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J Intern Med. 1999 Nov;246(5):503-7.

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

Author information

1
Division of Renal Medicine, Department of Clinical Science, Huddinge University Hospital, Karolinska Institute, Stockholm, Sweden. peter.stenvinkel@klinvet.ki.se

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) 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.

DESIGN:

Cross-sectional study.

SETTING:

Tertiary Referral Center and University Hospital.

SUBJECTS:

Ninety-six predialysis patients (mean age 52 +/- 1 years) with advanced CRF (glomerular filtration rate 7 +/- 1 mL min-1).

MAIN OUTCOME MEASURES:

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).

PMID:
10583720
[Indexed for MEDLINE]
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