title: Do ACE-inhibitors suppress tumour necrosis factor-alpha production in advanced chronic renal failure?
abstract: OBJECTIVE
  The serum levels of the catabolic cytokine TNF-alpha are often raised in malnourished chronic heart failure patients as well as in chronic renal failure (CRF) patients. Angiotensin-converting enzyme (ACE) inhibitors are often used in these patients and may decrease TNF-alpha and IL-1beta levels in vitro and in vivo. The aim of this study was to find out whether CRF patients with ongoing ACE-inhibitor treatment have lower TNF-alpha levels.
  
  
  METHODS
  Cross-sectional study.
  
  
  METHODS
  Tertiary Referral Center and University Hospital.
  
  
  METHODS
  Ninety-six predialysis patients (mean age 52 +/- 1 years) with advanced CRF (glomerular filtration rate 7 +/- 1 mL min-1).
  
  
  METHODS
  Plasma levels of TNF-alpha, subjective global assessment of nutritional status and data on ongoing antihypertensive treatment (ACE-inhibitors, beta blockers, calcium channel blockers and angiotensin II (AII) receptor blockers).
  
  
  RESULTS
  Patients treated with ACE-inhibitors (n = 44) had significantly lower plasma TNF-alpha levels (18.5 +/- 1.2 vs. 26.6 +/- 2.2 pg mL-1; P < 0.01) and were less frequently malnourished, relative to 52 patients not treated with ACE-inhibitors. No significant difference in TNF-alpha levels were observed when comparing patients with or without treatment with beta, calcium channel, or AII receptor blockers, respectively.
  
  
  CONCLUSIONS
  The present data suggest that the use of ACE-inhibitors is associated with lower plasma TNF-alpha and CRP levels as well as a lower prevalence of malnutrition in patients with advanced CRF. Further studies are needed to establish if there is a casual relationship between these findings and, if so, the molecular mechanism(s).
authors.affiliation: Division of Renal Medicine, Department of Clinical Science, Huddinge University Hospital, Karolinska Institute, Stockholm, Sweden. peter.stenvinkel@klinvet.ki.se
authors.forename: P
authors.initials: P
authors.lastname: Stenvinkel
authors.forename: P
authors.initials: P
authors.lastname: Andersson
authors.forename: T
authors.initials: T
authors.lastname: Wang
authors.forename: B
authors.initials: B
authors.lastname: Lindholm
authors.forename: J
authors.initials: J
authors.lastname: Bergström
authors.forename: J
authors.initials: J
authors.lastname: Palmblad
authors.forename: O
authors.initials: O
authors.lastname: Heimbürger
authors.forename: T
authors.initials: T
authors.lastname: Cederholm
mesh_terms: D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology*; D005260:Female; D006801:Humans; D007676:Kidney Failure, Chronic / Q000097:blood*; D008297:Male; D008875:Middle Aged; D009748:Nutrition Disorders / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000187:drug effects* / Q000378:metabolism*
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D014409:Tumor Necrosis Factor-alpha