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Multicenter Study
. 2018 Aug 10;8(1):11968.
doi: 10.1038/s41598-018-30361-5.

Hypoalbuminemia as a predictor of acute kidney injury during colistin treatment

Daniele Roberto Giacobbe  1 , Alessandra di Masi  2 , Loris Leboffe  2 , Valerio Del Bono  3 , Marianna Rossi  4 , Dario Cappiello  5 , Erika Coppo  6 , Anna Marchese  6 , Annarita Casulli  7 , Alessio Signori  8 , Andrea Novelli  9 , Katja Perrone  5 , Luigi Principe  10 , Alessandra Bandera  4 , Luca Enrico Vender  4 , Andrea Misin  11 , Pierpaolo Occhilupo  12 , Marcello Melone  5 , Paolo Ascenzi  2 , Andrea Gori  13 , Roberto Luzzati  11 , Claudio Viscoli  7 , Stefano Di Bella  11
Affiliations
Multicenter Study

Hypoalbuminemia as a predictor of acute kidney injury during colistin treatment

Daniele Roberto Giacobbe et al. Sci Rep. .

Abstract

This study aimed to assess the predictors of acute kidney injury (AKI) during colistin therapy in a cohort of patients with bloodstream infections (BSI) due to colistin-susceptible Gram-negative bacteria, focusing on the role of serum albumin levels. The study consisted of two parts: (1) a multicentre retrospective clinical study to assess the predictors of AKI during colistin therapy, defined according to the Kidney Disease: Improving Global Outcomes (KDIGO) criteria; and (2) bioinformatic and biochemical characterization of the possible interaction between human serum albumin and colistin. Among the 170 patients included in the study, 71 (42%), 35 (21%), and 11 (6%) developed KDIGO stage 1 (K1-AKI), KDIGO stage 2 (K2-AKI), and KDIGO stage 3 (K3-AKI), respectively. In multivariable analyses, serum albumin <2.5 g/dL was independently associated with K1-AKI (subdistribution hazard ratio [sHR] 1.85, 95% confidence interval [CI] 1.17-2.93, p = 0.009) and K2-AKI (sHR 2.37, 95% CI 1.15-4.87, p = 0.019). Bioinformatic and biochemical analyses provided additional information nurturing the discussion on how hypoalbuminemia favors development of AKI during colistin therapy. In conclusion, severe hypoalbuminemia independently predicted AKI during colistin therapy in a large cohort of patients with BSI due to colistin-susceptible Gram-negative bacteria. Further study is needed to clarify the underlying causal pathways.

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Conflict of interest statement

The authors declare no competing interests.

Figures

Figure 1
Figure 1
Flow chart of the patients inclusion process.
Figure 2
Figure 2
Cumulative incidence of acute kidney injury in the study population. KDIGO, Kidney Disease: Improving Global Outcomes; AKI, acute kidney injury.
Figure 3
Figure 3
Colistin recognition by ligand-free HSA. (A) Overall view of the best apparent free energy poses of ligand-free HSA-colistin complexes. (B) Overall view of the atomic details of colistin recognition at the FA8 site of HSA. Colistin is rendered in stick (orange). The picture was drawn with the UCSF-Chimera package. For details, see text.
See this image and copyright information in PMC

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