title: Possible involvement of TNF-alpha in left ventricular remodeling in hemodialysis patients.
abstract: BACKGROUND
  Tumor necrosis factor (TNF)-alpha causes hypertrophic as well as negative inotropic effects on cardiac myocytes. Circulating TNF-alpha levels are reported to be elevated in end-stage renal disease (ESRD) patients undergoing maintenance hemodialysis (HD). We investigated whether increased circulating TNF-alpha is associated with left ventricular remodeling against pressure and/or volume overload in HD patients with or without diabetes mellitus.
  
  
  METHODS
  Echocardiography and the measurement of plasma TNF-alpha and B-type natriuretic peptide (BNP) concentrations, one of the parameters indicating left ventricular wall stress, were performed on 176 ESRD patients undergoing maintenance HD (88 non-diabetic and 88 diabetic patients).
  
  
  RESULTS
  The mean plasma TNF-alpha concentrations were high, but did not differ between non-diabetic and diabetic patients (9.8 +/- 4.3 pg/mL vs. 9.9 +/- 5.4 pg/mL). In non-diabetic patients, plasma TNF-alpha concentration correlated positively with interventricular septal wall thickness (IVST) and relative left ventricular wall thickness (rLVWT), and inversely with left intraventricular dimensions, but did not correlate with left ventricular mass index (LVMI). In contrast, in diabetic patients, plasma TNF-alpha concentration correlated positively with plasma BNP concentration (r=0.821, p=0.0001) and left intraventricular dimensions, and inversely with rLVWT (r=-0.407, p=0.0001) and left ventricular fractional shortening (r=-0.445, p=0.0001).
  
  
  CONCLUSIONS
  Circulating TNF-alpha is possibly involved in concentric left ventricular remodeling in non-diabetic HD patients, whereas it is associated with eccentric left ventricular remodeling against sustained pressure and/or volume overload in diabetic HD patients.
authors.affiliation: Cardiovascular Division, Toujinkai Hospital, Kyoto, Japan. tojinkai.hosp@dream.com
authors.forename: Masato
authors.initials: M
authors.lastname: Nishimura
authors.forename: Tetsuya
authors.initials: T
authors.lastname: Hashimoto
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Kobayashi
authors.forename: Toyofumi
authors.initials: T
authors.lastname: Fukukda
authors.forename: Koji
authors.initials: K
authors.lastname: Okino
authors.forename: Noriyuki
authors.initials: N
authors.lastname: Yamamoto
authors.forename: Naoto
authors.initials: N
authors.lastname: Nakamura
authors.forename: Toshikazu
authors.initials: T
authors.lastname: Yoshikawa
authors.forename: Hakuo
authors.initials: H
authors.lastname: Takahashi
authors.forename: Toshihiko
authors.initials: T
authors.lastname: Ono
mesh_terms: D003928:Diabetic Nephropathies / Q000097:blood / Q000503:physiopathology / Q000628:therapy; D004452:Echocardiography; D005260:Female; D006801:Humans; D007676:Kidney Failure, Chronic / Q000097:blood / Q000503:physiopathology / Q000628:therapy; D008297:Male; D008875:Middle Aged; D020097:Natriuretic Peptide, Brain / Q000097:blood; D006435:Renal Dialysis; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis / Q000502:physiology*; D016277:Ventricular Function, Left; D020257:Ventricular Remodeling / Q000502:physiology*
chemical_list: D014409:Tumor Necrosis Factor-alpha; D020097:Natriuretic Peptide, Brain