Ferroportin inhibition attenuates plasma iron, oxidant stress, and renal injury following red blood cell transfusion in guinea pigs.

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Abstract

Red blood cell (RBC) transfusions result in the sequestration and metabolism of storage-damaged RBCs within the spleen and liver. These events are followed by increased plasma iron concentrations that can contribute to oxidant stress and cellular injury. We hypothesized that administration of a ferroportin inhibitor (FPN-INH) immediately after acute RBC exchange transfusion could attenuate posttransfusion circulatory compartment iron exposure, by retaining iron in spleen and hepatic macrophages.

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Journal

Journal ID (iso-abbrev): Transfusion

Title: Transfusion

Publisher: Wiley

ISSN (Electronic): 1537-2995

ISSN (Print): 0041-1132

Publication date (Electronic): Mar 2020

Volume: 60

Issue: 3

Affiliations

[1 ] Laboratory of Biochemistry and Vascular Biology, Division of Blood Components and Devices, Center of Biologics Evaluation and Research (CBER), FDA, Silver Spring, Maryland, USA.

[2 ] Division of Viral Products, Center of Biologics Evaluation and Research (CBER), FDA, Silver Spring, Maryland, USA.

[3 ] Department of Pathology, Center for Blood Oxygen Transport, Baltimore, Maryland, USA.

[4 ] Center for Blood Oxygen Transport and Hemostasis, Department of Pediatrics, University of Maryland Baltimore School of Medicine, Baltimore, Maryland, USA.

Article

DOI: 10.1111/trf.15720

PubMed ID: 32064619

SO-VID: bf1f85d0-fc2d-43d7-9ee5-44d44a051293

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