Evidence map›Paper›PMID 34226718›Full record

ReviewNature reviews. Nephrology2021

Pathophysiology of COVID-19-associated acute kidney injury.

Matthieu Legrand, Samira Bell, Lui Forni, Michael Joannidis, Jay L Koyner, Kathleen Liu, Vincenzo Cantaluppi

Open access · hybridAbstract readReview
In one paragraph

Review in Nature reviews. Nephrology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 305 papers, 7 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
305citing papers in PubMed, 7 pooled it
28.1field-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

305 citing papers in PubMed, 7 syntheses or guidelines pooled it, 510 citations in OpenAlex.

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 7 institutions in 5 countries.

Matthieu LegrandDepartment of Anesthesia and Perioperative Care, Division of Critical Care Medicine, University of California, San Francisco, CA, USA. matthieu.legrand@ucsf.edu.ORCID http://orcid.org/0000-0001-9788-5316
Samira BellDivision of Population Health and Genomics, School of Medicine, University of Dundee, Dundee, UK.ORCID http://orcid.org/0000-0001-9100-1575
Lui ForniIntensive Care Unit, Royal Surrey Hospital NHS Foundation Trust, Surrey, UK.ORCID http://orcid.org/0000-0002-0617-5309
Michael JoannidisDivision of Intensive Care and Emergency Medicine, Medical University of Innsbruck, Innsbruck, Austria.ORCID http://orcid.org/0000-0002-6996-0881
Jay L KoynerDivisions of Nephrology, Departments of Medicine, University of Chicago, Chicago, IL, USA.
Kathleen LiuDivisions of Nephrology and Critical Care Medicine, Departments of Medicine and Anesthesia, University of San Francisco, San Francisco, CA, USA.ORCID http://orcid.org/0000-0003-4891-8649
Vincenzo CantaluppiNephrology and Kidney Transplantation Unit, Department of Translational Medicine, University of Piemonte Orientale, Novara, Italy.
Innsbruck Medical University · ATUniversità degli Studi del Piemonte Orientale “Amedeo Avogadro” · ITUniversity of California, San Francisco · USUniversity of Chicago · USUniversity of Dundee · GBUniversity of San Francisco · USUniversity of Surrey · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although respiratory failure and hypoxaemia are the main manifestations of COVID-19, kidney involvement is also common. Available evidence supports a number of potential pathophysiological pathways through which acute kidney injury (AKI) can develop in the context of SARS-CoV-2 infection. Histopathological findings have highlighted both similarities and differences between AKI in patients with COVID-19 and in those with AKI in non-COVID-related sepsis. Acute tubular injury is common, although it is often mild, despite markedly reduced kidney function. Systemic haemodynamic instability very likely contributes to tubular injury. Despite descriptions of COVID-19 as a cytokine storm syndrome, levels of circulating cytokines are often lower in patients with COVID-19 than in patients with acute respiratory distress syndrome with causes other than COVID-19. Tissue inflammation and local immune cell infiltration have been repeatedly observed and might have a critical role in kidney injury, as might endothelial injury and microvascular thrombi. Findings of high viral load in patients who have died with AKI suggest a contribution of viral invasion in the kidneys, although the issue of renal tropism remains controversial. An impaired type I interferon response has also been reported in patients with severe COVID-19. In light of these observations, the potential pathophysiological mechanisms of COVID-19-associated AKI may provide insights into therapeutic strategies.

Indexed as

Acute Kidney InjuryAdaptive ImmunityBiopsyComplement System ProteinsCOVID-19Drug-Related Side Effects and Adverse ReactionsEndothelium, VascularExtracorporeal Membrane OxygenationHematuriaHumansImmunity, HumoralImmunity, InnateImmunosenescenceInflammationInterferon Type IKidneyComplement System ProteinsInterferon Type I

Identifiers

PMID34226718
PMCPMC8256398
OpenAlexW3183058561

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.