Key result
Acutely decompensated cardiorenal syndrome was associated with a higher degree of systemic inflammation compared to hypertensive controls, which was largely unaffected by in-hospital therapy.
Why the study?
Does current in-hospital therapy improve systemic inflammation and monocyte activation in patients with acutely decompensated cardiorenal syndrome?
Observational (n=15)
Does current in-hospital therapy improve systemic inflammation and monocyte activation in patients with acutely decompensated cardiorenal syndrome?
Absolute Event Rate: 6.9% vs 5.1%
p-value: p==0.07
Acutely decompensated cardiorenal syndrome is associated with elevated systemic inflammation and monocyte activation that are largely unaffected by current in-hospital therapies.
Inflammation persists despite in-hospital therapy in decompensated cardiorenal syndrome; hypothesis-generating for targeted anti-inflammatory trials.
Background A role for enteric endotoxin translocation has been postulated for heart-failure condition. In acutely decompensated cardiorenal syndrome (Ronco type 1 or type 3), the role of systemic inflammation remains unclear. Methods: Blood samples from 15 consecutively hospitalized cardiorenal syndrome (CRS) patients without pneumonia or urinary-tract infection were analyzed at admission and before hospital discharge. Methods included flow-cytometry analysis of monocyte function in terms of activation (CD14+/CD16+; CD14-/CD16+). Results were displayed as medians (per group) with standard deviation. ANOVA or Kruskal-Wallis test was performed, where applicable. Differences were considered as significant, if p<0.05. Results: Baseline parameters of renal and cardiac function were displayed in the Table. CRS Patients Hemodialysis Patients Hypertensive Patients p Age (years) 71.9 ± 9.1 71.3 ± 8.6 60.5 ± 13.7 <0.01 LVEF (%) 39.9 ± 15.7 54.0 ± 11.4 81.5 ± 4.9 <0.001 Creatinine (µmol/l) 270.0 ± 142.7 583.0 ± 248.7 67.0 ± 14.0 <0.0001 Urea (mmol/l) 22.4 ± 11.0 15.5 ± 5.3 3.5 ± 1.0 <0.0001 Brain-natriuretic peptide (ng/ml) 854.0 ± 1081.0 328.0 ± 299.8 21.5 ± 59.6 <0.0001 C-reactive protein (mg/dl) 36.9 ± 34.0 9.5 ± 13.2 1.9 ± 3.1 <0.001 Lipopolysaccharide-binding protein (ng/ml) 11.7 ± 7.9 10.4 ± 4.5 5.8 ± 1.6 =0.001 Procalcitonin (ng/ml) 0,2 ± 2.0 0.5 ± 1.0 0.0 ± 0.04 <0.0001 Interleukin-6 (pg/ml) 15.0 ± 23.6 14.6 ± 12.1 1.8 ± 1.5 <0.0001 Albumin (mg/dl) 34.0 ± 6.5 32.0 ± 4.1 41.0 ± 2.6 <0.0001 CD14+/CD16+ Monocytes 6.9 ± 2.7 7.9 ± 3.0 5.1 ± 2.3 =0.07 CD14-/CD16+ Monocytes 7.3 ± 5.8 9.5 ± 3.8 6.2 ± 2.8 ns Flow-cytometry analysis showed a tendency toward monocyte activation (CD14+/CD16+) both in CRS and hemodialysis patients. Individual comparisons between CRS/hypertensive patients and hemodialysis/hypertensive patients were significantly different. By discharge, one CRS patient died. No CRS patient required renal replacement therapy. Surviving CRS patients showed a normalization of urea (p<0.01), interleukin-6 tended to improve by discharge (p=0.01). Other prespecified parameters (Table) did not change by discharge. Conclusion Based on intergroup-comparisons, there is a higher degree of systemic inflammation in both CRS and hemodialysis patients than in hypertensive control patients. In CRS, systemic inflammation is hardly affected by current in-hospital therapy. More specific targets for therapy need to be identified to improve both systemic inflammation and outcome in CRS.
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Pliquett et al. (2015) conducted an observational in Acutely-decompensated cardiorenal syndrome (n=15). Acutely-decompensated cardiorenal syndrome vs. Hemodialysis and hypertensive patients was evaluated on CD14+/CD16+ Monocytes (p==0.07). Acutely decompensated cardiorenal syndrome was associated with a higher degree of systemic inflammation compared to hypertensive controls, which was largely unaffected by in-hospital therapy.
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