title: The relationship between inflammation, endothelial dysfunction and proteinuria in patients with diabetic nephropathy.
abstract: OBJECTIVE
  Diabetic nephropathy (DN) is a major manifestation of microangiopathy in patients with Diabetes Mellitus (DM). Inflammation is one of the major factors in the formation of endothelial dysfunction. Endothelial dysfunction is a major contributor to the complications of DM. The aim of the present study was to investigate the possible relationship between inflammation, endothelial dysfunction and proteinuria in patients with diabetic nephropathy.
  
  
  METHODS
  Plasma TNF-α and IL-6, pro-inflammatory cytokines, concentrations were measured in 25 patients with DN and in 30 diabetic control subjects. Also, we evaluated the markers of endothelial dysfunction such as flow mediated dilatation (FMD), nitrate-mediated dilatation (NMD) and carotid intima-media thickness (CIMT).
  
  
  RESULTS
  TNF-α, IL-6 and high-sensitivity C-reactive protein concentrations were significantly higher (p = 0.012, p = 0.006 and p < 0.001, respectively) in the patients with DN than the controls. And, urinary protein concentrations were significantly higher (p < 0.001) but eGFR levels were significantly lower (p < 0.001) in the patients with DN. FMD was significantly lower in DN patients (p < 0.001). We have observed that FMD correlated negatively with body mass index (r = -0.424, p < 0.05). And there was also a positive correlation between TNF-α and urinary protein concentrations in the patients with DN (p < 0.05).
  
  
  CONCLUSIONS
  TNF-α, IL-6, hsCRP and urinary protein concentrations are higher in the DN patients. There were no correlations among pro-inflammatory cytokines concentrations and markers of vascular endotelial disfunction. These findings did not show vascular endothelial dysfunction, but may indicate glomerular endothelial dysfunction.
authors.affiliation: Department of Endocrinology and Metabolism, Gulhane Military Medical Academy, Ankara, Turkey. ataslipinar@yahoo.com
authors.forename: Abdullah
authors.initials: A
authors.lastname: Taslipinar
authors.forename: Halil
authors.initials: H
authors.lastname: Yaman
authors.forename: Mahmut Ilker
authors.initials: MI
authors.lastname: Yilmaz
authors.forename: Seref
authors.initials: S
authors.lastname: Demirbas
authors.forename: Mutlu
authors.initials: M
authors.lastname: Saglam
authors.forename: Mine Yavuz
authors.initials: MY
authors.lastname: Taslipinar
authors.forename: Mehmet
authors.initials: M
authors.lastname: Agilli
authors.forename: Yasemin Gulcan
authors.initials: YG
authors.lastname: Kurt
authors.forename: Alper
authors.initials: A
authors.lastname: Sonmez
authors.forename: Omer
authors.initials: O
authors.lastname: Azal
authors.forename: Erol
authors.initials: E
authors.lastname: Bolu
authors.forename: Mujdat
authors.initials: M
authors.lastname: Yenicesu
authors.forename: Mustafa
authors.initials: M
authors.lastname: Kutlu
mesh_terms: D015415:Biomarkers / Q000097:blood*; D001808:Blood Vessels / Q000378:metabolism; D002097:C-Reactive Protein / Q000032:analysis; D059168:Carotid Intima-Media Thickness; D048909:Diabetes Complications; D003920:Diabetes Mellitus / Q000097:blood* / Q000503:physiopathology; D003928:Diabetic Nephropathies / Q000097:blood* / Q000150:complications / Q000503:physiopathology; D004727:Endothelium / Q000378:metabolism / Q000503:physiopathology*; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005919:Glomerular Filtration Rate; D006801:Humans; D007249:Inflammation / Q000097:blood* / Q000150:complications / Q000503:physiopathology; D015850:Interleukin-6 / Q000097:blood; D007678:Kidney Glomerulus / Q000378:metabolism / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D011507:Proteinuria / Q000097:blood* / Q000150:complications / Q000503:physiopathology; D014409:Tumor Necrosis Factor-alpha / Q000097:blood; D014664:Vasodilation
chemical_list: D015415:Biomarkers; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D002097:C-Reactive Protein