title: Expression of scavenger receptor CD36 in chronic renal failure patients.
abstract: BACKGROUND
  Patients with chronic renal failure (CRF) are at increased risk of atherosclerosis development. One of the major steps in pathogenesis of atherosclerosis is formation of foam cells. Scavenger receptor CD36 is among the major receptors for oxidized low density lipoproteins (oxLDL) and therefore it plays a crucial role in foam cell formation. The aim of the present study was to investigate the expression of CD36 on blood monocytes of CRF patients.
  
  
  METHODS
  Expression of CD36 on blood monocytes of CRF patients treated with hemodialysis (HD), peritoneal dialysis (PD), those not yet on dialysis (predialysis), and controls was assessed with the use of flow cytometry. Additionally, the major lipid peroxidation markers, malondialdehyde (MDA) and 4-hydroxyalkenals (HAE), were measured. Further, impact of treatment with HMG-CoA reductase inhibitors (statins) on CD36 expression in CRF patients was evaluated.
  
  
  RESULTS
  Expression of monocyte CD36, measured as mean fluorescence intensity (MFI) was significantly higher in HD and PD patients, when compared to controls without renal insufficiency (respectively: 1011 +/- 288 and 1000 +/- 309 vs. 710 +/- 313; P < 0.01 for both groups). This was not the case in predialysis group (828 +/- 363 vs. 710 +/- 313). Higher concentrations of lipid peroxidation indicators, MDA and HAE were observed in all three subgroups of CRF patients (2.1 +/- 0.51, 2.02 +/- 0.27, and 1.81 +/- 0.53 microm in HD, PD, and predialysis group, respectively, vs. 1.13 +/- 0.59 microm in controls; P < 0.01). Patients treated with statins showed significantly lower CD36 expression than patients without statin therapy.
  
  
  CONCLUSIONS
  The present study, for the first time, demonstrates increased expression of CD36 scavenger receptor in CRF patients. This may be a possible risk factor for accelerated atherogenesis observed in this group of patients.
authors.affiliation: Department of Nephrology, Transplantology and Internal Medicine, Medical University of Gdansk, Gdansk, Poland. chmiel@amg.gda.pl
authors.forename: Michal
authors.initials: M
authors.lastname: Chmielewski
authors.forename: Ewa
authors.initials: E
authors.lastname: Bryl
authors.forename: Lukasz
authors.initials: L
authors.lastname: Marzec
authors.forename: Ewa
authors.initials: E
authors.lastname: Aleksandrowicz
authors.forename: Jacek M
authors.initials: JM
authors.lastname: Witkowski
authors.forename: Boleslaw
authors.initials: B
authors.lastname: Rutkowski
mesh_terms: D050197:Atherosclerosis / Q000276:immunology; D018955:CD36 Antigens / Q000096:biosynthesis*; D005260:Female; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000494:pharmacology; D007676:Kidney Failure, Chronic / Q000276:immunology* / Q000628:therapy; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000187:drug effects / Q000276:immunology*; D006435:Renal Dialysis
chemical_list: D018955:CD36 Antigens; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors