title: Salutary effects of hemodialysis on low-density lipoprotein proinflammatory and high-density lipoprotein anti-inflammatory properties in patient with end-stage renal disease.
abstract: End-stage renal disease (ESRD) causes oxidative stress, inflammation, low-density lipoprotein (LDL) oxidation, high-density lipoprotein (HDL) deficiency and accelerated atherosclerosis. Uptake of oxidized LDL by macrophages results in foam cell and plaque formation. HDL mitigates atherosclerosis via reverse cholesterol transport and inhibition of LDL oxidation. ESRD heightens LDL inflammatory activity and suppresses HDL anti-inflammatory activity. The effect of hemodialysis on the LDL and HDL inflammatory properties is unknown. By removing the potential pro-oxidant/proinflammatory uremic toxins, dialysis may attenuate LDL inflammatory and HDL anti-inflammatory properties. Conversely, exposure to dialyzer membrane and tubing and influx of impurities from dialysate can intensify LDL and HDL inflammatory activities. This study examined the effect of hemodialysis on LDL and HDL inflammatory activities. Plasma samples were obtained from 12 normal control and 26 ESRD patients before and after hemodialysis with (16 patients) or without (10 patients) heparinization. HDL and LDL were isolated and tested for monocyte chemotactic activity in cultured endothelial cells. ESRD patients had increased LDL chemotactic activity, reduced HDL anti-inflammatory activity, paraoxonase and glutathione peroxidase levels, and elevated plasma IL-6 before dialysis. Hemodialysis partially improved LDL inflammatory and HDL anti-inflammatory activities and enhanced patients' HDL ability to suppress their LDL inflammatory activity. The salutary effect on LDL inflammatory activity was significantly greater in patients dialyzed with than those without heparin. ESRD heightens LDL inflammatory and impairs HDL anti-inflammatory activities. Hemodialysis partially improves LDL and HDL inflammatory activities. The salutary effects of hemodialysis are in part mediated by heparin, which is known to possess lipolytic and antioxidant properties.
authors.affiliation: Division of Nephrology and Hypertension, University of California, Irvine Medical Center, 101 The City Dr, 4th Floor City Tower, Orange, CA 92868, USA. ndvaziri@uci.edu
authors.forename: Nosratola D
authors.initials: ND
authors.lastname: Vaziri
authors.forename: Kaveh
authors.initials: K
authors.lastname: Navab
authors.forename: Pavan
authors.initials: P
authors.lastname: Gollapudi
authors.forename: Hamid
authors.initials: H
authors.lastname: Moradi
authors.forename: Madeleine V
authors.initials: MV
authors.lastname: Pahl
authors.forename: Cyril H
authors.initials: CH
authors.lastname: Barton
authors.forename: Alan M
authors.initials: AM
authors.lastname: Fogelman
authors.forename: Mohamad
authors.initials: M
authors.lastname: Navab
mesh_terms: D000328:Adult; D000893:Anti-Inflammatory Agents / Q000378:metabolism; D000925:Anticoagulants / Q000378:metabolism / Q000627:therapeutic use; D050197:Atherosclerosis / Q000209:etiology / Q000378:metabolism / Q000628:therapy; D008076:Cholesterol, HDL / Q000378:metabolism*; D057186:Comparative Effectiveness Research; D005260:Female; D006493:Heparin / Q000378:metabolism / Q000627:therapeutic use; D006801:Humans; D007249:Inflammation / Q000209:etiology / Q000378:metabolism / Q000628:therapy; D018836:Inflammation Mediators / Q000378:metabolism; D007676:Kidney Failure, Chronic / Q000150:complications / Q000378:metabolism* / Q000503:physiopathology / Q000628:therapy*; D015227:Lipid Peroxidation; D008077:Lipoproteins, LDL / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D010084:Oxidation-Reduction; D006435:Renal Dialysis; D014511:Uremia / Q000209:etiology / Q000378:metabolism / Q000628:therapy
chemical_list: D000893:Anti-Inflammatory Agents; D000925:Anticoagulants; D008076:Cholesterol, HDL; D018836:Inflammation Mediators; D008077:Lipoproteins, LDL; D006493:Heparin