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.

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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.

Contexto: la procalcitonina (PCT) podría ser útil en la evaluación de la función del injerto renal (IR) en el postrasplante inmediato, ya que sus niveles se incrementan posterior a la elevación de citocinas inflamatorias (IL-6, TNF-?) durante eventos de disfunción renal. Objetivo: determinar la asociación de la PCT sérica con la función del injerto renal en el periodo postrasplante inmediato. Metodología: cohorte retrospectiva de septiembre del 2018 a abril del 2019 en la División de Nefrología y Trasplantes, del Centro Médico Nacional de Occidente (CMNO), del Instituto Mexicano del Seguro Social (IMSS). Se incluyeron 62 receptores de trasplante renal de donante vivo (DV) y fallecido (DF) con determinación de PCT en los primeros 7 días del TR y el registro de eventos de disfunción temprana del injerto (DTI), fueron comparados con pacientes sin DTI (sDTI). Resultados: los receptores con DTI presentaron niveles más altos de PCT (13,90, 3,90, 1,22 ng/mL) comparado con el grupo sin DTI (0,32, 0,31 y 0,22 ng/ml) en los días 1, 3 y 5 respectivamente; p < 0,05. Conclusiones: la PCT es un marcador biológico asociado a DTI en el postrasplante renal inmediato.

Triggering receptor expressed on myeloid cells (TREM)-1 is a potent and early amplifier of the inflammatory response expressed on neutrophils and monocytes/macrophages. TREM-1, and its soluble form (sTREM-1), are increased in sepsis and other noninfectious inflammatory conditions. However, virtually no data are available in kidney disease. To determine serum sTREM-1 and its associated variables in patients on hemodialysis (HD), cross-sectional study including 264 HD patients and 148 controls. sTREM-1 was measured by quantitative sandwich enzyme immunoassay; soluble tumor necrosis factor receptor-1 (sTNF-R1), interleukin-6 (IL-6), and C-reactive protein (CRP) were also measured. All inflammation markers were significantly higher in HD patients than controls. Median (IQR) sTREM-1 was 1,006 (613–1,650) pg/mL but undetectable in controls. Considering only HD patients, sTREM-1 was positively correlated with IL-6 (r = 0.19, p = 0.008), and its levels were significantly higher in patients with arteriovenous fistula than in those with temporary catheter (1,226 vs. 743 pg/mL), in patients with 3 HD sessions/week than in those with 2 sessions/week (1,150 vs. 646 pg/mL), and in patients with >1 year on HD than in those with ≤1 year (1,100 vs. 948 pg/mL), whereas they were not different regarding age or presence of infection. Serum sTREM-1, sTNF-R1, IL-6, and CRP were higher in HD patients compared to controls. In HD patients, sTREM-1 displayed higher levels in individuals with arteriovenous fistula, 3 sessions/week and longer vintage, but not in those with infection or older age; in multivariate analysis, only the first two variables significantly predicted higher sTREM-1 levels.