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Renal involvement in idiopathic hypereosinophic syndrome
The hypereosinophilic syndromes (HESs) are a group of disorders marked by the sustained overproduction of eosinophils, in which eosinophilic infiltration and mediator release cause damage to multiple organs. In idiopathic HES, the underlying cause of hypereosinophilia (HE) remains unknown despite th...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Oxford University Press
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4400489/ https://www.ncbi.nlm.nih.gov/pubmed/26064485 http://dx.doi.org/10.1093/ckj/sft046 |
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author | Shehwaro, Nathalie Langlois, Anne Lyse Gueutin, Victor Izzedine, Hassane |
author_facet | Shehwaro, Nathalie Langlois, Anne Lyse Gueutin, Victor Izzedine, Hassane |
author_sort | Shehwaro, Nathalie |
collection | PubMed |
description | The hypereosinophilic syndromes (HESs) are a group of disorders marked by the sustained overproduction of eosinophils, in which eosinophilic infiltration and mediator release cause damage to multiple organs. In idiopathic HES, the underlying cause of hypereosinophilia (HE) remains unknown despite thorough aetiological work-up. Kidney disease is thought to be rare in HES. Renal manifestations described include eosinophilic interstitial nephritis, various types of glomerulopathies, thrombotic microangiopathy (TMA) and electrolyte disturbances. The diagnosis must be made in time, because a recovery of renal function can be obtained if treatment is initiated promptly. |
format | Online Article Text |
id | pubmed-4400489 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | Oxford University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-44004892015-06-10 Renal involvement in idiopathic hypereosinophic syndrome Shehwaro, Nathalie Langlois, Anne Lyse Gueutin, Victor Izzedine, Hassane Clin Kidney J Original Contributions The hypereosinophilic syndromes (HESs) are a group of disorders marked by the sustained overproduction of eosinophils, in which eosinophilic infiltration and mediator release cause damage to multiple organs. In idiopathic HES, the underlying cause of hypereosinophilia (HE) remains unknown despite thorough aetiological work-up. Kidney disease is thought to be rare in HES. Renal manifestations described include eosinophilic interstitial nephritis, various types of glomerulopathies, thrombotic microangiopathy (TMA) and electrolyte disturbances. The diagnosis must be made in time, because a recovery of renal function can be obtained if treatment is initiated promptly. Oxford University Press 2013-06 /pmc/articles/PMC4400489/ /pubmed/26064485 http://dx.doi.org/10.1093/ckj/sft046 Text en © The Author 2013. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For permissions, please email: journals.permissions@oup.com http://creativecommons.org/licenses/by-nc/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com |
spellingShingle | Original Contributions Shehwaro, Nathalie Langlois, Anne Lyse Gueutin, Victor Izzedine, Hassane Renal involvement in idiopathic hypereosinophic syndrome |
title | Renal involvement in idiopathic hypereosinophic syndrome |
title_full | Renal involvement in idiopathic hypereosinophic syndrome |
title_fullStr | Renal involvement in idiopathic hypereosinophic syndrome |
title_full_unstemmed | Renal involvement in idiopathic hypereosinophic syndrome |
title_short | Renal involvement in idiopathic hypereosinophic syndrome |
title_sort | renal involvement in idiopathic hypereosinophic syndrome |
topic | Original Contributions |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4400489/ https://www.ncbi.nlm.nih.gov/pubmed/26064485 http://dx.doi.org/10.1093/ckj/sft046 |
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