Evidence map›Paper›PMID 34307974›Full record

ReviewKidney international reports2021

Chronic Inflammation in Chronic Kidney Disease Progression: Role of Nrf2.

Peter Stenvinkel, Glenn M Chertow, Prasad Devarajan, Adeera Levin, Sharon P Andreoli, Sripal Bangalore, Bradley A Warady

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Kidney international reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 175 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
175citing papers in PubMed, 6 pooled it
25.0field-weighted citation impact, top 1% 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

175 citing papers in PubMed, 6 syntheses or guidelines pooled it, 268 citations in OpenAlex.

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115 more citing papers are in PubMed but not listed here.

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 7 institutions in 3 countries.

Peter StenvinkelDepartment of Renal Medicine M99, Karolinska University Hospital at Huddinge, Karolinska Institutet, Stockholm, Sweden.
Glenn M ChertowDivision of Nephrology, Stanford University, Stanford, California, USA.
Prasad DevarajanDepartment of Pediatrics, University of Cincinnati, Cincinnati, Ohio, USA.
Adeera LevinDepartment of Medicine, The University of British Columbia, Vancouver, Canada.
Sharon P AndreoliDepartment of Pediatrics, Indiana University School of Medicine, Indiana University, Indianapolis, Indiana, USA.
Sripal BangaloreDivision of Cardiology, New York University, New York, New York, USA.
Bradley A WaradyDivision of Pediatric Nephrology, Children's Mercy Kansas City, Kansas City, Missouri, USA.
Children's Mercy Hospital · USIndiana University – Purdue University Indianapolis · USKarolinska Institutet · SENew York University · USStanford University · USUniversity of British Columbia · CAUniversity of Cincinnati · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite recent advances in the management of chronic kidney disease (CKD), morbidity and mortality rates in these patients remain high. Although pressure-mediated injury is a well-recognized mechanism of disease progression in CKD, emerging data indicate that an intermediate phenotype involving chronic inflammation, oxidative stress, hypoxia, senescence, and mitochondrial dysfunction plays a key role in the etiology, progression, and pathophysiology of CKD. A variety of factors promote chronic inflammation in CKD, including oxidative stress and the adoption of a proinflammatory phenotype by resident kidney cells. Regulation of proinflammatory and anti-inflammatory factors through NF-κB- and nuclear factor, erythroid 2 like 2 (Nrf2)-mediated gene transcription, respectively, plays a critical role in the glomerular and tubular cell response to kidney injury. Chronic inflammation contributes to the decline in glomerular filtration rate (GFR) in CKD. Whereas the role of chronic inflammation in diabetic kidney disease (DKD) has been well-elucidated, there is now substantial evidence indicating unresolved inflammatory processes lead to fibrosis and eventual end-stage kidney disease (ESKD) in several other diseases, such as Alport syndrome, autosomal-dominant polycystic kidney disease (ADPKD), IgA nephropathy (IgAN), and focal segmental glomerulosclerosis (FSGS). In this review, we aim to clarify the mechanisms of chronic inflammation in the pathophysiology and disease progression across the spectrum of kidney diseases, with a focus on Nrf2.

Indexed as

chronic inflammationchronic kidney diseasemitochondrial dysfunctionNrf2oxidative stressresident kidney cells

Identifiers

PMID34307974
PMCPMC8258499
OpenAlexW3159180709

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.