Evidence map›Paper›PMID 32892687›Full record

ArticlePlatelets2021

Platelets and renal failure in the SARS-CoV-2 syndrome.

Muhanad Taha, Dahlia Sano, Samer Hanoudi, Zahia Esber, Morvarid Elahi, Ali Gabali, Teena Chopra, Sorin Draghici, Lobelia Samavati

Open access · greenAbstract read
In one paragraph

Article in Platelets, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.6field-weighted citation impact, top 18% 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

12 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Review
  11. Review
  12. Inflammatory stress in SARS-COV-2 associated Acute Kidney Injury.International journal of biological sciences · 2021
    Review
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

9 authors at 1 institution in 1 country.

Muhanad TahaDepartment of Internal Medicine, Division of Pulmonary, Critical Care and Sleep Medicine, Wayne State University, School of Medicine and Detroit Medical Center , Detroit, MI, USA.
Dahlia SanoDepartment of Internal Medicine, Division Hematology and Oncology; Wayne State University, School of Medicine and Detroit Medical Center , Detroit, MI, USA.
Samer HanoudiDepartment of Computer Science, Wayne State University , Detroit, MI, USA.
Zahia EsberDepartment of Internal Medicine, Division of Pulmonary, Critical Care and Sleep Medicine, Wayne State University, School of Medicine and Detroit Medical Center , Detroit, MI, USA.
Morvarid ElahiDepartment of Pathology, Wayne State University, School of Medicine and Detroit Medical Center , Detroit, MI, USA.
Ali GabaliDivision of Infectious Diseases, Wayne State University , Detroit, MI, USA.
Teena ChopraDivision of Infectious Diseases, Wayne State University , Detroit, MI, USA.
Sorin DraghiciDepartment of Computer Science, Wayne State University , Detroit, MI, USA.
Lobelia SamavatiDepartment of Internal Medicine, Division of Pulmonary, Critical Care and Sleep Medicine, Wayne State University, School of Medicine and Detroit Medical Center , Detroit, MI, USA.ORCID https://orcid.org/0000-0002-3327-2585
Wayne State University · US

Funding

A novel T7 phage display technology to detect sarcoidosis specific antigensR01HL150474 · NHLBI · WAYNE STATE UNIVERSITY · PI SAMAVATI, LOBELIA · 2020 to 2023
$1.8M
NHLBI NIH HHS R01 HL150474
6 · The paper itself

Abstract

The coronavirus disease 19 (COVID-19) is a highly transmittable viral infection caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). SARS-CoV-2 utilizes metallocarboxyl peptidase angiotensin receptor (ACE) 2 to gain entry into human cells. Activation of several proteases facilitates the interaction of viral spike proteins (S1) and ACE2 receptor. This leads to cleavage of host ACE2 receptors. ACE2 activity counterbalances the angiotensin II effect, its loss may lead to elevated angiotensin II levels with modulation of platelet function, size and activity. COVID-19 disease encompasses a spectrum of systemic involvement far beyond respiratory failure alone. Several features of this disease, including the etiology of acute kidney injury (AKI) and the hypercoagulable state, remain poorly understood. Here, we show that there is a high incidence of AKI (81%) in the critically ill adults with COVID-19 in the setting of elevated D-dimer, elevated ferritin, C reactive protein (CRP) and lactate dehydrogenase (LDH) levels. Strikingly, there were unique features of platelets in these patients, including larger, more granular platelets and a higher mean platelet volume (MPV). There was a significant correlation between measured D-dimer levels and MVP; but a negative correlation between MPV and glomerular filtration rates (GFR) in critically ill cohort. Our data suggest that activated platelets may play a role in renal failure and possibly hypercoagulability status in COVID19 patients.

Indexed as

PandemicsSARS-CoV-2Acute Kidney InjuryAdultAgedAged, 80 and overAngiotensin-Converting Enzyme 2Angiotensin IIBlood PlateletsComorbidityCOVID-19Diabetes MellitusFemaleFibrin Fibrinogen Degradation ProductsGlomerular Filtration RateHumansACE2 protein, humanAngiotensin-Converting Enzyme 2Angiotensin IIFibrin Fibrinogen Degradation Productsfibrin fragment DReceptors, VirusAKICOVID-19D-Dimerhypercoagulablemean platelet volumerenal failureSARS-CoV-2

Identifiers

PMID32892687
PMCPMC7855044
OpenAlexW3083154900

What OpenQuestion holds

Textmetadata
LicenceTDM
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.