Human kidney is a target for novel severe acute respiratory syndrome coronavirus 2 infection

Bo Diao, Chenhui Wang, Rongshuai Wang, Zeqing Feng, Ji Zhang, Han Yang, Yingjun Tan, Huiming Wang, Changsong Wang, Liang Liu, Ying Liu, Yueping Liu, Gang Wang, Zilin Yuan, Xiaotao Hou, Liang Ren (), Yuzhang Wu () and Yongwen Chen ()
Additional contact information
Bo Diao: Third Military Medical University
Chenhui Wang: Third Military Medical University
Rongshuai Wang: Huazhong University of Science and Technology
Zeqing Feng: Third Military Medical University
Ji Zhang: Third Military Medical University
Han Yang: Third Military Medical University
Yingjun Tan: Department of Medical Laboratory Center, General Hospital of Central Theater Command
Huiming Wang: Renmin Hospital of Wuhan University
Changsong Wang: 989th Hospital of PLA
Liang Liu: Hubei Chongxin Judicial Expertise Center
Ying Liu: Department of Medical Laboratory Center, General Hospital of Central Theater Command
Yueping Liu: Department of Medical Laboratory Center, General Hospital of Central Theater Command
Gang Wang: Department of Medical Laboratory Center, General Hospital of Central Theater Command
Zilin Yuan: Department of Medical Laboratory Center, General Hospital of Central Theater Command
Xiaotao Hou: Guangzhou KingMed Center for Clinical Laboratory Co., Ltd.
Liang Ren: Huazhong University of Science and Technology
Yuzhang Wu: Third Military Medical University
Yongwen Chen: Third Military Medical University

Nature Communications, 2021, vol. 12, issue 1, 1-9

Abstract: Abstract It is unclear whether severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can directly infect human kidney, thus leading to acute kidney injury (AKI). Here, we perform a retrospective analysis of clinical parameters from 85 patients with laboratory-confirmed coronavirus disease 2019 (COVID-19); moreover, kidney histopathology from six additional COVID-19 patients with post-mortem examinations was performed. We find that 27% (23/85) of patients exhibited AKI. The elderly patients and cases with comorbidities (hypertension and heart failure) are more prone to develop AKI. Haematoxylin & eosin staining shows that the kidneys from COVID-19 autopsies have moderate to severe tubular damage. In situ hybridization assays illustrate that viral RNA accumulates in tubules. Immunohistochemistry shows nucleocapsid and spike protein deposits in the tubules, and immunofluorescence double staining shows that both antigens are restricted to the angiotensin converting enzyme-II-positive tubules. SARS-CoV-2 infection triggers the expression of hypoxic damage-associated molecules, including DP2 and prostaglandin D synthase in infected tubules. Moreover, it enhances CD68+ macrophages infiltration into the tubulointerstitium, and complement C5b-9 deposition on tubules is also observed. These results suggest that SARS-CoV-2 directly infects human kidney to mediate tubular pathogenesis and AKI.

Date: 2021
References: Add references at CitEc
Citations: View citations in EconPapers (1)

Downloads: (external link)
https://www.nature.com/articles/s41467-021-22781-1 Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:12:y:2021:i:1:d:10.1038_s41467-021-22781-1

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/s41467-021-22781-1

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().