Systemic inflammation in acute cardiorenal syndrome: an observational pilot study

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

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.

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.