tetano
Editor, Senior Moderator
Nat Commun
. 2021 May 4;12(1):2506.
doi: 10.1038/s41467-021-22781-1.
Human kidney is a target for novel severe acute respiratory syndrome coronavirus 2 infection
Bo Diao[SUP] #[/SUP][SUP] 1 2 3 [/SUP], Chenhui Wang[SUP] #[/SUP][SUP] 1 [/SUP], Rongshuai Wang[SUP] #[/SUP][SUP] 4 [/SUP], Zeqing Feng[SUP] 1 [/SUP], Ji Zhang[SUP] 1 [/SUP], Han Yang[SUP] 1 [/SUP], Yingjun Tan[SUP] 2 [/SUP], Huiming Wang[SUP] 5 [/SUP], Changsong Wang[SUP] 6 [/SUP], Liang Liu[SUP] 7 [/SUP], Ying Liu[SUP] 2 [/SUP], Yueping Liu[SUP] 2 [/SUP], Gang Wang[SUP] 2 [/SUP], Zilin Yuan[SUP] 2 [/SUP], Xiaotao Hou[SUP] 8 [/SUP], Liang Ren[SUP] #[/SUP][SUP] 9 [/SUP], Yuzhang Wu[SUP] #[/SUP][SUP] 10 [/SUP], Yongwen Chen[SUP] #[/SUP][SUP] 11 [/SUP]
Affiliations
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.
. 2021 May 4;12(1):2506.
doi: 10.1038/s41467-021-22781-1.
Human kidney is a target for novel severe acute respiratory syndrome coronavirus 2 infection
Bo Diao[SUP] #[/SUP][SUP] 1 2 3 [/SUP], Chenhui Wang[SUP] #[/SUP][SUP] 1 [/SUP], Rongshuai Wang[SUP] #[/SUP][SUP] 4 [/SUP], Zeqing Feng[SUP] 1 [/SUP], Ji Zhang[SUP] 1 [/SUP], Han Yang[SUP] 1 [/SUP], Yingjun Tan[SUP] 2 [/SUP], Huiming Wang[SUP] 5 [/SUP], Changsong Wang[SUP] 6 [/SUP], Liang Liu[SUP] 7 [/SUP], Ying Liu[SUP] 2 [/SUP], Yueping Liu[SUP] 2 [/SUP], Gang Wang[SUP] 2 [/SUP], Zilin Yuan[SUP] 2 [/SUP], Xiaotao Hou[SUP] 8 [/SUP], Liang Ren[SUP] #[/SUP][SUP] 9 [/SUP], Yuzhang Wu[SUP] #[/SUP][SUP] 10 [/SUP], Yongwen Chen[SUP] #[/SUP][SUP] 11 [/SUP]
Affiliations
- PMID: 33947851
- DOI: 10.1038/s41467-021-22781-1
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.