glomerulosclerosis.