Interleukin-8 and acute kidney injury following cardiopulmonary bypass: a prospective cohort study

Abstract

Background: Cardiopulmonary bypass (CPB) elicits an inflammatory response mediated partly by neutrophils, which are activated and recruited by interleukin-8 (IL-8). We hypothesized that acute kidney injury (AKI) following CPB might be mediated by IL-8 and examined the association of perioperative plasma IL-8 levels with AKI in a prospective cohort.

Methods: Plasma IL-8 was measured before, and 2, 24 and 48 h following CPB. Two AKI definitions, a serum creatinine increase of > or = 0.3 mg/dl or 50% (AKI Network [AKIN] stage-1) or > or = 50% alone (AKI-50%), within the first 72 h, were used. Area under the receiver operator characteristic curves (AUCs) were generated and multivariable logistic regression analyses performed.

Results: A total of 143 patients were enrolled. The baseline mean serum creatinine was 1.1 mg/ dl (SD = 0.3), the CPB perfusion time was 112 min (SD = 43). Twenty-nine percent of the patients developed AKIN stage-1 and 13% AKI-50%. The plasma IL-8 level 2 h after CPB was higher in AKIN stage-1 (p = 0.03) and AKI-50% (p < 0.01), and predicted AKIN stage-1 (AUC = 0.62; p = 0.02) and AKI-50% (AUC = 0.72; p < 0.01). On multivariable analysis, the 2-hour plasma IL-8 level was associated with 1.36- and 1.59-fold higher odds for AKIN stage-1 and AKI-50%, respectively (p = 0.05).

Conclusion: Plasma IL-8 predicts the development of AKI following CPB, supporting a potential involvement for this chemokine in the pathogenesis of AKI.

Copyright 2009 S. Karger AG, Basel.

Figures

Fig. 1.

Plasma IL-8 profile following CPB. Error bars represent 25th, 50th (median) and 75th percentile values. ∗ p

Fig. 2.

Median plasma IL-8 profile following CPB stratified by AKIN stage-1 (a) and AKI-50% (b). The AKI group is displayed in gray and the non-AKI group in black. Error bars represent 25th and 75th percentile values. ∗ p < 0.05 vs. non-AKI by Wilcoxon rank sum test.