Evidence map›Paper›PMID 34502149›Full record

ArticleInternational journal of molecular sciences2021

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

Thayane Crestani, Renato O Crajoinas, Leonardo Jensen, Leno L Dima, Perrine Burdeyron, Thierry Hauet, Sebastien Giraud, Clara Steichen

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.4field-weighted citation impact, top 35% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed, 7 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 2 countries.

Thayane CrestaniLaboratory of Genetics and Molecular Cardiology, Heart Institute, University of São Paulo Medical School, São Paulo 05403-900, SP, Brazil.ORCID 0000-0002-3776-8596
Renato O CrajoinasLaboratory of Genetics and Molecular Cardiology, Heart Institute, University of São Paulo Medical School, São Paulo 05403-900, SP, Brazil.
Leonardo JensenLaboratory of Genetics and Molecular Cardiology, Heart Institute, University of São Paulo Medical School, São Paulo 05403-900, SP, Brazil.ORCID 0000-0002-1241-8960
Leno L DimaLaboratory of Genetics and Molecular Cardiology, Heart Institute, University of São Paulo Medical School, São Paulo 05403-900, SP, Brazil.
Perrine BurdeyronINSERM U1082 (IRTOMIT), F-86000 Poitiers, France.ORCID 0000-0001-8301-2717
Thierry HauetINSERM U1082 (IRTOMIT), F-86000 Poitiers, France.ORCID 0000-0002-0117-071X
Sebastien GiraudINSERM U1082 (IRTOMIT), F-86000 Poitiers, France.
Clara SteichenLaboratory of Genetics and Molecular Cardiology, Heart Institute, University of São Paulo Medical School, São Paulo 05403-900, SP, Brazil.
Inserm · FRUniversidade de São Paulo · BR

Funding

Fundação de Amparo à Pesquisa do Estado de São Paulo FAPESP2014/14086-7
6 · The paper itself

Abstract

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.

Indexed as

AnimalsBlood PressureDietFemaleGlomerular Filtration RateHeart DiseasesHeart RateHematocritHyperoxaluriaMaleOxalic AcidRatsRats, WistarRenal Insufficiency, ChronicOxalic Acidcardiac functionchronic kidney diseaseoxalaterat model

Identifiers

PMID34502149
PMCPMC8431202
OpenAlexW3194035057

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.