Evidence map›Paper›PMID 18488066›Full record

ReviewMolecular medicine (Cambridge, Mass.)

Renal hypoxia and dysoxia after reperfusion of the ischemic kidney.

Matthieu Legrand, Egbert G Mik, Tanja Johannes, Didier Payen, Can Ince

Open access · goldAbstract readReview
In one paragraph

Review in Molecular medicine (Cambridge, Mass.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 papers.

0numbers the graph read from it
0cells of the map it votes in
114citing papers in PubMed
8.8field-weighted citation impact, top 2% 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

114 citing papers in PubMed, 284 citations in OpenAlex.

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  13. Intraoperative blood pressure management during kidney transplantation: Grafts under pressure.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2024
    Article
  14. Acute kidney injury in patients with burns.Nature reviews. Nephrology · 2024
    Review
  15. Noninvasive measurement ofCommunications medicine · 2023
    Article
  16. Review
  17. Review
  18. Article
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54 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

5 authors at 4 institutions in 2 countries.

Matthieu LegrandDepartment of Physiology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands. m.m.legrand@amc.nl
Egbert G Mik
Tanja Johannes
Didier Payen
Can Ince
Erasmus MC · NLHôpital Lariboisière · FRUniversité Paris Cité · FRUniversity of Amsterdam · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ischemia is the most common cause of acute renal failure. Ischemic-induced renal tissue hypoxia is thought to be a major component in the development of acute renal failure in promoting the initial tubular damage. Renal oxygenation originates from a balance between oxygen supply and consumption. Recent investigations have provided new insights into alterations in oxygenation pathways in the ischemic kidney. These findings have identified a central role of microvascular dysfunction related to an imbalance between vasoconstrictors and vasodilators, endothelial damage and endothelium-leukocyte interactions, leading to decreased renal oxygen supply. Reduced microcirculatory oxygen supply may be associated with altered cellular oxygen consumption (dysoxia), because of mitochondrial dysfunction and activity of alternative oxygen-consuming pathways. Alterations in oxygen utilization and/or supply might therefore contribute to the occurrence of organ dysfunction. This view places oxygen pathways' alterations as a potential central player in the pathogenesis of acute kidney injury. Both in regulation of oxygen supply and consumption, nitric oxide seems to play a pivotal role. Furthermore, recent studies suggest that, following acute ischemic renal injury, persistent tissue hypoxia contributes to the development of chronic renal dysfunction. Adaptative mechanisms to renal hypoxia may be ineffective in more severe cases and lead to the development of chronic renal failure following ischemia-reperfusion. This paper is aimed at reviewing the current insights into oxygen transport pathways, from oxygen supply to oxygen consumption in the kidney and from the adaptation mechanisms to renal hypoxia. Their role in the development of ischemia-induced renal damage and ischemic acute renal failure are discussed.

Indexed as

Acute Kidney InjuryAnimalsHumansHypoxiaKidneyKidney DiseasesModels, BiologicalOxygen ConsumptionReperfusionReperfusion InjuryVasoconstrictionVasodilation

Identifiers

PMID18488066
PMCPMC2386087
OpenAlexW2161481747

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.