title: Do insulin resistance conditions further impair the lipid and inflammatory profile in end-stage renal disease patients on hemodialysis?
abstract: BACKGROUND
  Type 2 diabetes (T2DM) and chronic renal disease constitute important risk factors of atherosclerotic cardiovascular disease, associated with lipid abnormalities, and proinflammatory states. Advances in renal replacement therapy such as hemodialysis (HD) have not reduced morbi-mortality. It has not been elucidated if the concomitant presence of T2DM or metabolic syndrome with end-stage renal disease further impairs the atherogenic profiles.
  
  
  METHODS
  We studied 122 HD patients, among which 44 presented with T2DM (HD-T2DM) and 30 with metabolic syndrome (HD-MS); 48 had neither T2DM nor metabolic syndrome (HD-C). Lipoprotein profile, including atherogenic remnant lipoproteins (RLP), and inflammation markers--high sensitivity C-reactive protein (hsCRP), adiponectin, and interleukin-6 (IL-6)--were measured.
  
  
  RESULTS
  In all HD patients, triglycerides, free fatty acids, and RLP showed no differences between HD groups, whereas high-density lipoprotein cholesterol (HDL-C) was decreased, particularly in HD-T2DM and HD-MS, with respect to HD-C (P<0.01). Regarding inflammatory parameters, both IL-6 and hsCRP were found to be similar between HD groups. Adiponectin paradoxically shows higher values in relation to those expected for insulin resistance situations showing no differences between HD groups.
  
  
  CONCLUSIONS
  The presence of T2DM or metabolic syndrome did not worsen atherogenic lipoprotein levels, but did reduce HDL-C. Neither was the proinflammatory profile further altered in HD patients in the presence of insulin resistance conditions.
authors.affiliation: 1 Laboratory of Lipids and Lipoproteins, Department of Clinical Biochemistry, Faculty of Pharmacy and Biochemistry, INFIBIOC, University of Buenos Aires , Buenos Aires, Argentina .
authors.forename: Leonardo
authors.initials: L
authors.lastname: Cacciagiú
authors.forename: Ana I
authors.initials: AI
authors.lastname: González
authors.forename: Alicia
authors.initials: A
authors.lastname: Elbert
authors.forename: Guillermo
authors.initials: G
authors.lastname: De'Marziani
authors.forename: Tetsuo
authors.initials: T
authors.lastname: Machida
authors.forename: Masami
authors.initials: M
authors.lastname: Murakami
authors.forename: Graciela I
authors.initials: GI
authors.lastname: López
authors.forename: Regina
authors.initials: R
authors.lastname: Wikinski
authors.forename: Katsuyuki
authors.initials: K
authors.lastname: Nakajima
authors.forename: Laura
authors.initials: L
authors.lastname: Schreier
mesh_terms: D052242:Adiponectin / Q000097:blood; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D050197:Atherosclerosis / Q000097:blood / Q000276:immunology; D002097:C-Reactive Protein / Q000378:metabolism; D008076:Cholesterol, HDL / Q000097:blood; D003924:Diabetes Mellitus, Type 2 / Q000097:blood* / Q000276:immunology; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005260:Female; D006801:Humans; D007249:Inflammation / Q000097:blood*; D007333:Insulin Resistance; D015850:Interleukin-6 / Q000097:blood; D007676:Kidney Failure, Chronic / Q000097:blood* / Q000276:immunology; D008055:Lipids / Q000097:blood*; D008297:Male; D008875:Middle Aged; D006435:Renal Dialysis / Q000379:methods*; D012307:Risk Factors; D014280:Triglycerides / Q000097:blood
chemical_list: D052242:Adiponectin; D008076:Cholesterol, HDL; D005230:Fatty Acids, Nonesterified; D015850:Interleukin-6; D008055:Lipids; D014280:Triglycerides; D002097:C-Reactive Protein