Systemic inflammation in acute cardiorenal syndrome: an observational pilot study

Abstract

Aims: Acute cardiorenal syndrome (CRS) with and without consideration of the volume state was assessed with regard to inflammatory parameters.

Methods and results: Blood samples from patients with acute CRS (Ronco type 1 or 3, Group 1, n = 15), end-stage renal disease (Group 2, n = 12), hypertension (Group 3, n = 15), and, in a second cohort, with acute CRS and hypervolemia (Group 4, n = 9) and hypertension (Group 5, n = 10) were analysed with regard to lipopolysaccharide-binding protein (LBP), interleukins (ILs), and monocyte function (flow cytometry) both on admission (all groups) and on discharge (Groups 1 and 4). By discharge, one Group 1 patient died. LBP (ANOVA for Groups 1-3: P = 0.001) and IL-6 (Kruskal-Wallis for Groups 1-3: P < 0.0001) were higher in Group 1 (LBP: 11.7 ± 2.0 μg/mL; IL-6: 15.0 ± 6.1 pg/mL) and in Group 2 (LBP: 10.4 ± 1.4 μg/mL; IL-6: 14.6 ± 3.8 pg/mL) than in Group 3 (LBP: 5.8 ± 0.4 μg/mL; IL-6: 1.8 ± 0.4 pg/mL). In a direct comparison, the proportion of activated monocytes (CD14 and CD16 positive) was higher in Group 1 (6.9% ± 0.7%) vs. Group 3 (5.1% ± 0.6%; P = 0.018). Group 4 patients had higher IL-6 plasma levels (34.2 ± 10.1 pg/mL) than Group 1 patients (15.0 ± 6.1 pg/mL; P = 0.03). All other findings obtained in CRS groups (Groups 1 and 4) were comparable.

Conclusions: In acute CRS, a state of systemic inflammation was found, which is comparable with the end-stage renal disease situation. In comparison with hypertensive controls, a monocytic activation was found in acute CRS regardless of volume state.

Keywords: Cardiorenal syndrome; Heart failure; Inflammation; Monocyte function.