title: Type 2 diabetes in patients with end-stage renal disease is not associated with further increased serum inflammatory parameters.
abstract: BACKGROUND
  Cardiovascular morbidity and mortality is markedly increased in patients with end-stage renal disease (ESRD) undergoing hemodialysis (HD) and is further pronounced when diabetes mellitus is also present. As atherogenesis is mediated by inflammation of vessel walls and as evidence evolves that atherosclerosis and diabetes mellitus share a common inflammatory basis, we considered whether ESRD patients with additional diabetes mellitus exhibit increased inflammation levels exceeding those of ESRD patients without diabetes mellitus.
  
  
  METHODS
  The study included 20 ESRD patients with type 2 diabetes mellitus and 16 non-diabetic ESRD patients on long-term HD. The patients' clinical characteristics and serum levels of C-reactive protein (CRP), interleukin 6 (IL-6), soluble tumor necrosis factor receptor I (sTNF-RI), neopterin and fibrinogen were assessed.
  
  
  RESULTS
  There were no significant differences in serum levels of CRP, IL-6, neopterin, sTNF-RI and fibrinogen found in ESRD patients with and without diabetes mellitus. HD duration correlated significantly with neopterin (r=0.515, p<0.001) and sTNF-RI (r=0.429, p<0.05) serum levels. HD led to a significant reduction in neopterin levels whereas CRP, IL-6 and sTNF-RI levels did not change significantly.
  
  
  CONCLUSIONS
  With the inherent limitations of a small number of patients studied, we observed that the presence of type 2 diabetes mellitus in addition to ESRD was not associated with further increased serum levels of the examined inflammatory parameters. Our observations suggest that the worsened prognosis of diabetic ESRD patients is probably not explainable by superimposing inflammatory processes.
authors.affiliation: Second Department of Medicine, General Hospital Linz, Linz, Austria. gerd.bodlaj@akh.linz.at
authors.forename: Gerd
authors.initials: G
authors.lastname: Bodlaj
authors.forename: Jörg
authors.initials: J
authors.lastname: Berg
authors.forename: Robert
authors.initials: R
authors.lastname: Pichler
authors.forename: Thomas
authors.initials: T
authors.lastname: Sailer
authors.forename: Georg
authors.initials: G
authors.lastname: Biesenbach
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D015703:Antigens, CD / Q000097:blood; D001161:Arteriosclerosis / Q000097:blood / Q000175:diagnosis / Q000209:etiology; D002097:C-Reactive Protein / Q000032:analysis; D003924:Diabetes Mellitus, Type 2 / Q000097:blood* / Q000150:complications; D003928:Diabetic Nephropathies / Q000097:blood* / Q000628:therapy; D005260:Female; D005340:Fibrinogen / Q000032:analysis; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood*; D015850:Interleukin-6 / Q000097:blood; D007676:Kidney Failure, Chronic / Q000097:blood* / Q000628:therapy; D008297:Male; D008875:Middle Aged; D019798:Neopterin / Q000097:blood; D018124:Receptors, Tumor Necrosis Factor / Q000097:blood; D047888:Receptors, Tumor Necrosis Factor, Type I; D006435:Renal Dialysis
chemical_list: D015703:Antigens, CD; D018836:Inflammation Mediators; D015850:Interleukin-6; D018124:Receptors, Tumor Necrosis Factor; D047888:Receptors, Tumor Necrosis Factor, Type I; D019798:Neopterin; D005340:Fibrinogen; D002097:C-Reactive Protein