COVID-19 Research Paper Advance Articles

Expression profiles revealed potential kidney injury caused by SARS-CoV-2: a systematic analysis of ACE2 and clinical lessons learned from this discovery

Jukun Song1, *, , Jianguo Zhu2, *, , Weiming Chen2, , Guohua Zhu2, , Wei Wang2, , Chi Chen3, , Zhenyu Jia4, , Yan Zha5, , Ping Xu6, , Zheng Wang6, , Fa Sun2, , Xiangyan Zhang7, ,

  • 1 Department of Oral and Maxillofacial Surgery, Guizhou Provincial People’s Hospital, Guizhou, China
  • 2 Department of Urology, Guizhou Provincial People’s Hospital, Guizhou, China
  • 3 Department of Immunology and Microbiology, Guiyang College of Traditional Chinese Medicine, Guiyang, Guizhou, China
  • 4 Department of Botany and Plant Sciences, University of California, Riverside, CA 92507, USA
  • 5 Department of Nephrology, Guizhou Provincial People's Hospital, Guizhou, China
  • 6 The Second Hospital of Wuhan Iron and Steel Group Corporation, Hubei, China
  • 7 Department of Respiratory and Critical Care Medicine, Guizhou Provincial People's Hospital, Guizhou, China
* Equal contribution

Received: April 21, 2020       Accepted: October 1, 2020       Published: November 21, 2020
How to Cite

Copyright: © 2020 Song et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.


Background: Novel Coronavirus disease 2019 (COVID-19) was first detected in pneumonia patients in Wuhan, China in December 2019. Based on the current understanding, COVID-19 has become a global issue. Presumably, numerous studies have found that SARS-CoV-2 also transpires in kidney tissue with permanent viral loads. However, it is elusive as to whether SARS-CoV-2 can directly damage the kidney or induce acute renal failure. Hence, to comprehensively understand the impact of COVID-19 on kidney damage, we conducted a retrospective series of case studies to assess kidney functions. Additionally, ACE2 distribution in kidney tissue was analyzed through RNAseq data in open-access databases.

Results: According to the findings from transcriptome analysis, we revealed higher ACE2 expression levels in females than males. Similar results were more noticeable in the elderly than in young adults. Furthermore, single-cell RNA sequencing data analysis showed high ACE2 expression in kidney tubule and collecting duct principal cells as well as glomerular parietal epithelial cells. On their admission, the patient's serum creatinine and blood urea nitrogen (BUN) were elevated to between 36.13% and 16.80%, respectively. The estimated glomerular filtration rate (EGFR) of < 60 ml/min per 1.73 m2 was reported in 10.92 % of the patients. Notably, at admission, increased BUN time varied linearly following the generalized additive mixed model. Thus, the hourly-increase of BUN in patients was 0.495 (95%CI: 0.263, 0.726).

Conclusion: Based on clinical findings, it was ascertained that COVID-19 can damage renal function, but it seldom causes acute renal failure. Coronavirus may directly bind to ACE2-positive cells and damage kidney tissue in the analysis of scRNA-seq data in kidney tissue. Therefore, this evidence suggests that kidney tissue act as the SARS-CoV-2 infection site and the findings could provide insight into the pathophysiology of kidney damage.

Methods: We systematically analyzed ACE2 expression profiles in organs based on open-access datasets for healthy individuals. Meanwhile, single-cell sequencing data for kidney samples were collected and analyzed. Assessments on kidney functions were conducted on 119 selected COVID-19 positive patients admitted from 10th February – 18th March 2020, in hospital in Wuhan City, Hubei Province. Consequently, their clinical records and laboratory findings, such as the estimated glomerular filtration rate (eGFR), Blood Urea Nitrogen (BUN), Creatinine, and Comorbidities, were collected.


ACE2: Angiotensin-converting enzyme 2; COVID-19: coronavirus disease 2019; SARS-CoV-2: severe acute respiratory syndrome coronavirus 2.