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Brain–kidney crosstalk

Encephalopathy and altered higher mental functions are common clinical complications of acute kidney injury. Although sepsis is a major triggering factor, acute kidney injury predisposes to confusion by causing generalised inflammation, leading to increased permeability of the blood–brain barrier, e...

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Detalles Bibliográficos
Autores principales: Nongnuch, Arkom, Panorchan, Kwanpeemai, Davenport, Andrew
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4075125/
https://www.ncbi.nlm.nih.gov/pubmed/25043644
http://dx.doi.org/10.1186/cc13907
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author Nongnuch, Arkom
Panorchan, Kwanpeemai
Davenport, Andrew
author_facet Nongnuch, Arkom
Panorchan, Kwanpeemai
Davenport, Andrew
author_sort Nongnuch, Arkom
collection PubMed
description Encephalopathy and altered higher mental functions are common clinical complications of acute kidney injury. Although sepsis is a major triggering factor, acute kidney injury predisposes to confusion by causing generalised inflammation, leading to increased permeability of the blood–brain barrier, exacerbated by hyperosmolarity and metabolic acidosis due to the retention of products of nitrogen metabolism potentially resulting in increased brain water content. Downregulation of cell membrane transporters predisposes to alterations in neurotransmitter secretion and uptake, coupled with drug accumulation increasing the risk of encephalopathy. On the other hand, acute brain injury can induce a variety of changes in renal function ranging from altered function and electrolyte imbalances to inflammatory changes in brain death kidney donors.
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spelling pubmed-40751252015-06-05 Brain–kidney crosstalk Nongnuch, Arkom Panorchan, Kwanpeemai Davenport, Andrew Crit Care Review Encephalopathy and altered higher mental functions are common clinical complications of acute kidney injury. Although sepsis is a major triggering factor, acute kidney injury predisposes to confusion by causing generalised inflammation, leading to increased permeability of the blood–brain barrier, exacerbated by hyperosmolarity and metabolic acidosis due to the retention of products of nitrogen metabolism potentially resulting in increased brain water content. Downregulation of cell membrane transporters predisposes to alterations in neurotransmitter secretion and uptake, coupled with drug accumulation increasing the risk of encephalopathy. On the other hand, acute brain injury can induce a variety of changes in renal function ranging from altered function and electrolyte imbalances to inflammatory changes in brain death kidney donors. BioMed Central 2014 2014-06-05 /pmc/articles/PMC4075125/ /pubmed/25043644 http://dx.doi.org/10.1186/cc13907 Text en Copyright © 2014 Nongnuch et al.; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/4.0 The licensee has exclusive rights to distribute this article, in any medium, for 12 months following its publication. After this time, the article is available under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Review
Nongnuch, Arkom
Panorchan, Kwanpeemai
Davenport, Andrew
Brain–kidney crosstalk
title Brain–kidney crosstalk
title_full Brain–kidney crosstalk
title_fullStr Brain–kidney crosstalk
title_full_unstemmed Brain–kidney crosstalk
title_short Brain–kidney crosstalk
title_sort brain–kidney crosstalk
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4075125/
https://www.ncbi.nlm.nih.gov/pubmed/25043644
http://dx.doi.org/10.1186/cc13907
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