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Protective Role for Antioxidants in Acute Kidney Disease

Acute kidney injury causes significant morbidity and mortality in the community and clinic. Various pathologies, including renal and cardiovascular disease, traumatic injury/rhabdomyolysis, sepsis, and nephrotoxicity, that cause acute kidney injury (AKI), induce general or regional decreases in rena...

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Autores principales: Dennis, Joanne M., Witting, Paul K.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5537833/
https://www.ncbi.nlm.nih.gov/pubmed/28686196
http://dx.doi.org/10.3390/nu9070718
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author Dennis, Joanne M.
Witting, Paul K.
author_facet Dennis, Joanne M.
Witting, Paul K.
author_sort Dennis, Joanne M.
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description Acute kidney injury causes significant morbidity and mortality in the community and clinic. Various pathologies, including renal and cardiovascular disease, traumatic injury/rhabdomyolysis, sepsis, and nephrotoxicity, that cause acute kidney injury (AKI), induce general or regional decreases in renal blood flow. The ensuing renal hypoxia and ischemia promotes the formation of reactive oxygen species (ROS) such as superoxide radical anions, peroxides, and hydroxyl radicals, that can oxidatively damage biomolecules and membranes, and affect organelle function and induce renal tubule cell injury, inflammation, and vascular dysfunction. Acute kidney injury is associated with increased oxidative damage, and various endogenous and synthetic antioxidants that mitigate source and derived oxidants are beneficial in cell-based and animal studies. However, the benefit of synthetic antioxidant supplementation in human acute kidney injury and renal disease remains to be realized. The endogenous low-molecular weight, non-proteinaceous antioxidant, ascorbate (vitamin C), is a promising therapeutic in human renal injury in critical illness and nephrotoxicity. Ascorbate may exert significant protection by reducing reactive oxygen species and renal oxidative damage via its antioxidant activity, and/or by its non-antioxidant functions in maintaining hydroxylase and monooxygenase enzymes, and endothelium and vascular function. Ascorbate supplementation may be particularly important in renal injury patients with low vitamin C status.
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spelling pubmed-55378332017-08-04 Protective Role for Antioxidants in Acute Kidney Disease Dennis, Joanne M. Witting, Paul K. Nutrients Review Acute kidney injury causes significant morbidity and mortality in the community and clinic. Various pathologies, including renal and cardiovascular disease, traumatic injury/rhabdomyolysis, sepsis, and nephrotoxicity, that cause acute kidney injury (AKI), induce general or regional decreases in renal blood flow. The ensuing renal hypoxia and ischemia promotes the formation of reactive oxygen species (ROS) such as superoxide radical anions, peroxides, and hydroxyl radicals, that can oxidatively damage biomolecules and membranes, and affect organelle function and induce renal tubule cell injury, inflammation, and vascular dysfunction. Acute kidney injury is associated with increased oxidative damage, and various endogenous and synthetic antioxidants that mitigate source and derived oxidants are beneficial in cell-based and animal studies. However, the benefit of synthetic antioxidant supplementation in human acute kidney injury and renal disease remains to be realized. The endogenous low-molecular weight, non-proteinaceous antioxidant, ascorbate (vitamin C), is a promising therapeutic in human renal injury in critical illness and nephrotoxicity. Ascorbate may exert significant protection by reducing reactive oxygen species and renal oxidative damage via its antioxidant activity, and/or by its non-antioxidant functions in maintaining hydroxylase and monooxygenase enzymes, and endothelium and vascular function. Ascorbate supplementation may be particularly important in renal injury patients with low vitamin C status. MDPI 2017-07-07 /pmc/articles/PMC5537833/ /pubmed/28686196 http://dx.doi.org/10.3390/nu9070718 Text en © 2017 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Dennis, Joanne M.
Witting, Paul K.
Protective Role for Antioxidants in Acute Kidney Disease
title Protective Role for Antioxidants in Acute Kidney Disease
title_full Protective Role for Antioxidants in Acute Kidney Disease
title_fullStr Protective Role for Antioxidants in Acute Kidney Disease
title_full_unstemmed Protective Role for Antioxidants in Acute Kidney Disease
title_short Protective Role for Antioxidants in Acute Kidney Disease
title_sort protective role for antioxidants in acute kidney disease
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5537833/
https://www.ncbi.nlm.nih.gov/pubmed/28686196
http://dx.doi.org/10.3390/nu9070718
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