Predictors of acute kidney injury associated with intravenous colistin treatment |
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| Authors: | Jeong-Ah Kwon Jung Eun Lee Wooseong Huh Kyong Ran Peck Yoon-Goo Kim Dae Joong Kim Ha Young Oh |
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| Affiliation: | 1. Menzies School of Health Research, Charles Darwin University, Darwin, Northern Territory, Australia;2. Department of Medicine, Royal Darwin Hospital, Darwin, Northern Territory, Australia;3. Centre for Chronic Disease, The University of Queensland, Australia;4. SydPath, St Vincent''s Hospital, Sydney, Australia;5. Territory Pathology, Department of Health, Northern Territory Government, Australia;6. Department of Pathology, Monash Medical Centre, Clayton, Victoria, Australia;7. Flinders University Medical School, Northern Territory Medical Program, Darwin, Australia;8. Royal Perth Hospital, Perth, Australia;9. Cairns Base Hospital and Diabetes Centre, Cairns, Australia;10. Department of Medicine, University of Melbourne, Victoria, Australia;11. Department of Endocrinology and Diabetes, St Vincent''s Hospital Melbourne, Victoria, Australia;12. Centre for Population Health Research, University of South Australia, Australia |
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| Abstract: | Colistimethate sodium (CMS) was recently re-introduced into clinical practice as a last resort for the treatment of nosocomial infections caused by multiresistant bacteria. This retrospective cohort study was designed to identify predictors of acute kidney injury (AKI) associated with intravenous (i.v.) CMS treatment. From March 2007 to July 2008, 71 adult patients receiving CMS for ≥72 h were enrolled. AKI was defined using Risk, Injury, Failure, Loss and End-stage kidney disease (RIFLE) criteria according to serum creatinine. The median total dose of CMS was 54.3 mg/kg (range 27.5–94.5 mg/kg). AKI developed in 38 patients (53.5%). Cox regression analysis based of cumulative CMS dose (mg/kg) identified four independent predictors of AKI: male sex [hazard ratio (HR) = 3.55, 95% confidence interval (CI), 1.47–8.55]; concomitant use of a calcineurin inhibitor (HR = 6.74, 95% CI 2.49–18.24); hypoalbuminaemia (serum albumin level <2.0 g/dL) (HR = 6.29, 95% CI 2.04–19.39); and hyperbilirubinaemia (total bilirubin level >5 mg/dL) (HR = 3.53, 95% CI 1.17–10.71). In conclusion, AKI was a common complication of i.v. CMS treatment. Male sex, concomitant use of calcineurin inhibitors, hypoalbuminaemia and hyperbilirubinaemia were independent predictors of AKI. The effect of AKI on patient outcomes was not determined. |
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