RESEARCH Increased serum CXCL16 i

Full list of author information is available at the end of the articleof the body affecting the kidney (secondary NS) [1,2]. NS is characterized primarily by high proteinuria (>3 g/dL), hypoalbuminemia and edema resulting from damage to the glomerular filtration membrane, causing the kidney to leak large amounts of plasma protein from the blood into the urine. This trait is typically accompanied by lipoprotein, could directly stimulate mesangial cells to proliferate and secrete inflammatory factors, including IL-6, TGF-β, MCF-1, connective tissue growth factor and PDGF. In addition, LDL and oxLDL could promote the activation of renal immune cells, subsequently upre-gulating NF-κB activity and hastening the release of inflammatory factors [3]. Therefore, kidney inflammation may be the result of a hyperlipidemia-induced influx of inflammatory mediators. However, the mechanism of lipid deposition in the kidney, the initial step for th