Covid-19 and kidney injury: Pathophysiology and molecular mechanisms.
Acute Kidney Injury
/ immunology
Angiotensin-Converting Enzyme 2
/ genetics
COVID-19
/ immunology
Cytokine Release Syndrome
/ immunology
Cytokines
/ genetics
Disseminated Intravascular Coagulation
/ immunology
Host-Pathogen Interactions
/ genetics
Humans
Kidney Tubules, Proximal
/ immunology
Lymphopenia
/ immunology
Necrosis
/ immunology
Podocytes
/ immunology
Proteinuria
/ immunology
SARS-CoV-2
/ immunology
Sepsis
/ immunology
Serine Endopeptidases
/ genetics
Spike Glycoprotein, Coronavirus
/ genetics
SARS-CoV-2
acute kidney injury
angiotensin
bardikinin
coronovirus
proteinuria
renal injury
Journal
Reviews in medical virology
ISSN: 1099-1654
Titre abrégé: Rev Med Virol
Pays: England
ID NLM: 9112448
Informations de publication
Date de publication:
05 2021
05 2021
Historique:
revised:
16
09
2020
received:
11
07
2020
accepted:
17
09
2020
pubmed:
7
10
2020
medline:
1
6
2021
entrez:
6
10
2020
Statut:
ppublish
Résumé
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.
Identifiants
pubmed: 33022818
doi: 10.1002/rmv.2176
pmc: PMC7646060
doi:
Substances chimiques
Cytokines
0
Spike Glycoprotein, Coronavirus
0
spike protein, SARS-CoV-2
0
ACE2 protein, human
EC 3.4.17.23
Angiotensin-Converting Enzyme 2
EC 3.4.17.23
Serine Endopeptidases
EC 3.4.21.-
TMPRSS2 protein, human
EC 3.4.21.-
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
e2176Subventions
Organisme : Kidney Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
Informations de copyright
© 2020 John Wiley & Sons Ltd.
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