ABSTRACT
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is cause of a global pandemic which is demolishing global health and economy. SARS-CoV-2 infected patients are hospitalized with pneumonia where almost 20-30% of patients are led to kidney failure. The entry of SARS-CoV-2 into the systemic circulation leads to acute kidney injury (AKI) which may develop chronic kidney disease (CKD). In addition, patients who are diagnosed with AKI or CKD are at major risk of SARS-CoV-2 infection. Although a significant number of compounds have been proposed and the existing drugs have also been tested for repurposing, no specific therapy has been approved yet. SARS-CoV-2 invades human cells binding to the receptor of angiotensin-converting enzyme 2 (ACE2) via the receptor-binding domain. Cells that express ACE2 are susceptible to SARS-CoV-2 infection and the proportion of ACE2-positive cells in kidney proximal tubule is approximately 4%, indicating that SARS-CoV-2 might damage the kidney tubules leading to fatal kidney injury. Therefore, a better understanding of the potential mechanisms involved in SARS-CoV-2 infection-mediated kidney disease may unveil a novel therapeutic strategy against kidney diseases during COVID-19.
ABSTRACT
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is cause of a global pandemic which is demolishing global health and economy. SARS-CoV-2 infected patients are hospitalized with pneumonia where almost 20-30% of patients are led to kidney failure. The entry of SARS-CoV-2 into the systemic circulation leads to acute kidney injury (AKI) which may develop chronic kidney disease (CKD). In addition, patients who are diagnosed with AKI or CKD are at major risk of SARS-CoV-2 infection. Although a significant number of compounds have been proposed and the existing drugs have also been tested for repurposing, no specific therapy has been approved yet. SARS-CoV-2 invades human cells binding to the receptor of angiotensin-converting enzyme 2 (ACE2) via the receptor-binding domain. Cells that express ACE2 are susceptible to SARS-CoV-2 infection and the proportion of ACE2-positive cells in kidney proximal tubule is approximately 4%, indicating that SARS-CoV-2 might damage the kidney tubules leading to fatal kidney injury. Therefore, a better understanding of the potential mechanisms involved in SARS-CoV-2 infection-mediated kidney disease may unveil a novel therapeutic strategy against kidney diseases during COVID-19. © 2020, Bangladesh Society for Microbiology, Immunology and Advanced Biotechnology. All rights reserved.