A Sodium Oxalate-Rich Diet Induces Chronic Kidney Disease and Cardiac Dysfunction in Rats.


Journal

International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791

Informations de publication

Date de publication:
26 Aug 2021
Historique:
received: 26 07 2021
revised: 18 08 2021
accepted: 20 08 2021
entrez: 10 9 2021
pubmed: 11 9 2021
medline: 12 10 2021
Statut: epublish

Résumé

Chronic kidney disease (CKD) is a worldwide public health issue affecting 14% of the general population. However, research focusing on CKD mechanisms/treatment is limited because of a lack of animal models recapitulating the disease physiopathology, including its complications. We analyzed the effects of a three-week diet rich in sodium oxalate (OXA diet) on rats and showed that, compared to controls, rats developed a stable CKD with a 60% reduction in glomerular filtration rate, elevated blood urea levels and proteinuria. Histological analyses revealed massive cortical disorganization, tubular atrophy and fibrosis. Males and females were sensitive to the OXA diet, but decreasing the diet period to one week led to GFR significance but not stable diminution. Rats treated with the OXA diet also displayed classical CKD complications such as elevated blood pressure and reduced hematocrit. Functional cardiac analyses revealed that the OXA diet triggered significant cardiac dysfunction. Altogether, our results showed the feasibility of using a convenient and non-invasive strategy to induce CKD and its classical systemic complications in rats. This model, which avoids kidney mass loss or acute toxicity, has strong potential for research into CKD mechanisms and novel therapies, which could protect and postpone the use of dialysis or transplantation.

Identifiants

pubmed: 34502149
pii: ijms22179244
doi: 10.3390/ijms22179244
pmc: PMC8431202
pii:
doi:

Substances chimiques

Oxalic Acid 9E7R5L6H31

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : Fundação de Amparo à Pesquisa do Estado de São Paulo
ID : FAPESP2014/14086-7

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Auteurs

Thayane Crestani (T)

Laboratory of Genetics and Molecular Cardiology, Heart Institute, University of São Paulo Medical School, São Paulo 05403-900, SP, Brazil.

Renato O Crajoinas (RO)

Laboratory of Genetics and Molecular Cardiology, Heart Institute, University of São Paulo Medical School, São Paulo 05403-900, SP, Brazil.

Leonardo Jensen (L)

Laboratory of Genetics and Molecular Cardiology, Heart Institute, University of São Paulo Medical School, São Paulo 05403-900, SP, Brazil.

Leno L Dima (LL)

Laboratory of Genetics and Molecular Cardiology, Heart Institute, University of São Paulo Medical School, São Paulo 05403-900, SP, Brazil.

Perrine Burdeyron (P)

INSERM U1082 (IRTOMIT), F-86000 Poitiers, France.
Faculté de Médecine et Pharmacie, Université de Poitiers, F-86000 Poitiers, France.

Thierry Hauet (T)

INSERM U1082 (IRTOMIT), F-86000 Poitiers, France.
Faculté de Médecine et Pharmacie, Université de Poitiers, F-86000 Poitiers, France.
Service de Biochimie, CHU Poitiers, F-86000 Poitiers, France.

Sebastien Giraud (S)

INSERM U1082 (IRTOMIT), F-86000 Poitiers, France.
Service de Biochimie, CHU Poitiers, F-86000 Poitiers, France.

Clara Steichen (C)

Laboratory of Genetics and Molecular Cardiology, Heart Institute, University of São Paulo Medical School, São Paulo 05403-900, SP, Brazil.
INSERM U1082 (IRTOMIT), F-86000 Poitiers, France.
Faculté de Médecine et Pharmacie, Université de Poitiers, F-86000 Poitiers, France.

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Classifications MeSH