Evidence map›Paper›PMID 26847481›Full record

ReviewClinical medicine & research2016

Hypoxia: The Force that Drives Chronic Kidney Disease.

Qiangwei Fu, Sean P Colgan, Carl Simon Shelley

Abstract readReview
In one paragraph

Review in Clinical medicine & research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
91citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

91 citing papers in PubMed, 1 synthesis or guideline pooled it.

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31 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

3 authors.

Qiangwei FuKabara Cancer Research Institute, La Crosse, WI.
Sean P ColganMucosal Inflammation Program and University of Colorado School of Medicine, Aurora, CO.
Carl Simon ShelleyUniversity of Wisconsin School of Medicine and Public Health, Madison, WI simon.shelley@leukemiatherapeutics.com.

Funding

Mechanisms of Adenosine ProtectionR01DK095491 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI Sean P Colgan · 2012 to 2026
$4.9M
Hypoxia, HIF, and Mucosal InflammationR37DK050189 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI COLGAN, SEAN P · 2010 to 2019
$4.1M
Metabolic Regulation of Mucosal InflammationI01BX002182 · VA · VA EASTERN COLORADO HEALTH CARE SYSTEM · PI COLGAN, SEAN P · 2014 to 2025
–
BLRD VA I01 BX002182NIDDK NIH HHS R01 DK095491NIDDK NIH HHS R37 DK050189
6 · The paper itself

Abstract

In the United States the prevalence of end-stage renal disease (ESRD) reached epidemic proportions in 2012 with over 600,000 patients being treated. The rates of ESRD among the elderly are disproportionally high. Consequently, as life expectancy increases and the baby-boom generation reaches retirement age, the already heavy burden imposed by ESRD on the US health care system is set to increase dramatically. ESRD represents the terminal stage of chronic kidney disease (CKD). A large body of evidence indicating that CKD is driven by renal tissue hypoxia has led to the development of therapeutic strategies that increase kidney oxygenation and the contention that chronic hypoxia is the final common pathway to end-stage renal failure. Numerous studies have demonstrated that one of the most potent means by which hypoxic conditions within the kidney produce CKD is by inducing a sustained inflammatory attack by infiltrating leukocytes. Indispensable to this attack is the acquisition by leukocytes of an adhesive phenotype. It was thought that this process resulted exclusively from leukocytes responding to cytokines released from ischemic renal endothelium. However, recently it has been demonstrated that leukocytes also become activated independent of the hypoxic response of endothelial cells. It was found that this endothelium-independent mechanism involves leukocytes directly sensing hypoxia and responding by transcriptional induction of the genes that encode the β2-integrin family of adhesion molecules. This induction likely maintains the long-term inflammation by which hypoxia drives the pathogenesis of CKD. Consequently, targeting these transcriptional mechanisms would appear to represent a promising new therapeutic strategy.

Indexed as

HypoxiaAdultAgedAnemiaAnimalsAtherosclerosisCell AdhesionHumansHypercholesterolemiaHyperglycemiaHypertensionInflammationIntegrin beta ChainsKidney Failure, ChronicLeukocyte Common AntigensLeukocytesIntegrin beta ChainsLeukocyte Common AntigensLeukosialinPTPRC protein, humanSPN protein, humanCD43CD45Gene transcriptionHypoxiaKidney diseaseLeukocyte adhesionβ2-integrins

Identifiers

PMID26847481
PMCPMC4851450

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.