Evidence map›Paper›PMID 31116604›Full record

ArticleAmerican journal of physiology. Renal physiology2019

New mouse model of chronic kidney disease transitioned from ischemic acute kidney injury.

Jin Wei, Jie Zhang, Lei Wang, Shan Jiang, Liying Fu, Jacentha Buggs, Ruisheng Liu

Open access · bronzeAbstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 12% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Rodent models of AKI and AKI-CKD transition: an update in 2024.American journal of physiology. Renal physiology · 2024
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  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

7 authors at 3 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.
Shan JiangDepartment of Molecular Pharmacology and Physiology, University of South Florida College of Medicine , Tampa, Florida.
Liying FuTampa General Hospital , Tampa, Florida.
Jacentha BuggsTampa General Hospital , Tampa, Florida.
Ruisheng LiuDepartment of Molecular Pharmacology and Physiology, University of South Florida College of Medicine , Tampa, Florida.
University of South Florida · USFlorida College · USTampa General Hospital · US

Funding

Role of tubuloglomerular feedback in the development of hypertension in diabetesR01HL142814 · NHLBI · UNIVERSITY OF SOUTH FLORIDA · PI LIU, RUISHENG · 2019 to 2022
$2.4M
Renal hemodynamics and hypertension during pregnancyR01HL137987 · NHLBI · UNIVERSITY OF SOUTH FLORIDA · PI LIU, RUISHENG · 2018 to 2021
$1.6M
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
NHLBI NIH HHS R01 HL137987NHLBI NIH HHS R01 HL142814NIDDK NIH HHS R01 DK098582NIDDK NIH HHS R01 DK099276
6 · The paper itself

Abstract

Acute kidney injury (AKI) significantly increases the risk of development of chronic kidney disease (CKD), which is closely associated with the severity of AKI. However, the underlying mechanisms for the AKI to CKD transition remain unclear. Several animal models with AKI to CKD transition have been generated and widely used in research; however, none of them exhibit the typical changes in glomerular filtration rate or plasma creatinine, the hallmarks of CKD. In the present study, we developed a novel model with a typical phenotype of AKI to CKD transition in C57BL/6 mice. In this model, life-threatening ischemia-reperfusion injury was performed in one kidney, whereas the contralateral kidney was kept intact to maintain animal survival; then, after 2 wk of recovery, when the renal function of the injured kidney restored above the survival threshold, the contralateral intact kidney was removed. Animals of this two-stage unilateral ischemia-reperfusion injury model with pedicle clamping of 21 and 24 min exhibited an incomplete recovery from AKI and subsequent progression of CKD with characteristics of a progressive decline in glomerular filtration rate, increase in plasma creatinine, worsening of proteinuria, and deleterious histopathological changes, including interstitial fibrosis and glomerulosclerosis. In conclusion, a new model of the AKI to CKD transition was generated in C57BL/6 mice.

Indexed as

KidneyAcute Kidney InjuryAnimalsBiomarkersConstrictionCreatinineDisease Models, AnimalDisease ProgressionFibrosisGlomerular Filtration RateMice, Inbred C57BLNephrectomyOrgan SizePhenotypeProteinuriaRenal Insufficiency, ChronicBiomarkersCreatinineacute kidney injuryanimal modelchronic kidney diseaseischemia-reperfusion injury

Identifiers

PMID31116604
PMCPMC6732455
OpenAlexW2946401691

What Socratic 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 Socratic graph.