Cardiotrophin-1 administration prevents the renal toxicity of iodinated contrast media in rats

[EN]Although generally reversible, contrast media toxicity often induces contrast-induced nephropathy (CIN), which is associated with longer hospitalization time, the need for dialysis, and higher incidence of later cardiovascular events and higher mortality. Preventive cotreatments have been assaye...

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Autores: Quirós Luis, Yaremi, Sánchez González, Penelope D., López Hernández, Francisco José, Morales Martín, Ana Isabel, López-Novoa, José M.
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2013
País:España
Institución:Universidad de Salamanca (USAL)
Repositorio:GREDOS. Repositorio Institucional de la Universidad de Salamanca
OAI Identifier:oai:gredos.usal.es:10366/169133
Acceso en línea:http://hdl.handle.net/10366/169133
Access Level:acceso embargado
Palabra clave:Acute kidney injury
Contrast-induced nephropathy
Contrast
Nephrotoxicity
Cardiotrophin-1
Nephroprotection
Cytokines
Rats
Animals
Kidney
Contrast Media
3209 Farmacología
medios de contraste
riñón
animales
ratas
citocinas
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oai_identifier_str oai:gredos.usal.es:10366/169133
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spelling Cardiotrophin-1 administration prevents the renal toxicity of iodinated contrast media in ratsQuirós Luis, YaremiSánchez González, Penelope D.López Hernández, Francisco JoséMorales Martín, Ana IsabelLópez-Novoa, José M.Acute kidney injuryContrast-induced nephropathyContrastNephrotoxicityCardiotrophin-1NephroprotectionCytokinesRatsAnimalsKidneyContrast Media3209 Farmacologíamedios de contrasteriñónanimalesratascitocinas[EN]Although generally reversible, contrast media toxicity often induces contrast-induced nephropathy (CIN), which is associated with longer hospitalization time, the need for dialysis, and higher incidence of later cardiovascular events and higher mortality. Preventive cotreatments have been assayed at the preclinical and clinical levels, but recent meta-analysis has not demonstrated a beneficial effect, which supports the search for new nephroprotective strategies. We have assessed if the administration of cardiotrophin-1 (CT-1), an endogenous cytokine with protective properties on the heart and liver, might mitigate CIN in rats. We have developed a model of CIN induced by the administration of the contrast medium gastrographin iv (3.7mg/kg) in rats sensitized by previous administration of subnephrotoxic doses of gentamicin (50mg/kg/day, ip) for 6 days. The severity of CIN was assessed by the measurement of renal function; renal histological damage; urinary excretion of markers of tubular damage, including N-acetyl beta glucosaminidase (NAG), kidney injury molecule 1 (KIM-1), and plasminogen activator inhibitor 1; lipid peroxidation; and renal apoptosis. Treatment with CT-1 almost completely prevented the renal tissue damage, as evidenced by almost total prevention of tubular desepithelization and tubular obstruction, reduced caspase activation, and cell proliferation. Besides, CT-1 also prevented the increment in renal tissue levels of renal tissue injury markers NAG, KIM-1, and neutrophil gelatinase-associated lipocalin. Oxidative stress, a hallmark of CIN, was also prevented by CT-1. Administration of CT-1 also prevented the derangement in kidney function induced by CIN. Renal hemodynamics, also impaired by the contrast medium, was normal in rats cotreated with CT-1. CT-1 administration significantly prevents the alterations in renal function and structure observed in a rat model of CIN.Digna Biotech S.L. to Bio-inRen S.L. (Spain); Instituto de Salud Carlos III (Retic 016/2006, RedinRen). The Renal and Cardiovascular Pathophysiology Unit holds the Excellence Group mention (GR-100) and awarded by the Junta de Castilla y León.Oxford University Pressinfo202620262013info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://hdl.handle.net/10366/169133reponame:GREDOS. Repositorio Institucional de la Universidad de Salamancainstname:Universidad de Salamanca (USAL)InglésRetic 016/2006Attribution-NonCommercial-NoDerivatives 4.0 Internacionalhttp://creativecommons.org/licenses/by-nc-nd/4.0/info:eu-repo/semantics/embargoedAccessoai:gredos.usal.es:10366/1691332026-06-07T06:28:51Z
dc.title.none.fl_str_mv Cardiotrophin-1 administration prevents the renal toxicity of iodinated contrast media in rats
title Cardiotrophin-1 administration prevents the renal toxicity of iodinated contrast media in rats
spellingShingle Cardiotrophin-1 administration prevents the renal toxicity of iodinated contrast media in rats
Quirós Luis, Yaremi
Acute kidney injury
Contrast-induced nephropathy
Contrast
Nephrotoxicity
Cardiotrophin-1
Nephroprotection
Cytokines
Rats
Animals
Kidney
Contrast Media
3209 Farmacología
medios de contraste
riñón
animales
ratas
citocinas
title_short Cardiotrophin-1 administration prevents the renal toxicity of iodinated contrast media in rats
title_full Cardiotrophin-1 administration prevents the renal toxicity of iodinated contrast media in rats
title_fullStr Cardiotrophin-1 administration prevents the renal toxicity of iodinated contrast media in rats
title_full_unstemmed Cardiotrophin-1 administration prevents the renal toxicity of iodinated contrast media in rats
title_sort Cardiotrophin-1 administration prevents the renal toxicity of iodinated contrast media in rats
dc.creator.none.fl_str_mv Quirós Luis, Yaremi
Sánchez González, Penelope D.
López Hernández, Francisco José
Morales Martín, Ana Isabel
López-Novoa, José M.
author Quirós Luis, Yaremi
author_facet Quirós Luis, Yaremi
Sánchez González, Penelope D.
López Hernández, Francisco José
Morales Martín, Ana Isabel
López-Novoa, José M.
author_role author
author2 Sánchez González, Penelope D.
López Hernández, Francisco José
Morales Martín, Ana Isabel
López-Novoa, José M.
author2_role author
author
author
author
dc.subject.none.fl_str_mv Acute kidney injury
Contrast-induced nephropathy
Contrast
Nephrotoxicity
Cardiotrophin-1
Nephroprotection
Cytokines
Rats
Animals
Kidney
Contrast Media
3209 Farmacología
medios de contraste
riñón
animales
ratas
citocinas
topic Acute kidney injury
Contrast-induced nephropathy
Contrast
Nephrotoxicity
Cardiotrophin-1
Nephroprotection
Cytokines
Rats
Animals
Kidney
Contrast Media
3209 Farmacología
medios de contraste
riñón
animales
ratas
citocinas
description [EN]Although generally reversible, contrast media toxicity often induces contrast-induced nephropathy (CIN), which is associated with longer hospitalization time, the need for dialysis, and higher incidence of later cardiovascular events and higher mortality. Preventive cotreatments have been assayed at the preclinical and clinical levels, but recent meta-analysis has not demonstrated a beneficial effect, which supports the search for new nephroprotective strategies. We have assessed if the administration of cardiotrophin-1 (CT-1), an endogenous cytokine with protective properties on the heart and liver, might mitigate CIN in rats. We have developed a model of CIN induced by the administration of the contrast medium gastrographin iv (3.7mg/kg) in rats sensitized by previous administration of subnephrotoxic doses of gentamicin (50mg/kg/day, ip) for 6 days. The severity of CIN was assessed by the measurement of renal function; renal histological damage; urinary excretion of markers of tubular damage, including N-acetyl beta glucosaminidase (NAG), kidney injury molecule 1 (KIM-1), and plasminogen activator inhibitor 1; lipid peroxidation; and renal apoptosis. Treatment with CT-1 almost completely prevented the renal tissue damage, as evidenced by almost total prevention of tubular desepithelization and tubular obstruction, reduced caspase activation, and cell proliferation. Besides, CT-1 also prevented the increment in renal tissue levels of renal tissue injury markers NAG, KIM-1, and neutrophil gelatinase-associated lipocalin. Oxidative stress, a hallmark of CIN, was also prevented by CT-1. Administration of CT-1 also prevented the derangement in kidney function induced by CIN. Renal hemodynamics, also impaired by the contrast medium, was normal in rats cotreated with CT-1. CT-1 administration significantly prevents the alterations in renal function and structure observed in a rat model of CIN.
publishDate 2013
dc.date.none.fl_str_mv 2013
2026
2026
info
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/10366/169133
url http://hdl.handle.net/10366/169133
dc.language.none.fl_str_mv Inglés
language_invalid_str_mv Inglés
dc.relation.none.fl_str_mv Retic 016/2006
dc.rights.none.fl_str_mv Attribution-NonCommercial-NoDerivatives 4.0 Internacional
http://creativecommons.org/licenses/by-nc-nd/4.0/
info:eu-repo/semantics/embargoedAccess
rights_invalid_str_mv Attribution-NonCommercial-NoDerivatives 4.0 Internacional
http://creativecommons.org/licenses/by-nc-nd/4.0/
eu_rights_str_mv embargoedAccess
dc.publisher.none.fl_str_mv Oxford University Press
publisher.none.fl_str_mv Oxford University Press
dc.source.none.fl_str_mv reponame:GREDOS. Repositorio Institucional de la Universidad de Salamanca
instname:Universidad de Salamanca (USAL)
instname_str Universidad de Salamanca (USAL)
reponame_str GREDOS. Repositorio Institucional de la Universidad de Salamanca
collection GREDOS. Repositorio Institucional de la Universidad de Salamanca
repository.name.fl_str_mv
repository.mail.fl_str_mv
_version_ 1869403360316096512
score 15.198674

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