Do ACE-inhibitors suppress tumour necrosis factor-alpha production in advanced chronic renal failure?

Citation
P. Stenvinkel et al., Do ACE-inhibitors suppress tumour necrosis factor-alpha production in advanced chronic renal failure?, J INTERN M, 246(5), 1999, pp. 503-507
Citations number
22
Categorie Soggetti
General & Internal Medicine","Medical Research General Topics
Journal title
JOURNAL OF INTERNAL MEDICINE
ISSN journal
09546820 → ACNP
Volume
246
Issue
5
Year of publication
1999
Pages
503 - 507
Database
ISI
SICI code
0954-6820(199911)246:5<503:DASTNF>2.0.ZU;2-T
Abstract
Objectives. 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) inhibito rs are often used in these patients and may decrease TNF-alpha and IL-1 bet a levels in vitro and in vivo. The aim of this study was to find out whethe r CRF patients with ongoing ACE-inhibitor treatment have lower TNF-alpha le vels. Design. Cross-sectional study. Setting. Tertiary Referral Center and University Hospital. Subjects. Ninety-six predialysis patients (mean age 52 +/- 1 years) with ad vanced CRF (glomerular filtration rate 7 +/- 1 mL min(-1)). Main outcome measures. Plasma levels of TNF-alpha, subjective global assess ment 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 lo wer 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 tre ated with ACE-inhibitors. No significant difference in TNF-alpha levels wer e observed when comparing patients with or without treatment with beta, cal cium channel, or AII receptor blockers, respectively. Conclusions. The present data suggest that the use of ACE-inhibitors is ass ociated with lower plasma TNP-alpha and CRP levels as well as a lower preva lence of malnutrition in patients with advanced CRF. Further studies are ne eded to establish if there is a casual relationship between these findings and, if so, the molecular mechanism(s).