Acute sodium overload produces renal tubulointerstitial inflammation in normal rats

Autores
Roson, Maria Ines; Cavallero, Carmen Susana; Della Penna, Silvana; Cao, Gabriel Fernando; Gorzalczany, Susana Beatriz; Pandolfo, Marcela; Kuprewicz, A.; Canessa, O.; Toblli, Jorge Eduardo; Fernandez, Belisario Enrique
Año de publicación
2006
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
The aim of the present study was to determine whether acute sodium overload could trigger an inflammatory reaction in the tubulointerstitial (TI) compartment in normal rats. Four groups of Sprague-Dawley rats received increasing NaCl concentrations by intravenous infusion. Control (C): Na + 0.15M; G1: Na+ 0.5M; G2: Na+ 1.0M; and G3: Na+ 1.5M. Creatinine clearance, mean arterial pressure (MAP), renal blood flow (RBF), and sodium fractional excretion were determined. Transforming growth factor β1 (TGF-β1), α-smooth muscle actin (α-SMA), RANTES, transcription factor nuclear factor-kappa B (NF-κB), and angiotensin II (ANG II) were evaluated in kidneys by immunohistochemistry. Animals with NaCl overload showed normal glomerular function without MAP and RBF modifications and exhibited a concentration-dependent natriuretic response. Plasmatic sodium increased in G2 (P < 0.01) and G3 (P < 0.001). Light microscopy did not show renal morphological damage. Immunohistochemistry revealed an increased number of ANG II-positive tubular cells in G2 and G3, and positive immunostaining for NF-κB only in G3 (P < 0.01). Increased staining of α-SMA in the interstitium (P < 0.01), TGF-β1 in tubular cells (P < 0.01), and a significant percentage (P < 0.01) of positive immunostaining for RANTES in tubular epithelium and in glomerular and peritubular endothelium were detected in G3>G2>C group. These results suggest that an acute sodium overload is able 'per se' to initiate TI endothelial inflammatory reaction (glomerular and peritubular) and incipient fibrosis in normal rats, independently of hemodynamic modifications. Furthermore, these findings are consistent with the possibility that activation of NF-κB and local ANG II may be involved in the pathway of this inflammatory process.
Fil: Roson, Maria Ines. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Cavallero, Carmen Susana. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Della Penna, Silvana. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina
Fil: Cao, Gabriel Fernando. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Hospital Alemán; Argentina
Fil: Gorzalczany, Susana Beatriz. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina
Fil: Pandolfo, Marcela. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina
Fil: Kuprewicz, A.. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina
Fil: Canessa, O.. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina
Fil: Toblli, Jorge Eduardo. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Hospital Alemán; Argentina
Fil: Fernandez, Belisario Enrique. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina
Materia
RANTES
RENAL TUBULOINTERSTITIAL INFLAMMATION
SMOOTH MUSCLE ACTIN
SODIUM OVERLOAD
TRANSFORMING GROWTH FACTOR
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/96242
Acceder
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oai_identifier_str oai:ri.conicet.gov.ar:11336/96242
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Acute sodium overload produces renal tubulointerstitial inflammation in normal ratsRoson, Maria InesCavallero, Carmen SusanaDella Penna, SilvanaCao, Gabriel FernandoGorzalczany, Susana BeatrizPandolfo, MarcelaKuprewicz, A.Canessa, O.Toblli, Jorge EduardoFernandez, Belisario EnriqueRANTESRENAL TUBULOINTERSTITIAL INFLAMMATIONSMOOTH MUSCLE ACTINSODIUM OVERLOADTRANSFORMING GROWTH FACTORhttps://purl.org/becyt/ford/3.3https://purl.org/becyt/ford/3The aim of the present study was to determine whether acute sodium overload could trigger an inflammatory reaction in the tubulointerstitial (TI) compartment in normal rats. Four groups of Sprague-Dawley rats received increasing NaCl concentrations by intravenous infusion. Control (C): Na + 0.15M; G1: Na+ 0.5M; G2: Na+ 1.0M; and G3: Na+ 1.5M. Creatinine clearance, mean arterial pressure (MAP), renal blood flow (RBF), and sodium fractional excretion were determined. Transforming growth factor β1 (TGF-β1), α-smooth muscle actin (α-SMA), RANTES, transcription factor nuclear factor-kappa B (NF-κB), and angiotensin II (ANG II) were evaluated in kidneys by immunohistochemistry. Animals with NaCl overload showed normal glomerular function without MAP and RBF modifications and exhibited a concentration-dependent natriuretic response. Plasmatic sodium increased in G2 (P < 0.01) and G3 (P < 0.001). Light microscopy did not show renal morphological damage. Immunohistochemistry revealed an increased number of ANG II-positive tubular cells in G2 and G3, and positive immunostaining for NF-κB only in G3 (P < 0.01). Increased staining of α-SMA in the interstitium (P < 0.01), TGF-β1 in tubular cells (P < 0.01), and a significant percentage (P < 0.01) of positive immunostaining for RANTES in tubular epithelium and in glomerular and peritubular endothelium were detected in G3>G2>C group. These results suggest that an acute sodium overload is able 'per se' to initiate TI endothelial inflammatory reaction (glomerular and peritubular) and incipient fibrosis in normal rats, independently of hemodynamic modifications. Furthermore, these findings are consistent with the possibility that activation of NF-κB and local ANG II may be involved in the pathway of this inflammatory process.Fil: Roson, Maria Ines. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Cavallero, Carmen Susana. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Della Penna, Silvana. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; ArgentinaFil: Cao, Gabriel Fernando. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Hospital Alemán; ArgentinaFil: Gorzalczany, Susana Beatriz. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; ArgentinaFil: Pandolfo, Marcela. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; ArgentinaFil: Kuprewicz, A.. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; ArgentinaFil: Canessa, O.. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; ArgentinaFil: Toblli, Jorge Eduardo. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Hospital Alemán; ArgentinaFil: Fernandez, Belisario Enrique. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; ArgentinaNature Publishing Group2006-10info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/96242Roson, Maria Ines; Cavallero, Carmen Susana; Della Penna, Silvana; Cao, Gabriel Fernando; Gorzalczany, Susana Beatriz; et al.; Acute sodium overload produces renal tubulointerstitial inflammation in normal rats; Nature Publishing Group; Kidney International; 70; 8; 10-2006; 1439-14460085-2538CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/pii/S0085253815521716info:eu-repo/semantics/altIdentifier/doi/10.1038/sj.ki.5001831info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-10T13:20:34Zoai:ri.conicet.gov.ar:11336/96242instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-10 13:20:35.229CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Acute sodium overload produces renal tubulointerstitial inflammation in normal rats
title Acute sodium overload produces renal tubulointerstitial inflammation in normal rats
spellingShingle Acute sodium overload produces renal tubulointerstitial inflammation in normal rats
Roson, Maria Ines
RANTES
RENAL TUBULOINTERSTITIAL INFLAMMATION
SMOOTH MUSCLE ACTIN
SODIUM OVERLOAD
TRANSFORMING GROWTH FACTOR
title_short Acute sodium overload produces renal tubulointerstitial inflammation in normal rats
title_full Acute sodium overload produces renal tubulointerstitial inflammation in normal rats
title_fullStr Acute sodium overload produces renal tubulointerstitial inflammation in normal rats
title_full_unstemmed Acute sodium overload produces renal tubulointerstitial inflammation in normal rats
title_sort Acute sodium overload produces renal tubulointerstitial inflammation in normal rats
dc.creator.none.fl_str_mv Roson, Maria Ines
Cavallero, Carmen Susana
Della Penna, Silvana
Cao, Gabriel Fernando
Gorzalczany, Susana Beatriz
Pandolfo, Marcela
Kuprewicz, A.
Canessa, O.
Toblli, Jorge Eduardo
Fernandez, Belisario Enrique
author Roson, Maria Ines
author_facet Roson, Maria Ines
Cavallero, Carmen Susana
Della Penna, Silvana
Cao, Gabriel Fernando
Gorzalczany, Susana Beatriz
Pandolfo, Marcela
Kuprewicz, A.
Canessa, O.
Toblli, Jorge Eduardo
Fernandez, Belisario Enrique
author_role author
author2 Cavallero, Carmen Susana
Della Penna, Silvana
Cao, Gabriel Fernando
Gorzalczany, Susana Beatriz
Pandolfo, Marcela
Kuprewicz, A.
Canessa, O.
Toblli, Jorge Eduardo
Fernandez, Belisario Enrique
author2_role author
author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv RANTES
RENAL TUBULOINTERSTITIAL INFLAMMATION
SMOOTH MUSCLE ACTIN
SODIUM OVERLOAD
TRANSFORMING GROWTH FACTOR
topic RANTES
RENAL TUBULOINTERSTITIAL INFLAMMATION
SMOOTH MUSCLE ACTIN
SODIUM OVERLOAD
TRANSFORMING GROWTH FACTOR
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.3
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv The aim of the present study was to determine whether acute sodium overload could trigger an inflammatory reaction in the tubulointerstitial (TI) compartment in normal rats. Four groups of Sprague-Dawley rats received increasing NaCl concentrations by intravenous infusion. Control (C): Na + 0.15M; G1: Na+ 0.5M; G2: Na+ 1.0M; and G3: Na+ 1.5M. Creatinine clearance, mean arterial pressure (MAP), renal blood flow (RBF), and sodium fractional excretion were determined. Transforming growth factor β1 (TGF-β1), α-smooth muscle actin (α-SMA), RANTES, transcription factor nuclear factor-kappa B (NF-κB), and angiotensin II (ANG II) were evaluated in kidneys by immunohistochemistry. Animals with NaCl overload showed normal glomerular function without MAP and RBF modifications and exhibited a concentration-dependent natriuretic response. Plasmatic sodium increased in G2 (P < 0.01) and G3 (P < 0.001). Light microscopy did not show renal morphological damage. Immunohistochemistry revealed an increased number of ANG II-positive tubular cells in G2 and G3, and positive immunostaining for NF-κB only in G3 (P < 0.01). Increased staining of α-SMA in the interstitium (P < 0.01), TGF-β1 in tubular cells (P < 0.01), and a significant percentage (P < 0.01) of positive immunostaining for RANTES in tubular epithelium and in glomerular and peritubular endothelium were detected in G3>G2>C group. These results suggest that an acute sodium overload is able 'per se' to initiate TI endothelial inflammatory reaction (glomerular and peritubular) and incipient fibrosis in normal rats, independently of hemodynamic modifications. Furthermore, these findings are consistent with the possibility that activation of NF-κB and local ANG II may be involved in the pathway of this inflammatory process.
Fil: Roson, Maria Ines. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Cavallero, Carmen Susana. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Della Penna, Silvana. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina
Fil: Cao, Gabriel Fernando. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Hospital Alemán; Argentina
Fil: Gorzalczany, Susana Beatriz. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina
Fil: Pandolfo, Marcela. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina
Fil: Kuprewicz, A.. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina
Fil: Canessa, O.. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina
Fil: Toblli, Jorge Eduardo. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Hospital Alemán; Argentina
Fil: Fernandez, Belisario Enrique. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina
description The aim of the present study was to determine whether acute sodium overload could trigger an inflammatory reaction in the tubulointerstitial (TI) compartment in normal rats. Four groups of Sprague-Dawley rats received increasing NaCl concentrations by intravenous infusion. Control (C): Na + 0.15M; G1: Na+ 0.5M; G2: Na+ 1.0M; and G3: Na+ 1.5M. Creatinine clearance, mean arterial pressure (MAP), renal blood flow (RBF), and sodium fractional excretion were determined. Transforming growth factor β1 (TGF-β1), α-smooth muscle actin (α-SMA), RANTES, transcription factor nuclear factor-kappa B (NF-κB), and angiotensin II (ANG II) were evaluated in kidneys by immunohistochemistry. Animals with NaCl overload showed normal glomerular function without MAP and RBF modifications and exhibited a concentration-dependent natriuretic response. Plasmatic sodium increased in G2 (P < 0.01) and G3 (P < 0.001). Light microscopy did not show renal morphological damage. Immunohistochemistry revealed an increased number of ANG II-positive tubular cells in G2 and G3, and positive immunostaining for NF-κB only in G3 (P < 0.01). Increased staining of α-SMA in the interstitium (P < 0.01), TGF-β1 in tubular cells (P < 0.01), and a significant percentage (P < 0.01) of positive immunostaining for RANTES in tubular epithelium and in glomerular and peritubular endothelium were detected in G3>G2>C group. These results suggest that an acute sodium overload is able 'per se' to initiate TI endothelial inflammatory reaction (glomerular and peritubular) and incipient fibrosis in normal rats, independently of hemodynamic modifications. Furthermore, these findings are consistent with the possibility that activation of NF-κB and local ANG II may be involved in the pathway of this inflammatory process.
publishDate 2006
dc.date.none.fl_str_mv 2006-10
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/96242
Roson, Maria Ines; Cavallero, Carmen Susana; Della Penna, Silvana; Cao, Gabriel Fernando; Gorzalczany, Susana Beatriz; et al.; Acute sodium overload produces renal tubulointerstitial inflammation in normal rats; Nature Publishing Group; Kidney International; 70; 8; 10-2006; 1439-1446
0085-2538
CONICET Digital
CONICET
url http://hdl.handle.net/11336/96242
identifier_str_mv Roson, Maria Ines; Cavallero, Carmen Susana; Della Penna, Silvana; Cao, Gabriel Fernando; Gorzalczany, Susana Beatriz; et al.; Acute sodium overload produces renal tubulointerstitial inflammation in normal rats; Nature Publishing Group; Kidney International; 70; 8; 10-2006; 1439-1446
0085-2538
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/pii/S0085253815521716
info:eu-repo/semantics/altIdentifier/doi/10.1038/sj.ki.5001831
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
application/pdf
application/pdf
application/pdf
application/pdf
application/pdf
dc.publisher.none.fl_str_mv Nature Publishing Group
publisher.none.fl_str_mv Nature Publishing Group
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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