title: Disturbed tumor necrosis factor system is linked with lower eGFR and chronic inflammation in hypertension.
abstract: BACKGROUND
  The relationship between tumor necrosis factor (TNF)-related parameters and cardiorenal metabolic factors is still controversial in clinical hypertension.
  
  
  METHODS
  Normotensive men (NT, n=60) and treated stage 2 and 3 essential hypertensive men (HT, n=89) were enrolled in this study. The relationship between TNF-related parameters and cardiorenal metabolic factors was examined in NT and HT, separately.
  
  
  RESULTS
  HT showed higher rates of insulin resistance and enhanced chronic inflammation compared with NT. The levels of soluble TNF receptor 1 and 2 were significantly higher in HT than in NT, although TNF-α levels were unexpectedly lower in HT than in NT. Regression analysis indicated that the TNF-related parameters were closely linked with mild renal dysfunction both in NT and HT, and moderately related to chronic inflammation only in HT. HT taking inhibitors of the renin-angiotensin system showed improved insulin resistance, but no difference in the TNF-related parameters.
  
  
  CONCLUSIONS
  These results suggest that the disturbed TNF system is closely linked with chronic inflammation rather than with insulin resistance in HT.
authors.forename: Takashi
authors.initials: T
authors.lastname: Eguchi
authors.forename: Tatsuya
authors.initials: T
authors.lastname: Maruyama
authors.forename: Yoichi
authors.initials: Y
authors.lastname: Ohno
authors.forename: Toshiyuki
authors.initials: T
authors.lastname: Morii
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Hirose
authors.forename: Tsuneo
authors.initials: T
authors.lastname: Takenaka
authors.forename: Hiromichi
authors.initials: H
authors.lastname: Suzuki
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Kawabe
authors.forename: Ikuo
authors.initials: I
authors.lastname: Saito
authors.forename: Matsuhiko
authors.initials: M
authors.lastname: Hayashi
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Itoh
mesh_terms: D000368:Aged; D001794:Blood Pressure / Q000235:genetics; D002908:Chronic Disease; D000075222:Essential Hypertension; D005919:Glomerular Filtration Rate; D006801:Humans; D006973:Hypertension / Q000235:genetics* / Q000503:physiopathology; D007249:Inflammation / Q000235:genetics* / Q000503:physiopathology; D007333:Insulin Resistance / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D018124:Receptors, Tumor Necrosis Factor / Q000096:biosynthesis; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis* / Q000235:genetics
chemical_list: D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha