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
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).