Evidence map›Paper›PMID 29412703›Full record

ArticleAmerican journal of physiology. Renal physiology2018

A new low-nephron CKD model with hypertension, progressive decline of renal function, and enhanced inflammation in C57BL/6 mice.

Jin Wei, Jie Zhang, Lei Wang, Byeong Jake Cha, Shan Jiang, Ruisheng Liu

Open access · greenAbstract readComparative Study
PubMed Full text at PMC Publisher
In one paragraph

Article in American journal of physiology. Renal physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 2 pooled it
1.8field-weighted citation impact, top 15% 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

23 citing papers in PubMed, 2 syntheses or guidelines pooled it, 23 citations in OpenAlex.

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  19. A mouse model of renal ischemia-reperfusion injury solely induced by cold ischemia.American journal of physiology. Renal physiology · 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

6 authors at 2 institutions in 1 country.

Jin WeiDepartment of Molecular Pharmacology and Physiology, University of South Florida College of Medicine , Tampa, Florida.
Jie ZhangDepartment of Molecular Pharmacology and Physiology, University of South Florida College of Medicine , Tampa, Florida.
Lei WangDepartment of Molecular Pharmacology and Physiology, University of South Florida College of Medicine , Tampa, Florida.
Byeong Jake ChaDepartment of Molecular Pharmacology and Physiology, University of South Florida College of Medicine , Tampa, Florida.
Shan JiangDepartment of Molecular Pharmacology and Physiology, University of South Florida College of Medicine , Tampa, Florida.
Ruisheng LiuDepartment of Molecular Pharmacology and Physiology, University of South Florida College of Medicine , Tampa, Florida.
Florida College · USUniversity of South Florida · US

Funding

Tubuloglomerular feedback and salt-sensitive hypertensionR01DK098582 · NIDDK · UNIVERSITY OF SOUTH FLORIDA · PI LIU, RUISHENG · 2013 to 2016
$1.3M
Primary cilia and modulation of the renal microcirculationR01DK099276 · NIDDK · UNIVERSITY OF SOUTH FLORIDA · PI LIU, RUISHENG · 2014 to 2017
$980k
NIDDK NIH HHS R01 DK098582NIDDK NIH HHS R01 DK099276
6 · The paper itself

Abstract

Chronic kidney disease (CKD) is a major health issue in the US. The typical five-sixths nephrectomy (typical 5/6 NX) is a widely used experimental CKD model. However, the typical 5/6 NX model is hypertensive in rats but strain dependent in mice. In particular, C57BL/6 mice with the typical 5/6 NX exhibits normal blood pressure and well-preserved renal function. The goal of the present study was to create a new hypertensive CKD model in C57BL/6 mice. We first characterized the vascular architecture originated from each renal artery branch by confocal laser-scanning microscopy with fluorescent lectin. Then, a novel 5/6 NX-BL model was generated by uninephrectomy combined with 2/3 renal infarction via a ligation of upper renal artery branch on the contralateral kidney. Compared with 5/6 NX-C, the 5/6 NX-BL model exhibited elevated mean arterial pressure (137.6 ± 13.9 vs. 104.7 ± 8.2 mmHg), decreased glomerular filtration rate (82.9 ± 19.2 vs. 125.0 ± 13.9 µl/min) with a reciprocal increase in plasma creatinine (0.31 ± 0.03 vs. 0.19 ± 0.04 mg/dl), and significant renal injury as assessed by proteinuria, histology with light, and transmission electron microscopy. In addition, inflammatory status, as indicated by the level of proinflammatory cytokine TNFα and the leukocyte counts, was significantly upregulated in 5/6 NX-BL compared with the 5/6 NX-C. In summary, we developed a new hypertensive CKD model in C57BL/6 mice with 5/6 renal mass reduction by uninephrectomy and upper renal artery branch ligation on the contralateral kidney. This 5/6 NX-BL model exhibits an infarction zone-dependent hypertension and progressive deterioration of the renal function accompanied by enhanced inflammatory response.

Indexed as

Arterial PressureGlomerular Filtration RateAlbuminuriaAnimalsBiomarkersCreatinineDisease Models, AnimalDisease ProgressionHypertension, RenovascularInflammationInflammation MediatorsKidneyLigationMice, Inbred C57BLNephrectomyRenal ArteryBiomarkersCreatinineInflammation MediatorsReninTumor Necrosis Factor-alphachronic kidney disease

Identifiers

PMID29412703
PMCPMC6031904
OpenAlexW2786351196

What OpenQuestion holds

Textmetadata
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.