Aquaporin-2 in the early stages of the adenine-induced chronic kidney disease model.

Chronic kidney disease (CKD) is one of the leading health problems in the world. It is silent in the early stages and gradually progresses, inducing renal physiological and structural alterations. Moreover, CKD is associated with impaired life quality, increased risk for cardiovascular diseases, and...

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Main Authors: Lucas H Oronel, Maria Ortiz, Carolina Yarza, Sofía Gayone, Carlos Davio, Mónica Majowicz, Maria Florencia Albertoni Borghese
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2025-01-01
Series:PLoS ONE
Online Access:https://doi.org/10.1371/journal.pone.0314827
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author Lucas H Oronel
Maria Ortiz
Carolina Yarza
Sofía Gayone
Carlos Davio
Mónica Majowicz
Maria Florencia Albertoni Borghese
author_facet Lucas H Oronel
Maria Ortiz
Carolina Yarza
Sofía Gayone
Carlos Davio
Mónica Majowicz
Maria Florencia Albertoni Borghese
author_sort Lucas H Oronel
collection DOAJ
description Chronic kidney disease (CKD) is one of the leading health problems in the world. It is silent in the early stages and gradually progresses, inducing renal physiological and structural alterations. Moreover, CKD is associated with impaired life quality, increased risk for cardiovascular diseases, and reduced life expectancy. Different CKD animal models differ in underlying etiology, time of onset, and associated diseases. The 0.25% adenine diet induces progressive kidney damage, constituting an adequate model mimicking human CKD. Vasopressin (VP) was postulated as a mediator of CKD, mainly acting through its V2 receptors. However, the molecular mechanisms involved in the pathogenesis of this condition and its progression still are not entirely understood. This study aimed to evaluate if AQP2 expression is altered in an adenine-induced model of CKD in rats at early stages of development (two weeks) and to assess a potential beneficial effect of Tolvaptan (a V2 receptor antagonist) treatment. We showed an increased renal medullary AQP2 expression at two weeks of adenine administration. This increase was mainly cytoplasmic, explaining the increased urinary volume of CKD rats and suggesting a possible non-canonical role for AQP2. In addition, Tolvaptan effectively inhibited the V2 receptor in both control and CKD rats, decreasing AQP2 expression and increasing diuresis. Moreover, Tolvaptan slightly reduced BUN and plasma creatinine. On the other hand, the renal alterations induced by adenine in CKD rats were not prevented by Tolvaptan.
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spelling doaj-art-c21457f132ec461dad2966046bd94d382025-02-05T05:31:49ZengPublic Library of Science (PLoS)PLoS ONE1932-62032025-01-01201e031482710.1371/journal.pone.0314827Aquaporin-2 in the early stages of the adenine-induced chronic kidney disease model.Lucas H OronelMaria OrtizCarolina YarzaSofía GayoneCarlos DavioMónica MajowiczMaria Florencia Albertoni BorgheseChronic kidney disease (CKD) is one of the leading health problems in the world. It is silent in the early stages and gradually progresses, inducing renal physiological and structural alterations. Moreover, CKD is associated with impaired life quality, increased risk for cardiovascular diseases, and reduced life expectancy. Different CKD animal models differ in underlying etiology, time of onset, and associated diseases. The 0.25% adenine diet induces progressive kidney damage, constituting an adequate model mimicking human CKD. Vasopressin (VP) was postulated as a mediator of CKD, mainly acting through its V2 receptors. However, the molecular mechanisms involved in the pathogenesis of this condition and its progression still are not entirely understood. This study aimed to evaluate if AQP2 expression is altered in an adenine-induced model of CKD in rats at early stages of development (two weeks) and to assess a potential beneficial effect of Tolvaptan (a V2 receptor antagonist) treatment. We showed an increased renal medullary AQP2 expression at two weeks of adenine administration. This increase was mainly cytoplasmic, explaining the increased urinary volume of CKD rats and suggesting a possible non-canonical role for AQP2. In addition, Tolvaptan effectively inhibited the V2 receptor in both control and CKD rats, decreasing AQP2 expression and increasing diuresis. Moreover, Tolvaptan slightly reduced BUN and plasma creatinine. On the other hand, the renal alterations induced by adenine in CKD rats were not prevented by Tolvaptan.https://doi.org/10.1371/journal.pone.0314827
spellingShingle Lucas H Oronel
Maria Ortiz
Carolina Yarza
Sofía Gayone
Carlos Davio
Mónica Majowicz
Maria Florencia Albertoni Borghese
Aquaporin-2 in the early stages of the adenine-induced chronic kidney disease model.
PLoS ONE
title Aquaporin-2 in the early stages of the adenine-induced chronic kidney disease model.
title_full Aquaporin-2 in the early stages of the adenine-induced chronic kidney disease model.
title_fullStr Aquaporin-2 in the early stages of the adenine-induced chronic kidney disease model.
title_full_unstemmed Aquaporin-2 in the early stages of the adenine-induced chronic kidney disease model.
title_short Aquaporin-2 in the early stages of the adenine-induced chronic kidney disease model.
title_sort aquaporin 2 in the early stages of the adenine induced chronic kidney disease model
url https://doi.org/10.1371/journal.pone.0314827
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