Patients with impaired renal function often have atherogenic dyslipidemia, including high TG and low HDL-C levels, which occurs as a result of impaired TG-rich lipoprotein catabolism associated with decreased lipoprotein lipase (LPL) activity or impaired HDL maturation caused by reduced lecithin-cholesterol acyltransferase (LCAT) activity [7,32,33,34,35]. This evidence concerns the gene LCAT and metabolic syndrome.