Evidence map›Paper›PMID 26064882›Full record

ArticleBioMed research international2015

Development of a Model of Chronic Kidney Disease in the C57BL/6 Mouse with Properties of Progressive Human CKD.

Zahraa Mohammed-Ali, Gaile L Cruz, Chao Lu, Rachel E Carlisle, Kaitlyn E Werner, Kjetil Ask, Jeffrey G Dickhout

Open access · hybridAbstract read
In one paragraph

Article in BioMed research international, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

12 citing papers in PubMed, 13 citations in OpenAlex.

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  9. Euthanasia via COMolecular reproduction and development · 2019
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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

7 authors at 1 institution in 1 country.

Zahraa Mohammed-AliDepartment of Medicine, Division of Nephrology, McMaster University and St. Joseph's Healthcare Hamilton, Hamilton, ON, Canada L8N 4A6.ORCID 0000-0001-8436-0553
Gaile L CruzDepartment of Medicine, Division of Nephrology, McMaster University and St. Joseph's Healthcare Hamilton, Hamilton, ON, Canada L8N 4A6.
Chao LuDepartment of Medicine, Division of Nephrology, McMaster University and St. Joseph's Healthcare Hamilton, Hamilton, ON, Canada L8N 4A6.
Rachel E CarlisleDepartment of Medicine, Division of Nephrology, McMaster University and St. Joseph's Healthcare Hamilton, Hamilton, ON, Canada L8N 4A6.
Kaitlyn E WernerDepartment of Medicine, Division of Nephrology, McMaster University and St. Joseph's Healthcare Hamilton, Hamilton, ON, Canada L8N 4A6.
Kjetil AskDepartment of Medicine, Division of Respirology, McMaster University and St. Joseph's Healthcare Hamilton, Hamilton, ON, Canada L8N 4A6.
Jeffrey G DickhoutDepartment of Medicine, Division of Nephrology, McMaster University and St. Joseph's Healthcare Hamilton, Hamilton, ON, Canada L8N 4A6.
St. Joseph’s Healthcare Hamilton · CA

Funding

Canadian Institutes of Health Research MOP-133484Canadian Institutes of Health Research OSO-115895
6 · The paper itself

Abstract

Chronic kidney disease (CKD) is a major healthcare problem with increasing prevalence in the population. CKD leads to end stage renal disease and increases the risk of cardiovascular disease. As such, it is important to study the mechanisms underlying CKD progression. To this end, an animal model was developed to allow the testing of new treatment strategies or molecular targets for CKD prevention. Many underlying risk factors result in CKD but the disease itself has common features, including renal interstitial fibrosis, tubular epithelial cell loss through apoptosis, glomerular damage, and renal inflammation. Further, CKD shows differences in prevalence between the genders with premenopausal women being relatively resistant to CKD. We sought to develop and characterize an animal model with these common features of human CKD in the C57BL/6 mouse. Mice of this genetic background have been used to produce transgenic strains that are commercially available. Thus, a CKD model in this strain would allow the testing of the effects of numerous genes on the severity or progression of CKD with minimal cost. This paper describes such a mouse model of CKD utilizing angiotensin II and deoxycorticosterone acetate as inducers.

Indexed as

Disease Models, AnimalDisease ProgressionAngiotensin IIAnimalsDesoxycorticosterone AcetateFemaleHumansMaleMiceRenal Insufficiency, ChronicAngiotensin IIDesoxycorticosterone Acetate

Identifiers

PMID26064882
PMCPMC4433637
OpenAlexW2032545317

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.