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Saudi Journal of Kidney Diseases and Transplantation
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Year : 2020  |  Volume : 31  |  Issue : 6  |  Page : 1456-1457
Coronavirus disease 2019: Implications of severe acute respiratory syndrome coronavirus 2 in acute kidney injury

1 Mylan Pharmaceutical Company, Riyadh, Saudi Arabia
2 GlaxoSmithKline (GSK) Pharmaceutical Company, Riyadh, Saudi Arabia

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Date of Web Publication29-Jan-2021

How to cite this article:
Alenazi AA, AlDkhil LM. Coronavirus disease 2019: Implications of severe acute respiratory syndrome coronavirus 2 in acute kidney injury. Saudi J Kidney Dis Transpl 2020;31:1456-7

How to cite this URL:
Alenazi AA, AlDkhil LM. Coronavirus disease 2019: Implications of severe acute respiratory syndrome coronavirus 2 in acute kidney injury. Saudi J Kidney Dis Transpl [serial online] 2020 [cited 2021 Jun 25];31:1456-7. Available from: https://www.sjkdt.org/text.asp?2020/31/6/1456/308374

To the Editor,

On New Year’s Eve 2019, the Chinese health authorities, yet again almost after two decades, reported an outbreak of a new type of viral pneumonia on December 31, 2019. Later, it was confirmed as coronavirus (CoV) outbreak; however, this time with severe acute respiratory syndrome CoV 2 (SARS-CoV-2), the pathogenic viral organism of coronavirus disease 2019 (COVID-19). The organism supposedly originated from wildlife animal (bats) in the southern China seafood wholesale market in Wuhan city of Hubei Province, China, which resulted in the immediate closure of the market. With rapidly growing numbersin China and global spillover thereafter, the World Health Organization (WHO) declared COVID-19 as Public Health Emergency of International Concern on 30 January 30, 2020. As of June 22, 2020 WHO Situation Report, 8,860,331 confirmed cases and 465,740 deaths have been documented worldwide.[1],[2]

Undeniably, SARS-CoV-2 can cause multi-organ damage. Recent research studies have reported acute kidney injury (AKI) in COVID-19 patients, one of the vital organ systems. A relevant preprint of the study documented 23% incidence of AKI in COVID-19 subjects. Interestingly, the authors found acute tubular necrosis with infiltration of macrophages and lymphocytes upon histological examination of six of the deceased COVID-19 patients.[3]

Besides acute tubular necrosis, another paper mentioned hemosiderin deposits, peritubular accumulation of erythrocytes, glomerular deposits of fibrin thrombi, endothelial injury, rhabdomyolysis-related pigment casts, and inflammation. Particularly, the study also underlined the likelihood of subclinical kidney damage, given the fact that few of the COVID-19 subjects showed no clinical proof of AKI such as deranged serum creatinine and/or blood urea nitrogen.[4] Hypercoagulable state secondary to COVID-19 infection has also been confirmed in scientific literature and can precipitate acute tubular necrosis and, consequently, permanent kidney injury.[5] Activation of pro-coagulation process by SARS-CoV-2 can trigger complement system which can injure the kidney and is associated with poor clinical outcomes, supported by a study of Diao et al.[3] The SARS-CoV-2 enters host cells through angiotensin-converting enzyme 2 receptors which is abundantly expressed by kidneys in podocytes and proximal tubule. This might explain the direct kidney injury (podo-cytopathy and microangiopathy) by SARS-CoV-2 and might account for collapsing glomerulopathy and proteinuria described earlierin COVID-19 confirmed cases.[6],[7] It is of particular interest to note that nucleocapsid of SARS-CoV-2 and even nucleocapsid related inclusion bodies in cytoplasm have been evidenced in kidney tubules, a characteristic feature that has been previously discovered with other virus-driven kidney microstructural insult.[3]

In a nutshell, these findings strongly suggest the indirect and direct antagonistic role of SARS-CoV-2 in the pathophysiological development of AKI. It has perhaps implications in renal medicine; however, clear cut assumptions regarding pathogenesis and specific treatment strategy would be unsuitable at this point in time. Therefore, research studies directed at comprehensive appraisal of the clinical characteristics, including genomics, of the COVID-19 patients with renal disease manifestations would be of great importance and, if appropriately designed, could help in determining novel findings and interventions.

Conflict of interest: None declared.

   References Top

He F, Deng Y, Li W. Coronavirus disease 2019 (COVID-19): What we know? J Med Virol 2020;97:719-25.  Back to cited text no. 1
Coronavirus disease (COVID-19) Situation Report – 154. 2020. https://www.who.int/docs/default-source/coronaviruse/situation-reports/20200622-covid-19-sitrep-154.pdf?sfvrsn=d0249d8d_2. [Last accessed 2020 Jun 23].  Back to cited text no. 2
Diao B, Wang C, Wang R, et al. Human kidney is a target for novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. medRxiv 2020.  Back to cited text no. 3
Su H, Yang M, Wan C, et al. Renal histopathological analysis of 26 postmortem findings of patients with COVID-19 in China. Kidney Int 2020;98:219-27.  Back to cited text no. 4
Tang N, Li D, Wang X, Ziyong S. Abnormal coagulation parameters are associated with poor prognosis in patients with novel coronavirus pneumonia. J Thromb Haemost 2020;18:844-7.  Back to cited text no. 5
Cheng Y, Luo R, Wang K, et al. Kidney disease is associated with in-hospital death of patients with COVID-19. Kidney Int 2020;97:829-38.  Back to cited text no. 6
Larsen C, Bourne TD, Wilson JD, Sagga O, Sharshir MA. Collapsing glomerulopathy in a patient with COVID-19. Kidney Int Rep 2020; 5:935-9.  Back to cited text no. 7

Correspondence Address:
Abeer Ageel Alenazi
Mylan Pharmaceutical Company, Riyadh
Saudi Arabia
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DOI: 10.4103/1319-2442.308374

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