Evidence map›Paper›PMID 22496773›Full record

ArticlePloS one2012

Diabetic kidney disease in FVB/NJ Akita mice: temporal pattern of kidney injury and urinary nephrin excretion.

Jae-Hyung Chang, Seung-Yeol Paik, Lan Mao, William Eisner, Patrick J Flannery, Liming Wang, Yuping Tang, Natalie Mattocks, Samy Hadjadj, Jean-Michel Goujon and 3 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

36 citing papers in PubMed, 49 citations in OpenAlex.

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  18. Modelling diabetic nephropathy in mice.Nature reviews. Nephrology · 2018
    Review
  19. Podocyte-specific knockout of cyclooxygenase 2 exacerbates diabetic kidney disease.American journal of physiology. Renal physiology · 2017
    Article
  20. Article
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

13 authors at 7 institutions in 3 countries.

Jae-Hyung ChangDivision of Nephrology, Department of Medicine, Duke University Medical Center, Durham, North Carolina, United States of America.
Seung-Yeol Paik
Lan Mao
William Eisner
Patrick J Flannery
Liming Wang
Yuping Tang
Natalie Mattocks
Samy Hadjadj
Jean-Michel Goujon
Phillip Ruiz
Susan B Gurley
Robert F Spurney
Durham VA Medical Center · USDuke University · USChung-Ang University · KRDuke Medical Center · USInserm · FRUniversité de Poitiers · FRUniversity of Miami · US

Funding

Role of Gq Signaling in Promoting Podocyte Injury in Diabetes MellitusR01DK087707 · NIDDK · DUKE UNIVERSITY · PI SPURNEY, ROBERT · 2011 to 2014
$1.4M
A Novel Mouse Model of Podocyte InjuryR01DK075688 · NIDDK · DUKE UNIVERSITY · PI SPURNEY, ROBERT · 2009 to 2011
$1.2M
Mechanisms of proteinuria induced by RhoA GTPasesI01BX000791 · VA · DURHAM VA MEDICAL CENTER · PI SPURNEY, ROBERT · 2011 to 2014
–
BLRD VA I01 BX000791NIDDK NIH HHS 3R01DK075688-01A2S1NIDDK NIH HHS R01 DK075688NIDDK NIH HHS R01-DK075688NIDDK NIH HHS R01 DK087707
6 · The paper itself

Abstract

Akita mice are a genetic model of type 1 diabetes. In the present studies, we investigated the phenotype of Akita mice on the FVB/NJ background and examined urinary nephrin excretion as a marker of kidney injury. Male Akita mice were compared with non-diabetic controls for functional and structural characteristics of renal and cardiac disease. Podocyte number and apoptosis as well as urinary nephrin excretion were determined in both groups. Male FVB/NJ Akita mice developed sustained hyperglycemia and albuminuria by 4 and 8 weeks of age, respectively. These abnormalities were accompanied by a significant increase in systolic blood pressure in 10-week old Akita mice, which was associated with functional, structural and molecular characteristics of cardiac hypertrophy. By 20 weeks of age, Akita mice developed a 10-fold increase in albuminuria, renal and glomerular hypertrophy and a decrease in the number of podocytes. Mild-to-moderate glomerular mesangial expansion was observed in Akita mice at 30 weeks of age. In 4-week old Akita mice, the onset of hyperglycemia was accompanied by increased podocyte apoptosis and enhanced excretion of nephrin in urine before the development of albuminuria. Urinary nephrin excretion was also significantly increased in albuminuric Akita mice at 16 and 20 weeks of age and correlated with the albumin excretion rate. These data suggest that: 1. FVB/NJ Akita mice have phenotypic characteristics that may be useful for studying the mechanisms of kidney and cardiac injury in diabetes, and 2. Enhanced urinary nephrin excretion is associated with kidney injury in FVB/NJ Akita mice and is detectable early in the disease process.

Indexed as

AlbuminuriaAnimalsBiomarkersBlotting, WesternDiabetes ComplicationsDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 1Diabetic NephropathiesDisease Models, AnimalHyperglycemiaImmunoenzyme TechniquesKidneyMaleMembrane ProteinsMiceMice, Inbred StrainsBiomarkersMembrane ProteinsnephrinRNA, Messenger

Identifiers

PMID22496773
PMCPMC3319540
OpenAlexW2095488781

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LicenceCC BY
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Registered trials

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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.