Evidence map›Paper›PMID 32791255›Full record

ArticleKidney international2020

SARS-CoV-2 causes a specific dysfunction of the kidney proximal tubule.

Alexis Werion, Leila Belkhir, Marie Perrot, Gregory Schmit, Selda Aydin, Zhiyong Chen, Andrea Penaloza, Julien De Greef, Halil Yildiz, Lucie Pothen and 11 more

Open access · bronzeAbstract read
In one paragraph

Article in Kidney international, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 140 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
140citing papers in PubMed, 2 pooled it
17.7field-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

140 citing papers in PubMed, 2 syntheses or guidelines pooled it, 234 citations in OpenAlex.

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80 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

21 authors at 3 institutions in 3 countries.

Alexis WerionDivision of Nephrology, Cliniques universitaires Saint-Luc, Brussels, Belgium.
Leila BelkhirDivision of Internal Medicine and Infectious Diseases, Cliniques universitaires Saint-Luc, Brussels, Belgium; Institut de Recherche Expérimentale et Clinique, UCLouvain, Brussels, Belgium.
Marie PerrotDivision of Nephrology, Cliniques universitaires Saint-Luc, Brussels, Belgium.
Gregory SchmitDepartment of Laboratory Medicine, Microbiology and Pathology, Cliniques universitaires Saint-Luc, Brussels, Belgium; Centre of Forensic Medicine, Cliniques universitaires Saint-Luc, Brussels, Belgium.
Selda AydinInstitut de Recherche Expérimentale et Clinique, UCLouvain, Brussels, Belgium; Department of Laboratory Medicine, Microbiology and Pathology, Cliniques universitaires Saint-Luc, Brussels, Belgium.
Zhiyong ChenDepartment of Physiology, Mechanisms of Inherited Kidney Disorders Group, University of Zurich, Zurich, Switzerland.
Andrea PenalozaDepartment of Emergency Medicine, Cliniques universitaires Saint-Luc, Brussels, Belgium.
Julien De GreefDivision of Internal Medicine and Infectious Diseases, Cliniques universitaires Saint-Luc, Brussels, Belgium; Institut de Recherche Expérimentale et Clinique, UCLouvain, Brussels, Belgium.
Halil YildizDivision of Internal Medicine and Infectious Diseases, Cliniques universitaires Saint-Luc, Brussels, Belgium; Institut de Recherche Expérimentale et Clinique, UCLouvain, Brussels, Belgium.
Lucie PothenDivision of Internal Medicine and Infectious Diseases, Cliniques universitaires Saint-Luc, Brussels, Belgium; Institut de Recherche Expérimentale et Clinique, UCLouvain, Brussels, Belgium.
Jean Cyr YombiDivision of Internal Medicine and Infectious Diseases, Cliniques universitaires Saint-Luc, Brussels, Belgium; Institut de Recherche Expérimentale et Clinique, UCLouvain, Brussels, Belgium.
Joseph DewulfDepartment of Laboratory Medicine, Microbiology and Pathology, Cliniques universitaires Saint-Luc, Brussels, Belgium.
Anais ScohyDepartment of Laboratory Medicine, Microbiology and Pathology, Cliniques universitaires Saint-Luc, Brussels, Belgium.
Ludovic GérardInstitut de Recherche Expérimentale et Clinique, UCLouvain, Brussels, Belgium; Department of Intensive Care Medicine, Cliniques universitaires Saint-Luc, Brussels, Belgium.
Xavier WitteboleInstitut de Recherche Expérimentale et Clinique, UCLouvain, Brussels, Belgium; Department of Intensive Care Medicine, Cliniques universitaires Saint-Luc, Brussels, Belgium.
Pierre-François LaterreInstitut de Recherche Expérimentale et Clinique, UCLouvain, Brussels, Belgium; Department of Intensive Care Medicine, Cliniques universitaires Saint-Luc, Brussels, Belgium.
Sara E MillerDepartment of Pathology, Duke University Medical Center, Durham, North Carolina, USA.
Olivier DevuystDivision of Nephrology, Cliniques universitaires Saint-Luc, Brussels, Belgium; Institut de Recherche Expérimentale et Clinique, UCLouvain, Brussels, Belgium; Department of Physiology, Mechanisms of Inherited Kidney Disorders Group, University of Zurich, Zurich, Switzerland.
Michel JadoulDivision of Nephrology, Cliniques universitaires Saint-Luc, Brussels, Belgium; Department of Emergency Medicine, Cliniques universitaires Saint-Luc, Brussels, Belgium.
Johann MorelleDivision of Nephrology, Cliniques universitaires Saint-Luc, Brussels, Belgium; Institut de Recherche Expérimentale et Clinique, UCLouvain, Brussels, Belgium. Electronic address: johann.morelle@uclouvain.be.
Cliniques universitaires Saint-Luc (CUSL) COVID-19 Research Group
Cliniques Universitaires Saint-Luc · BEDuke Medical Center · USUniversity of Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Coronavirus disease 2019 (COVID-19) is commonly associated with kidney damage, and the angiotensin converting enzyme 2 (ACE2) receptor for SARS-CoV-2 is highly expressed in the proximal tubule cells. Whether patients with COVID-19 present specific manifestations of proximal tubule dysfunction remains unknown. To test this, we examined a cohort of 49 patients requiring hospitalization in a large academic hospital in Brussels, Belgium. There was evidence of proximal tubule dysfunction in a subset of patients with COVID-19, as attested by low-molecular-weight proteinuria (70-80%), neutral aminoaciduria (46%), and defective handling of uric acid (46%) or phosphate (19%). None of the patients had normoglycemic glucosuria. Proximal tubule dysfunction was independent of pre-existing comorbidities, glomerular proteinuria, nephrotoxic medications or viral load. At the structural level, kidneys from patients with COVID-19 showed prominent tubular injury, including in the initial part of the proximal tubule, with brush border loss, acute tubular necrosis, intraluminal debris, and a marked decrease in the expression of megalin in the brush border. Transmission electron microscopy identified particles resembling coronaviruses in vacuoles or cisternae of the endoplasmic reticulum in proximal tubule cells. Among features of proximal tubule dysfunction, hypouricemia with inappropriate uricosuria was independently associated with disease severity and with a significant increase in the risk of respiratory failure requiring invasive mechanical ventilation using Cox (adjusted hazard ratio 6.2, 95% CI 1.9-20.1) or competing risks (adjusted sub-distribution hazard ratio 12.1, 95% CI 2.7-55.4) survival models. Thus, our data establish that SARS-CoV-2 causes specific manifestations of proximal tubule dysfunction and provide novel insights into COVID-19 severity and outcome.

Indexed as

AgedAged, 80 and overBelgiumBetacoronavirusCase-Control StudiesCoronavirus InfectionsCOVID-19HumansKidney Tubules, ProximalMaleMiddle AgedPandemicsPneumonia, ViralSARS-CoV-2COVID-19kidneyrenal Fanconi syndromesevere acute respiratory syndrome

Identifiers

PMID32791255
PMCPMC7416689
OpenAlexW3047897956

What OpenQuestion holds

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Registered trials

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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.