Evidence map›Paper›PMID 24511135›Full record

ArticleJournal of the American Society of Nephrology : JASN2014

Severe renal mass reduction impairs recovery and promotes fibrosis after AKI.

Aaron J Polichnowski, Rongpei Lan, Hui Geng, Karen A Griffin, Manjeri A Venkatachalam, Anil K Bidani

Open access · bronzeAbstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
4.6field-weighted citation impact, top 5% 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

46 citing papers in PubMed, 72 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

6 authors at 2 institutions in 1 country.

Aaron J PolichnowskiDivision of Nephrology and Hypertension, Department of Medicine, Loyola University and Hines Veterans Affaris Hospital, Maywood, Illinois; and.
Rongpei LanDepartment of Pathology, University of Texas Health Science Center, San Antonio, Texas.
Hui GengDepartment of Pathology, University of Texas Health Science Center, San Antonio, Texas.
Karen A GriffinDivision of Nephrology and Hypertension, Department of Medicine, Loyola University and Hines Veterans Affaris Hospital, Maywood, Illinois; and.
Manjeri A VenkatachalamDepartment of Pathology, University of Texas Health Science Center, San Antonio, Texas.
Anil K BidaniDivision of Nephrology and Hypertension, Department of Medicine, Loyola University and Hines Veterans Affaris Hospital, Maywood, Illinois; and abidani@lumc.edu.
The University of Texas Health Science Center at San Antonio · USLoyola University Medical Center · US

Funding

PATHOLOGY OF HYPERTENSIVE INJURY IN REMNANT KIDNEYSR01DK040426 · NIDDK · RUSH UNIVERSITY MEDICAL CENTER · PI BIDANI, ANIL K · 1990 to 2011
$2.8M
Dynamic BP load and diabetic nephropathy phenotype.R01DK061653 · NIDDK · LOYOLA UNIVERSITY CHICAGO · PI GRIFFIN, KAREN A. · 2002 to 2014
$2.1M
Nitric Oxide Deficiency in Hypertensive NephropathiesIK2BX001285 · VA · EDWARD HINES JR VA HOSPITAL · PI POLICHNOWSKI, AARON JAMES · 2011 to 2015
–
BLRD VA IK2 BX001285NIDDK NIH HHS DK40426NIDDK NIH HHS DK61653NIDDK NIH HHS R01 DK040426NIDDK NIH HHS R01 DK061653
6 · The paper itself

Abstract

Preexisting CKD may affect the severity of and/or recovery from AKI. We assessed the impact of prior graded normotensive renal mass reduction on ischemia-reperfusion-induced AKI. Rats underwent 40 minutes of ischemia 2 weeks after right uninephrectomy and surgical excision of both poles of the left kidney (75% reduction of renal mass), right uninephrectomy (50% reduction of renal mass), or sham reduction of renal mass. The severity of AKI was comparable among groups, which was reflected by similarly increased serum creatinine (SCr; approximately 4.5 mg/dl) at 2 days, tubule necrosis at 3 days, and vimentin-expressing regenerating tubules at 7 days postischemia-reperfusion. However, SCr remained elevated compared with preischemia-reperfusion values, and more tubules failed to differentiate during late recovery 4 weeks after ischemia-reperfusion in rats with 75% renal mass reduction relative to other groups. Tubules that failed to differentiate continued to produce vimentin, exhibited vicarious proliferative signaling, and expressed less vascular endothelial growth factor but more profibrotic peptides. The disproportionate failure of regenerating tubules to redifferentiate in rats with 75% renal mass reduction associated with more severe capillary rarefaction and greater tubulointerstitial fibrosis. Furthermore, initially normotensive rats with 75% renal mass reduction developed hypertension and proteinuria, 2-4 weeks postischemia-reperfusion. In summary, severe (>50%) renal mass reduction disproportionately compromised tubule repair, diminished capillary density, and promoted fibrosis with hypertension after ischemia-reperfusion-induced AKI in rats, suggesting that accelerated declines of renal function may occur after AKI in patients with preexisting CKD.

Indexed as

Acute Kidney InjuryAnimalsFibrosisKidneyKidney TubulesMaleOrgan SizeRatsRats, Sprague-DawleySeverity of Illness Index

Identifiers

PMID24511135
PMCPMC4073422
OpenAlexW2160803520

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.