Urinary Metabolomics From a Dose-Fractionated Polymyxin B Rat Model of Acute Kidney Injury.


Journal

International journal of antimicrobial agents
ISSN: 1872-7913
Titre abrégé: Int J Antimicrob Agents
Pays: Netherlands
ID NLM: 9111860

Informations de publication

Date de publication:
Jul 2022
Historique:
received: 22 10 2021
revised: 18 02 2022
accepted: 11 04 2022
pubmed: 24 4 2022
medline: 24 6 2022
entrez: 23 4 2022
Statut: ppublish

Résumé

Polymyxin B treatment is limited by kidney injury. This study sought to identify Polymyxin B-related urinary metabolomic profile modifications for early detection of polymyxin-associated nephrotoxicity. Samples were obtained from a previously conducted study. Male Sprague-Dawley rats received dose-fractionated polymyxin B (12 mg/kg/day) once daily (QD), twice daily (BID), and thrice daily (TID) for three days, with urinary biomarkers and kidney histopathology scores determined. Daily urine was analysed for metabolites via 1H nuclear magnetic resonance (NMR). Principal components analyses identified spectral data trends with orthogonal partial least square discriminant analysis applied to classify metabolic differences. Metabolomes were compared across groups (i.e., those receiving QD, BID, TID, and control) using a mixed-effects models. Spearman correlation was performed for injury biomarkers and the metabolome. A total of 25 rats were treated with Polymyxin B, and n = 2 received saline, contributing 77 urinary samples. Pre-dosing samples clustered well, characterised by higher amounts of citrate, 2-oxoglutarate, and hippurate. Day 1 samples showed higher taurine; day 3 samples had higher lactate, acetate and creatine. Taurine was the only metabolite that significantly increased in both BID and TID compared with the QD group. Day 1 taurine correlated with increasing histopathology scores (rho = 0.4167, P = 0.038) and kidney injury molecule-1 (KIM-1) (rho = 0.4052, P = 0.036), whereas KIM-1 on day 1 and day 3 did not reach significance with histopathology (rho = 0.3248, P = 0.11 and rho = 0.3739, P = 0.066). Polymyxin B causes increased amounts of urinary taurine on day 1, which then normalizes to baseline concentrations. Taurine may provide one of the earlier signals of acute kidney damage caused by polymyxin B.

Sections du résumé

BACKGROUND BACKGROUND
Polymyxin B treatment is limited by kidney injury. This study sought to identify Polymyxin B-related urinary metabolomic profile modifications for early detection of polymyxin-associated nephrotoxicity.
METHODS METHODS
Samples were obtained from a previously conducted study. Male Sprague-Dawley rats received dose-fractionated polymyxin B (12 mg/kg/day) once daily (QD), twice daily (BID), and thrice daily (TID) for three days, with urinary biomarkers and kidney histopathology scores determined. Daily urine was analysed for metabolites via 1H nuclear magnetic resonance (NMR). Principal components analyses identified spectral data trends with orthogonal partial least square discriminant analysis applied to classify metabolic differences. Metabolomes were compared across groups (i.e., those receiving QD, BID, TID, and control) using a mixed-effects models. Spearman correlation was performed for injury biomarkers and the metabolome.
RESULTS RESULTS
A total of 25 rats were treated with Polymyxin B, and n = 2 received saline, contributing 77 urinary samples. Pre-dosing samples clustered well, characterised by higher amounts of citrate, 2-oxoglutarate, and hippurate. Day 1 samples showed higher taurine; day 3 samples had higher lactate, acetate and creatine. Taurine was the only metabolite that significantly increased in both BID and TID compared with the QD group. Day 1 taurine correlated with increasing histopathology scores (rho = 0.4167, P = 0.038) and kidney injury molecule-1 (KIM-1) (rho = 0.4052, P = 0.036), whereas KIM-1 on day 1 and day 3 did not reach significance with histopathology (rho = 0.3248, P = 0.11 and rho = 0.3739, P = 0.066).
CONCLUSIONS CONCLUSIONS
Polymyxin B causes increased amounts of urinary taurine on day 1, which then normalizes to baseline concentrations. Taurine may provide one of the earlier signals of acute kidney damage caused by polymyxin B.

Identifiants

pubmed: 35460851
pii: S0924-8579(22)00097-8
doi: 10.1016/j.ijantimicag.2022.106593
pii:
doi:

Substances chimiques

Biomarkers 0
Taurine 1EQV5MLY3D
Polymyxin B J2VZ07J96K

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

106593

Informations de copyright

Copyright © 2022 Elsevier Ltd and International Society of Antimicrobial Chemotherapy. All rights reserved.

Auteurs

Emanuela Locci (E)

Department of Medical Sciences and Public Health, Section of Legal Medicine, University of Cagliari, Cagliari, Italy.

Jiajun Liu (J)

Midwestern University, Downers Grove, IL, USA; Midwestern University Chicago College of Pharmacy Pharmacometrics Center of Excellence, Downers Grove, IL, USA; Northwestern Memorial Hospital, Chicago, IL, USA.

Gwendolyn M Pais (GM)

Midwestern University, Downers Grove, IL, USA; Midwestern University Chicago College of Pharmacy Pharmacometrics Center of Excellence, Downers Grove, IL, USA.

Alberto Chighine (A)

Department of Medical Sciences and Public Health, Section of Legal Medicine, University of Cagliari, Cagliari, Italy.

Dariusc Andrea Kahnamoei (DA)

Department of Medical Sciences and Public Health, Section of Legal Medicine, University of Cagliari, Cagliari, Italy.

Theodoros Xanthos (T)

School of Medicine, European University Cyprus, Cyprus.

Athanasios Chalkias (A)

University of Thessaly, Faculty of Medicine, Department of Anesthesiology, Larisa, Greece; Outcomes Research Consortium, Cleveland, OH, USA.

Andrew Lee (A)

Northwestern University, Chicago, IL, USA.

Alan R Hauser (AR)

Northwestern University, Chicago, IL, USA.

Jack Chang (J)

Midwestern University, Downers Grove, IL, USA; Midwestern University Chicago College of Pharmacy Pharmacometrics Center of Excellence, Downers Grove, IL, USA; Northwestern Memorial Hospital, Chicago, IL, USA.

Nathaniel J Rhodes (NJ)

Midwestern University, Downers Grove, IL, USA; Midwestern University Chicago College of Pharmacy Pharmacometrics Center of Excellence, Downers Grove, IL, USA; Northwestern Memorial Hospital, Chicago, IL, USA.

Ernesto d'Aloja (E)

Department of Medical Sciences and Public Health, Section of Legal Medicine, University of Cagliari, Cagliari, Italy.

Marc H Scheetz (MH)

Midwestern University, Downers Grove, IL, USA; Midwestern University Chicago College of Pharmacy Pharmacometrics Center of Excellence, Downers Grove, IL, USA; Northwestern Memorial Hospital, Chicago, IL, USA. Electronic address: mschee@midwestern.edu.

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Classifications MeSH