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

• Published in: Nature communications Vol. 12; no. 1; pp. 2506 - 9
• Main Authors: Diao, Bo, Wang, Chenhui, Wang, Rongshuai, Feng, Zeqing, Zhang, Ji, Yang, Han, Tan, Yingjun, Wang, Huiming, Wang, Changsong, Liu, Liang, Liu, Ying, Liu, Yueping, Wang, Gang, Yuan, Zilin, Hou, Xiaotao, Ren, Liang, Wu, Yuzhang, Chen, Yongwen
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 04.05.2021; Nature Publishing Group; Nature Portfolio
• Subjects: 101/1; 14/32; 14/63; 631/326/596/4130; 692/4022/1585; 692/699/1585/4; 82/51; Acute Kidney Injury - epidemiology; Acute Kidney Injury - etiology; Acute Kidney Injury - pathology; Acute Kidney Injury - virology; Adult; Aged; Aged, 80 and over; Angiotensin; Angiotensin-Converting Enzyme 2 - metabolism; Antigens; Antigens, Viral - genetics; Antigens, Viral - metabolism; Autopsies; Autopsy; China - epidemiology; Congestive heart failure; Coronaviridae; Coronaviruses; COVID-19; COVID-19 - complications; COVID-19 - epidemiology; COVID-19 - virology; Damage accumulation; Female; Histopathology; Humanities and Social Sciences; Humans; Hybridization; Hypertension; Hypoxia; Immunity, Innate; Immunofluorescence; Immunohistochemistry; Injury analysis; Kidney Function Tests; Kidney Tubules - metabolism; Kidney Tubules - pathology; Kidney Tubules - virology; Kidneys; Macrophages; Male; Middle Aged; multidisciplinary; Nucleocapsids; Pandemics; Pathogenesis; Peptidyl-dipeptidase A; Prostaglandin D2 synthase; Respiratory diseases; Retrospective Studies; SARS-CoV-2 - genetics; SARS-CoV-2 - isolation & purification; SARS-CoV-2 - pathogenicity; Science; Science (multidisciplinary); Severe acute respiratory syndrome coronavirus 2; Spike protein; Staining; Tubules; Viral diseases; Viral Proteins - genetics; Viral Proteins - metabolism; Young Adult; China
• ISSN: 2041-1723; 2041-1723
• DOI: 10.1038/s41467-021-22781-1

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. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can lead to acute kidney injury. The authors describe that SARS-COV-2 can directly infect human kidney, possibly mediating tubular pathogenesis.