This study compared the effect of enalapril versus placebo on serum tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, and C-reactive protein (CRP) in hemodialysis in a randomized, double- blinded, controlled clinical trial. Patients without infection or antiinflammatory drugs were randomly allocated to a study (n = 13, enalapril, 20 mg/day) or control (n = 12, placebo) group; all had arteriovenous fistula. Serum TNF-alpha, IL-6, and CRP were measured at 0, 1, and 3 months. Systolic blood pressure (baseline vs. final) was 151 +/- 25 vs. 135 +/- 19 mm Hg (p < 0.05) in the study group and 154 +/- 21 vs. 144 +/- 27 mm Hg in control group; diastolic blood pressure was 86 +/- 9 vs. 76 +/- 13 and 91 +/- 16 vs. 81 +/- 18 mm Hg, respectively; median (percentiles 25%-75%) IL-6 (baseline vs. final) was 4.2 (3-8) vs. 4.1 (2-9) pg/mL and 6.3 (3-9) vs. 6.7 (3-8) pg/mL; and CRP was 1.9 (1-7) vs. 3.0 (1-12) mg/L and 4.7 (1-16) vs. 3.9 (2-16) mg/L, respectively. TNF-alpha was detected in only two patients. Enalapril significantly reduced blood pressure in hemodialysis patients, but it did not decrease IL-6 and CRP compared with placebo.

To evaluate individual and combined effect of captopril and telmisartan on systemic inflammation markers of hemodialysis (HD) patients. Randomized, double-blinded, controlled clinical trial. Patients on HD at least 2 months, with arteriovenous fistula, were randomly allocated to groups: (1) captopril/placebo (N 13); (2) telmisartan/placebo (N 13); (3) captopril + telmisartan (N 12); or (4) placebo/placebo (N 12). During 3 months, patients received oral drugs as follows: captopril 50 mg/day, telmisartan 80 mg/day or placebo. Patients excluded if they had conditions or were on drugs potentially influencing on inflammation. Clinical and biochemical evaluations were performed monthly. Serum tumor necrosis factor alpha (TNFα), interleukin 6 (IL-6), and C-reactive protein (CRP) were measured at 0, 1 and 3 months. Baseline, demographic, clinical and biochemical variables were comparable between groups. Baseline versus final inflammatory markers were: captopril/placebo TNFα, 2.47 (0.1–4.5) versus 1.73 (0.3–3.8) pg/ml; IL-6, 17.03 (7.2–23) versus 7.90 (0.7–19) pg/ml; CRP, 4.21 (1.6–18) versus 5.9 (3.0–28) mg/l; telmisartan/placebo TNFα, 3.03 (2.3–4.6) versus 1.70 (1.2–2.0) pg/ml; IL-6, 14.10 (5.5–23) versus 9.85 (6.2–13) pg/ml; CRP, 5.74 (2.1–13) versus 10.60 (1.5–27) mg/l; captopril + telmisartan TNFα, 1.43 (0.7–5.4) versus 0.40 (0.1–2.1) pg/ml; IL-6, 10.05 (4.9–23) versus 4.00 (0.7–7.7) pg/ml (p < 0.05); CRP, 3.26 (0.7–12) versus 2.83 (0.6–6.5) mg/l; placebo/placebo TNFα, 3.13 (1.6–5.6) versus 1.64 (1.6–2.3) pg/ml; IL-6, 8.12 (5.4–16) versus 7.60 (2.4–15) pg/ml; CRP, 5.23 (1.9–16) versus 3.13 (1.5–18) mg/l. Monotherapy with captopril or telmisartan display a trend, but their combined treatment significantly decreased serum levels of IL-6. No remarkable changes on TNFα and CRP were observed.