Covid‐19 and kidney injury: Pathophysiology and molecular mechanisms

Elham Ahmadian; Seyed Mahdi Hosseiniyan Khatibi; Saiedeh Razi Soofiyani; Sima Abediazar; Mohammadali M. Shoja; Mohammadreza Ardalan; Sepideh Zununi Vahed

doi:10.1002/rmv.2176

journal article Oct 06, 2020

Covid‐19 and kidney injury: Pathophysiology and molecular mechanisms

Elham Ahmadian Seyed Mahdi Hosseiniyan Khatibi Saiedeh Razi Soofiyani Sima Abediazar Mohammadali M. Shoja Mohammadreza Ardalan Sepideh Zununi Vahed

Reviews in Medical Virology Vol. 31 No. 3 · Wiley

View at Publisher Save 10.1002/rmv.2176

Abstract

SummaryThe 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.

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References

108

[1]

10.1016/j.jaut.2020.102434

[2]

10.1016/s2213-2600(20)30229-0

[3]

10.1016/j.kint.2020.03.005

[4]

Endothelial cell infection and endotheliitis in COVID-19

Zsuzsanna Varga, Andreas J Flammer, Peter Steiger et al.

The Lancet 10.1016/s0140-6736(20)30937-5

[5]

Presenting Characteristics, Comorbidities, and Outcomes Among 5700 Patients Hospitalized With COVID-19 in the New York City Area

Safiya Richardson, Jamie S. Hirsch, Mangala Narasimhan et al.

JAMA 10.1001/jama.2020.6775

[6]

10.34172/npj.2020.22

[7]

10.34172/jnp.2020.35

[8]

Pan XW "Identification of a potential mechanism of acute kidney injury during the COVID‐19 outbreak: a study based on single‐cell transcriptome analysis" Intensive Care Med (2020)

[9]

Diao B "Human kidney is a target for novel severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) infection" medRxiv Prepr (2020)

[10]

10.1016/j.ekir.2020.03.024

[11]

10.34172/jrip.2020.19

[12]

10.1002/rmv.2134

[13]

10.1159/000507471

[14]

10.1172/jci138871

[15]

10.1038/s41581-020-0284-7

[16]

Li Z "Caution on kidney dysfunctions of COVID‐19 patients" medRxiv Prepr (2020)

[17]

Cheng Y "Kidney impairment is associated with in‐hospital death of COVID‐19 patients" medRxiv (2020)

[18]

10.1016/j.kint.2020.03.001

[19]

10.1681/asn.2020030276

[20]

10.1080/22221751.2020.1760144

[21]

10.1093/cid/ciaa248

[22]

10.1016/j.ekir.2020.04.002

[23]

10.1016/j.bbrc.2020.03.044

[24]

10.1681/asn.2006050423

[25]

10.34172/jnp.2020.37

[26]

Wang K "SARS‐CoV‐2 invades host cells via a novel route: CD147‐spike protein" BioRxiv (2020)

[27]

Structure, Function, and Antigenicity of the SARS-CoV-2 Spike Glycoprotein

Alexandra C. Walls, Young-Jun Park, M. Alejandra Tortorici et al.

Cell 10.1016/j.cell.2020.02.058

[28]

10.3390/ijms21093275

[29]

10.1111/j.1523-1755.2005.67130.x

[30]

Diao B "Diagnosis of acute respiratory syndrome coronavirus 2 infection by detection of nucleocapsid protein" medRxiv (2020)

[31]

10.1038/ki.2008.497

[32]

10.1093/ndt/gft320

[33]

10.1016/s0140-6736(03)13410-1

[34]

SARS-CoV-2 Cell Entry Depends on ACE2 and TMPRSS2 and Is Blocked by a Clinically Proven Protease Inhibitor

Markus Hoffmann, Hannah Kleine-Weber, Simon Schroeder et al.

Cell 10.1016/j.cell.2020.02.052

[35]

10.1002/1096-9896(2000)9999:9999<::aid-path743>3.0.co;2-t

[36]

10.1016/j.stem.2018.10.010

[37]

10.1073/pnas.1908706116

[38]

10.1128/jvi.02232-10

[39]

Renal histopathological analysis of 26 postmortem findings of patients with COVID-19 in China

Hua Su, Ming Yang, Cheng Wan et al.

Kidney International 10.1016/j.kint.2020.04.003

[40]

10.1016/j.antiviral.2015.01.011

[41]

10.1152/ajprenal.00316.2016

[42]

10.1128/jvi.00415-08

[43]

10.1128/jvi.01818-18

[44]

10.1186/1743-422x-10-359

[45]

10.1681/asn.2020040419

[46]

10.1001/jama.2020.1623

[47]

Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China

Chaolin Huang, Yeming Wang, Xingwang Li et al.

The Lancet 10.1016/s0140-6736(20)30183-5

[48]

Clinical Characteristics of 138 Hospitalized Patients With 2019 Novel Coronavirus–Infected Pneumonia in Wuhan, China

Dawei Wang, Bo Hu, Chang Hu et al.

JAMA 10.1001/jama.2020.1585

[49]

10.7326/0003-4819-139-9-200311040-00005

[50]

10.1111/j.1523-1755.2005.67130.x

Showing 50 of 108 references

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Published: Oct 06, 2020
Vol/Issue: 31(3)
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Elham Ahmadian