Do ACE-inhibitors suppress tumour necrosis factor-α production in advanced chronic renal failure?
Article first published online: 25 DEC 2001
Journal of Internal Medicine
Volume 246, Issue 5, pages 503–507, November 1999
How to Cite
Stenvinkel, P., Andersson, P., Wang, T., Lindholm, B., Bergström, J., Palmblad, J., Heimbürger, O. and Cederholm, T. (1999), Do ACE-inhibitors suppress tumour necrosis factor-α production in advanced chronic renal failure?. Journal of Internal Medicine, 246: 503–507. doi: 10.1046/j.1365-2796.1999.00560.x
- Issue published online: 25 DEC 2001
- Article first published online: 25 DEC 2001
- chronic renal failure;
Abstract. Stenvinkel P, Andersson P, Wang T, Lindholm B, Bergström J, Palmblad J, Heimbürger O, Cederholm T (Huddinge University Hospital and Karolinska Institute, Stockholm; Sweden). Do ACE-inhibitors suppress tumour necrosis factor-α production in advanced chronic renal failure? J Intern Med 1999; 246: 503–507.
Objectives. The serum levels of the catabolic cytokine TNF-α 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-α and IL-1β 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-α 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-α, 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-α 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-α 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-α 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).