title: Association of low-grade inflammation with nephropathy in type 2 diabetic patients: role of elevated CRP-levels and 2 different gene-polymorphisms of proinflammatory cytokines.
abstract: BACKGROUND
  Chronic inflammatory processes are thought to play a key role in the development of micro- and macrovascular complications in type 2 diabetes mellitus. An association between low -grade inflammation and type 2 diabetes has been described in some studies. We assayed the association of two frequent polymorphisms in proinflammatory cytokines: the interleukin 6 G(-174)C promoter polymorphism [IL-6G(-174)C], the exon 2 interleukin receptor antagonist insertion deletion polymorphism [IL1RA]) and serum CRP levels with the prevalence of diabetic nephropathy in patients suffering from type 2 diabetes mellitus.
  
  
  METHODS
  A total of 141 patients with type 2 diabetes mellitus, with and without diabetic nephropathy was genotyped for the above mentioned polymorphisms: 66 with normoalbuminuria, 31 with microalbuminuria and 44 with macroalbuminuria. CRP levels were analysed by a high sensitivity - immunnephelometric assay.
  
  
  RESULTS
  While a significant association be-tween macroalbuminuria and CRP could be observed (p<0,015), no associations were found between IL-6G(-174)C or IL1RA genotype and any stage of nephropathy. CRP-levels were similar in the 3 different IL-6G(-174)C genotypes as well as in the 2 IL1RA genotypes.
  
  
  CONCLUSIONS
  In type 2 diabetic subjects elevated CRP levels are associated with an increased prevalence of albuminuria. The two investigated proinflammatory polymorphisms do not seem to contribute to initiation of nephropathy in type 2 diabetic patients but we cannot exclude effects of these polymorphisms on course of nephropathy.
authors.affiliation: Department of Medical and Chemical Laboratory Diagnostics, University of Vienna, Medical School, Vienna, Austria.
authors.forename: H
authors.initials: H
authors.lastname: Abrahamian
authors.forename: G
authors.initials: G
authors.lastname: Endler
authors.forename: M
authors.initials: M
authors.lastname: Exner
authors.forename: H
authors.initials: H
authors.lastname: Mauler
authors.forename: M
authors.initials: M
authors.lastname: Raith
authors.forename: L
authors.initials: L
authors.lastname: Endler
authors.forename: H
authors.initials: H
authors.lastname: Rumpold
authors.forename: M
authors.initials: M
authors.lastname: Gerdov
authors.forename: C
authors.initials: C
authors.lastname: Mannhalter
authors.forename: R
authors.initials: R
authors.lastname: Prager
authors.forename: K
authors.initials: K
authors.lastname: Irsigler
authors.forename: O F
authors.initials: OF
authors.lastname: Wagner
mesh_terms: D000368:Aged; D002097:C-Reactive Protein / Q000032:analysis*; D003924:Diabetes Mellitus, Type 2 / Q000097:blood* / Q000235:genetics*; D003928:Diabetic Nephropathies / Q000097:blood* / Q000235:genetics*; D005260:Female; D006801:Humans; D007249:Inflammation / Q000097:blood / Q000235:genetics; D018836:Inflammation Mediators / Q000097:blood; D053590:Interleukin 1 Receptor Antagonist Protein / Q000097:blood / Q000235:genetics; D015850:Interleukin-6 / Q000097:blood / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D016254:Mutagenesis, Insertional; D011110:Polymorphism, Genetic; D017384:Sequence Deletion
chemical_list: C507763:IL1RN protein, human; D018836:Inflammation Mediators; D053590:Interleukin 1 Receptor Antagonist Protein; D015850:Interleukin-6; D002097:C-Reactive Protein