Evidence map›Paper›PMID 36751625›Full record

ArticleClinical kidney journal2023

Urinary angiotensin-converting enzyme 2 and metabolomics in COVID-19-mediated kidney injury.

Ander Vergara, Kaiming Wang, Daniele Colombo, Mahmoud Gheblawi, Jaslyn Rasmuson, Rupasri Mandal, Franca Del Nonno, Brian Chiu, James W Scholey, María José Soler and 2 more

Open access · goldAbstract read
In one paragraph

Article in Clinical kidney journal, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 11% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.

  1. Pooled it
  2. Review
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  5. Understanding Renal Tubular Function: Key Mechanisms, Clinical Relevance, and Comprehensive Urine Assessment.Pathophysiology : the official journal of the International Society for Pathophysiology · 2025
    Review
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  7. Article
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  11. Review
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  14. Altered kidney distribution and loss of ACE2 into the urine in acute kidney injury.American journal of physiology. Renal physiology · 2024
    Article
  15. Review
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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

12 authors at 5 institutions in 3 countries.

Ander VergaraDepartment of Medicine, Division of Cardiology, University of Alberta, Edmonton, Alberta, Canada.ORCID https://orcid.org/0000-0003-1926-0147
Kaiming WangDepartment of Medicine, Division of Cardiology, University of Alberta, Edmonton, Alberta, Canada.
Daniele ColomboDepartment of Pathology, National Institute for Infectious Diseases "Lazzaro Spallanzani," IRCCS, Rome, Italy.
Mahmoud GheblawiDepartment of Medicine, Division of Cardiology, University of Alberta, Edmonton, Alberta, Canada.
Jaslyn RasmusonDepartment of Medicine, Division of Cardiology, University of Alberta, Edmonton, Alberta, Canada.
Rupasri MandalMetabolomics Innovation Center, University of Alberta, Edmonton, Alberta, Canada.
Franca Del NonnoDepartment of Pathology, National Institute for Infectious Diseases "Lazzaro Spallanzani," IRCCS, Rome, Italy.
Brian ChiuDepartment of Laboratory Medicine and Pathology, University of Alberta Hospital, Edmonton, Alberta, Canada.
James W ScholeyDepartment of Medicine, Division of Nephrology, University Health Network, Toronto, Ontario, Canada.
María José SolerDepartment of Nephrology, Vall d'Hebron University Hospital, Barcelona, Spain.ORCID https://orcid.org/0000-0003-3621-0766
David S WishartMetabolomics Innovation Center, University of Alberta, Edmonton, Alberta, Canada.
Gavin Y OuditDepartment of Medicine, Division of Cardiology, University of Alberta, Edmonton, Alberta, Canada.
University of Alberta · CAIstituto Nazionale per le Malattie Infettive Lazzaro Spallanzani · ITAlberta Hospital Edmonton · CAUniversity Health Network · CAVall d'Hebron Institut de Recerca · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Angiotensin-converting enzyme 2 (ACE2), the receptor for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is highly expressed in the kidneys. Beyond serving as a crucial endogenous regulator of the renin-angiotensin system, ACE2 also possess a unique function to facilitate amino acid absorption. Our observational study sought to explore the relationship between urine ACE2 (uACE2) and renal outcomes in coronavirus disease 2019 (COVID-19). Methods: In a cohort of 104 patients with COVID-19 without acute kidney injury (AKI), 43 patients with COVID-19-mediated AKI and 36 non-COVID-19 controls, we measured uACE2, urine tumour necrosis factor receptors I and II (uTNF-RI and uTNF-RII) and neutrophil gelatinase-associated lipocalin (uNGAL). We also assessed ACE2 staining in autopsy kidney samples and generated a propensity score-matched subgroup of patients to perform a targeted urine metabolomic study to describe the characteristic signature of COVID-19. Results: uACE2 is increased in patients with COVID-19 and further increased in those that developed AKI. After adjusting uACE2 levels for age, sex and previous comorbidities, increased uACE2 was independently associated with a >3-fold higher risk of developing AKI [odds ratio 3.05 (95% confidence interval 1.23‒7.58), Conclusions: Elevated uACE2 is related to AKI in patients with COVID-19. The loss of tubular ACE2 during SARS-CoV-2 infection demonstrates a potential link between aminoaciduria and proximal tubular injury.

Indexed as

acute kidney injuryangiotensin-converting enzyme 2COVID-19metabolomicsrenin–angiotensin system

Identifiers

PMID36751625
PMCPMC9494506
OpenAlexW4297876438

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.