Reduced lipoprotein lipase (LPL) synthesis [47], VLDL deficiency [48, 49], decreased LDL receptor (LDLR) sensitivity, and impaired clearance of apoB-100 [50–52] are additional mechanisms contributing to the increase in TG, apoB-containing lipoproteins (such as VLDL, IDL, and LDL), Lp (a), and total cholesterol in nephrotic syndrome [46]. This evidence concerns the gene LPL and nephrotic syndrome.