Evidence map›Paper›PMID 33022818›Full record

ReviewReviews in medical virology2021

Covid-19 and kidney injury: Pathophysiology and molecular mechanisms.

Elham Ahmadian, Seyed Mahdi Hosseiniyan Khatibi, Saiedeh Razi Soofiyani, Sima Abediazar, Mohammadali M Shoja, Mohammadreza Ardalan, Sepideh Zununi Vahed

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

Review in Reviews in medical virology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 213 papers, 9 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
213citing papers in PubMed, 9 pooled it
49.6field-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

213 citing papers in PubMed, 9 syntheses or guidelines pooled it, 364 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Pooled it
  6. Pooled it
  7. Pooled it
  8. Pooled it
  9. Pooled it
  10. Trial
  11. Trial
  12. Review
  13. Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

153 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 2 institutions in 2 countries.

Elham AhmadianKidney Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Seyed Mahdi Hosseiniyan KhatibiKidney Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Saiedeh Razi SoofiyaniClinical Research Development Unit, Sina Educational, Research and Treatment Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Sima AbediazarKidney Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Mohammadali M ShojaDepartment of Surgery, University of Illinois at Chicago-Metropolitan Group Hospitals (UIC-MGH), Chicago, Illinois, USA.
Mohammadreza ArdalanKidney Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Sepideh Zununi VahedKidney Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.ORCID https://orcid.org/0000-0003-0179-4562
Tabriz University of Medical Sciences · IRUniversity of Illinois Chicago · US

Funding

Kidney Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
6 · The paper itself

Abstract

The novel coronavirus (SARS-CoV-2) has turned into a life-threatening pandemic disease (Covid-19). About 5% of patients with Covid-19 have severe symptoms including septic shock, acute respiratory distress syndrome, and the failure of several organs, while most of them have mild symptoms. Frequently, the kidneys are involved through direct or indirect mechanisms. Kidney involvement mainly manifests itself as proteinuria and acute kidney injury (AKI). The SARS-CoV-2-induced kidney damage is expected to be multifactorial; directly it can infect the kidney podocytes and proximal tubular cells and based on an angiotensin-converting enzyme 2 (ACE2) pathway it can lead to acute tubular necrosis, protein leakage in Bowman's capsule, collapsing glomerulopathy and mitochondrial impairment. The SARS-CoV-2-driven dysregulation of the immune responses including cytokine storm, macrophage activation syndrome, and lymphopenia can be other causes of the AKI. Organ interactions, endothelial dysfunction, hypercoagulability, rhabdomyolysis, and sepsis are other potential mechanisms of AKI. Moreover, lower oxygen delivery to kidney may cause an ischaemic injury. Understanding the fundamental molecular pathways and pathophysiology of kidney injury and AKI in Covid-19 is necessary to develop management strategies and design effective therapies.

Indexed as

Acute Kidney InjuryAngiotensin-Converting Enzyme 2COVID-19Cytokine Release SyndromeCytokinesDisseminated Intravascular CoagulationHost-Pathogen InteractionsHumansKidney Tubules, ProximalLymphopeniaNecrosisPodocytesProteinuriaSARS-CoV-2SepsisSerine EndopeptidasesACE2 protein, humanAngiotensin-Converting Enzyme 2CytokinesSerine EndopeptidasesSpike Glycoprotein, Coronavirusspike protein, SARS-CoV-2TMPRSS2 protein, humanacute kidney injuryangiotensinbardikinincoronovirusproteinuriarenal injurySARS-CoV-2

Identifiers

PMID33022818
PMCPMC7646060
OpenAlexW3090321510

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.