Evidence map›Paper›PMID 33796285›Full record

ReviewClinical kidney journal2021

Renin-angiotensin system blockade in the COVID-19 pandemic.

Jordana B Cohen, Andrew M South, Hossam A Shaltout, Matthew R Sinclair, Matthew A Sparks

Open access · goldAbstract readReview
In one paragraph

Review in Clinical kidney journal, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.5field-weighted citation impact, top 15% 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

14 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. COVID-19 and the cardiovascular system: an update.The American journal of the medical sciences · 2022
    Review
  6. Kidney implications of SARS-CoV2 infection in children.Pediatric nephrology (Berlin, Germany) · 2022
    Review
  7. Farewell from theClinical kidney journal · 2022
    Article
  8. Review
  9. Review
  10. Observational
  11. Shining More Light on RAS Inhibition during the COVID-19 Pandemic.Clinical journal of the American Society of Nephrology : CJASN · 2021
    Article
  12. Article
  13. Article
  14. Article
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.

Jordana B CohenRenal-Electrolyte and Hypertension Division, Department of Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.ORCID https://orcid.org/0000-0003-4649-079X
Andrew M SouthSection of Nephrology, Department of Pediatrics, Brenner Children's Hospital, Wake Forest School of Medicine, Winston Salem, NC, USA.ORCID https://orcid.org/0000-0002-3204-4142
Hossam A ShaltoutDepartment of Surgery, Hypertension and Vascular Research, Wake Forest School of Medicine, Winston Salem, NC, USA.
Matthew R SinclairDivision of Nephrology, Department of Medicine, Duke University School of Medicine, Durham, NC, USA.
Matthew A SparksDivision of Nephrology, Department of Medicine, Duke University School of Medicine, Durham, NC, USA.ORCID https://orcid.org/0000-0003-2075-2691
Duke University · USBrenner Children's Hospital · USUniversity of Pennsylvania · USWake Forest University · US

Funding

The role of angiotensin-(1-7) in hypertension and hypertension-induced heart and kidney damageK23HL148394 · NHLBI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI SOUTH, ANDREW MICHAEL · 2020 to 2024
$783k
NHLBI NIH HHS K23 HL148394NHLBI NIH HHS L40 HL148910
6 · The paper itself

Abstract

In the early months of the coronavirus disease 2019 (COVID-19) pandemic, a hypothesis emerged suggesting that pharmacologic inhibitors of the renin-angiotensin system (RAS) may increase COVID-19 severity. This hypothesis was based on the role of angiotensin-converting enzyme 2 (ACE2), a counterregulatory component of the RAS, as the binding site for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), allowing viral entry into host cells. Extrapolations from prior evidence led to speculation that upregulation of ACE2 by RAS blockade may increase the risk of adverse outcomes from COVID-19. However, counterarguments pointed to evidence of potential protective effects of ACE2 and RAS blockade with regard to acute lung injury, as well as substantial risks from discontinuing these commonly used and important medications. Here we provide an overview of classic RAS physiology and the crucial role of ACE2 in systemic pathways affected by COVID-19. Additionally, we critically review the physiologic and epidemiologic evidence surrounding the interactions between RAS blockade and COVID-19. We review recently published trial evidence and propose important future directions to improve upon our understanding of these relationships.

Indexed as

angiotensin-converting enzyme 2angiotensin-converting enzyme inhibitorangiotensin II receptor blockercoronavirusCOVID-19hypertensionrenin–angiotensin systemSARS-CoV-2

Identifiers

PMID33796285
PMCPMC7929063
OpenAlexW3143236622

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.