Evidence map›Paper›PMID 32461141›Full record

ReviewKidney international2020

The case of complement activation in COVID-19 multiorgan impact.

Marina Noris, Ariela Benigni, Giuseppe Remuzzi

Open access · bronzeAbstract readReview
In one paragraph

Review in Kidney international, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 224 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
224citing papers in PubMed, 6 pooled it
7.8field-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

224 citing papers in PubMed, 6 syntheses or guidelines pooled it, 352 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Pooled it
  6. Renal Injury by SARS-CoV-2 Infection: A Systematic Review.Kidney diseases (Basel, Switzerland) · 2021
    Pooled it
  7. Trial
  8. Article
  9. Review
  10. Review
  11. Article
  12. Observational
  13. Neutrophils and NETs in kidney disease.Nature reviews. Nephrology · 2025
    Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Preeclampsia in the Context of COVID-19: Mechanisms, Pathophysiology, and Clinical Outcomes.American journal of reproductive immunology (New York, N.Y. : 1989) · 2024
    Review
  20. Article

164 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 at 1 institution in 1 country.

Marina NorisIstituto di Ricerche Farmacologiche Mario Negri IRCCS, Clinical Research Center for Rare Diseases Aldo e Cele Daccò and Centro Anna Maria Astori, Science and Technology Park Kilometro Rosso, Bergamo, Italy.
Ariela BenigniIstituto di Ricerche Farmacologiche Mario Negri IRCCS, Clinical Research Center for Rare Diseases Aldo e Cele Daccò and Centro Anna Maria Astori, Science and Technology Park Kilometro Rosso, Bergamo, Italy.
Giuseppe RemuzziIstituto di Ricerche Farmacologiche Mario Negri IRCCS, Clinical Research Center for Rare Diseases Aldo e Cele Daccò and Centro Anna Maria Astori, Science and Technology Park Kilometro Rosso, Bergamo, Italy. Electronic address: giuseppe.remuzzi@marionegri.it.
Mario Negri Institute for Pharmacological Research · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The novel coronavirus disease COVID-19 originates in the lungs, but it may extend to other organs, causing, in severe cases, multiorgan damage, including cardiac injury and acute kidney injury. In severe cases, the presence of kidney injury is associated with increased risk of death, highlighting the relevance of this organ as a target of SARS-CoV-2 infection. COVID-19-associated tissue injury is not primarily mediated by viral infection, but rather is a result of the inflammatory host immune response, which drives hypercytokinemia and aggressive inflammation that affect lung parenchymal cells, diminishing oxygen uptake, but also endothelial cells, resulting in endotheliitis and thrombotic events and intravascular coagulation. The complement system represents the first response of the host immune system to SARS-CoV-2 infection, but there is growing evidence that unrestrained activation of complement induced by the virus in the lungs and other organs plays a major role in acute and chronic inflammation, endothelial cell dysfunction, thrombus formation, and intravascular coagulation, and ultimately contributes to multiple organ failure and death. In this review, we discuss the relative role of the different complement activation products in the pathogenesis of COVID-19-associated tissue inflammation and thrombosis and propose the hypothesis that blockade of the terminal complement pathway may represent a potential therapeutic option for the prevention and treatment of lung and multiorgan damage.

Indexed as

BetacoronavirusComplement ActivationAnimalsComplement C5aCoronavirus InfectionsCOVID-19Endothelial CellsHumansInflammationMannose-Binding LectinMicePandemicsPneumonia, ViralSARS-CoV-2ThrombosisVascular DiseasesComplement C5aMannose-Binding LectinC5 inhibitioncomplement activationcomplement terminal pathwayCOVID-19kidney injuryvascular injury

Identifiers

PMID32461141
PMCPMC7246017
OpenAlexW3027964178

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.