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Author: Saad Alharbi, Khalid; Al-Abbasi, Fahad A; Prasad Agrawal, Gopal; Sharma, Ajay; Kowti, Rajesh; Kazmi, Imran
Title: Impact of COVID-19 on Nephrology Patients: A Mechanistic Outlook for Pathogenesis of Acute Kidney Injury.
  • Cord-id: 43d3rcvj
  • Document date: 2020_7_15
  • ID: 43d3rcvj
    Snippet: Context Some research has indicated that SARS-CoV-2 has had effects on the various functions of the renal system. Acute kidney injury (AKI) is a dangerous and broadly spread pathological illness. Objective In this review, we emphasize that AKI can be a severe complication of COVID-19 and highlight the importance of assessing, defining, and reporting the course of AKI. Design The research team performed a literature review, searching relevant literature databases. We searched four databases, PubM
    Document: Context Some research has indicated that SARS-CoV-2 has had effects on the various functions of the renal system. Acute kidney injury (AKI) is a dangerous and broadly spread pathological illness. Objective In this review, we emphasize that AKI can be a severe complication of COVID-19 and highlight the importance of assessing, defining, and reporting the course of AKI. Design The research team performed a literature review, searching relevant literature databases. We searched four databases, PubMed, EMBASE, Web of Science and CNKI (Chinese Database), to identify studies reporting COVID-19. Articles published on or before May 10, 2020 were eligible for inclusion. We used the following search terms: "Coronavirus" or "2019-nCoV" or "COVID-19" or "AKI" or "renal failure" or "nephrology". Setting This study was take place at Jouf University, Sakaka, Al-Jouf, Saudi Arabia. Results The review showed that AKI patients, who were susceptible to a cytokine storm, showed clinical deterioration. This result allowed the current research team to develop a hypothesis of a set of adverse events in COVID-19 that proposes the modification of inflammatory pathways by stimulation of nAChRα7. The stimulation could occur by way of IL-6 / JAK2 / STAT3 / SOCS3 and NF-κB (p65)/IL-18, which work together to induce AKI and increase overall renal-related diagnostic markers, such as plasma creatinine and tubular cell damage. In addition, the functioning of the cholinergic anti-inflammatory pathway may be determined by nicotine. Pharmacological nicotine products are widely available, and their role in COVID-19-mediated AKI can be further evaluated. Conclusions The research team concluded that the dysregulation of the cholinergic anti-inflammatory system could explain most of the clinical features of severe COVID-19.

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