Urinary Exosomes Identify Inflammatory Pathways in Vancomycin Associated Acute Kidney Injury.


Journal

International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791

Informations de publication

Date de publication:
10 Mar 2021
Historique:
received: 29 12 2020
revised: 23 02 2021
accepted: 25 02 2021
entrez: 3 4 2021
pubmed: 4 4 2021
medline: 4 5 2021
Statut: epublish

Résumé

Vancomycin is commonly used as a first line therapy for gram positive organisms such as methicillin resistant Urine samples from patients with V-AKI who were enrolled in the DIRECT study and matched healthy controls from the UAB-UCSD O'Brien Center Biorepository were included in the analysis. Exosomes were extracted using solvent exclusion principle and polyethylene glycol induced precipitation. Protein identity and quantification was determined by label-free liquid chromatography mass spectrometry (LC/MS). The mean peak serum creatinine was 3.7 ± 1.4 mg/dL and time to kidney injury was 4.0 ± 3.0 days. At discharge, 90% of patients demonstrated partial recovery; 33% experienced full recovery by day 28. Proteomic analyses on five V-AKI and 7 control samples revealed 2009 proteins in all samples and 251 proteins significantly associated with V-AKI (Pi-score > 1). The top discriminatory proteins were complement C3, complement C4, galectin-3-binding protein, fibrinogen, alpha-2 macroglobulin, immunoglobulin heavy constant mu and serotransferrin. Urinary exosomes reveal up-regulation of inflammatory proteins after nephrotoxic injury in V-AKI. Further studies are necessary in a large patient sample to confirm these findings for elucidation of pathophysiologic mechanisms and validation of potential injury biomarkers.

Sections du résumé

BACKGROUND BACKGROUND
Vancomycin is commonly used as a first line therapy for gram positive organisms such as methicillin resistant
METHODS METHODS
Urine samples from patients with V-AKI who were enrolled in the DIRECT study and matched healthy controls from the UAB-UCSD O'Brien Center Biorepository were included in the analysis. Exosomes were extracted using solvent exclusion principle and polyethylene glycol induced precipitation. Protein identity and quantification was determined by label-free liquid chromatography mass spectrometry (LC/MS). The mean peak serum creatinine was 3.7 ± 1.4 mg/dL and time to kidney injury was 4.0 ± 3.0 days. At discharge, 90% of patients demonstrated partial recovery; 33% experienced full recovery by day 28. Proteomic analyses on five V-AKI and 7 control samples revealed 2009 proteins in all samples and 251 proteins significantly associated with V-AKI (Pi-score > 1). The top discriminatory proteins were complement C3, complement C4, galectin-3-binding protein, fibrinogen, alpha-2 macroglobulin, immunoglobulin heavy constant mu and serotransferrin.
CONCLUSION CONCLUSIONS
Urinary exosomes reveal up-regulation of inflammatory proteins after nephrotoxic injury in V-AKI. Further studies are necessary in a large patient sample to confirm these findings for elucidation of pathophysiologic mechanisms and validation of potential injury biomarkers.

Identifiants

pubmed: 33801801
pii: ijms22062784
doi: 10.3390/ijms22062784
pmc: PMC7999309
pii:
doi:

Substances chimiques

Biomarkers 0
Vancomycin 6Q205EH1VU
Creatinine AYI8EX34EU

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : NIDDK NIH HHS
ID : P30 DK079337
Pays : United States
Organisme : International Serious Adverse Events Consortium
ID : 12-1325

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Auteurs

Linda Awdishu (L)

Skaggs School of Pharmacy and Pharmaceutical Sciences, University of California, San Diego, CA 92093, USA.

Amy Le (A)

Skaggs School of Pharmacy and Pharmaceutical Sciences, University of California, San Diego, CA 92093, USA.

Jordan Amato (J)

Skaggs School of Pharmacy and Pharmaceutical Sciences, University of California, San Diego, CA 92093, USA.

Vidhyut Jani (V)

Skaggs School of Pharmacy and Pharmaceutical Sciences, University of California, San Diego, CA 92093, USA.

Soma Bal (S)

School of Medicine, University of California, San Diego, CA 92093, USA.

Robert H Mills (RH)

Skaggs School of Pharmacy and Pharmaceutical Sciences, University of California, San Diego, CA 92093, USA.

Marvic Carrillo-Terrazas (M)

Skaggs School of Pharmacy and Pharmaceutical Sciences, University of California, San Diego, CA 92093, USA.

David J Gonzalez (DJ)

Skaggs School of Pharmacy and Pharmaceutical Sciences, University of California, San Diego, CA 92093, USA.

Ashita Tolwani (A)

School of Medicine, University of Alabama, Birmingham, AL 35233, USA.

Anjali Acharya (A)

Albert Einstein College of Medicine, The Bronx, NY 10461, USA.

Jorge Cerda (J)

Albany Medical College, Albany, NY 12208, USA.

Melanie S Joy (MS)

Division of Renal Diseases and Hypertension, Skaggs School of Pharmacy and Pharmaceutical, Aurora, CO 80045, USA.
School of Medicine, University of Colorado, Aurora, CO 80045, USA.

Paola Nicoletti (P)

Mount Sinai School of Medicine, New York, NY 10029, USA.

Etienne Macedo (E)

School of Medicine, University of California, San Diego, CA 92093, USA.

Sucheta Vaingankar (S)

School of Medicine, University of California, San Diego, CA 92093, USA.

Ravindra Mehta (R)

School of Medicine, University of California, San Diego, CA 92093, USA.

Satish P RamachandraRao (SP)

Department of Cellular and Molecular Medicine, University of Michigan Medical System, Ann Arbor, MI 48109, USA.

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Classifications MeSH