UC Irvine

Key PointsHeavy glomerular proteinuria (nephrotic syndrome) and advanced chronic kidney disease (CKD) can elicit profound changes in the structure and function of HDLHDL abnormalities in nephrotic syndrome impair reverse cholesterol transport and consequently promote foam cell formation, atherosclerosis, and glomerulosclerosisHDL abnormalities in nephrotic syndrome are largely due to lecithin–cholesteryl acyltransferase (LCAT) deficiency caused by urinary losses, elevated plasma cholesterol ester transfer protein levels, hypoalbuminaemia, and/or reduced expression levels of hepatic HDL docking receptor (SRB1)HDL abnormalities in CKD are caused by deficiencies in ApoA-1, ApoA-2, LCAT, paraoxonase-1, glutathione peroxidase, elevated levels of ACAT-1, and increased oxidative and myeloperoxidase modifications to HDL cargoOxidative and myeloperoxidase modifications to ApoA-1, ApoA-2 and SRB1 impair HDL-mediated reverse cholesterol transport and HDL antioxidant and anti-inflammatory activityHDL abnormalities contribute to endothelial dysfunction, accelerated atherosclerosis, oxidative stress, and systemic inflammation in patients with CKD