Targeting TLR-4 Signaling to Treat COVID-19-induced Acute Kidney Injury
Meaad A. Almazmomi1,2★, Mohammed Alsieni2★ Corresponding author
- 1Pharmaceutical Care Department, Ministry of National Guard—Health Affairs, Jeddah, Saudi Arabia.
- 2Pharmacology Department, Faculty of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia.
CORRESPONDENCE
Meaad A. Almazmomi
Pharmaceutical Care Department, Ministry of National Guard—Health Affairs, Jeddah 22384, Saudi Arabia.
ORCID: 0000-0001-7946-9239
Received: 27-09-2022; Accepted: 08-12-2022.
Volume 13, Issue 4 · pp. 316–329 · PUBLISHED 2022 · DOI: 10.1177/0976500X221147798
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ABSTRACT
The newly discovered severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) has turned into a potentially fatal pandemic illness. Numerous acute kidney injury (AKI) cases have been reported, although diffuse alveolar destruction and acute respiratory failure are the major symptoms of SARS-CoV-2 infection. The AKI, often known as a sudden loss of kidney function, carries a greater risk of mortality and morbidity. AKI was the second most frequent cause of death after acute respiratory distress syndrome (ARDS) in critically ill patients with coronavirus disease 2019 (COVID-19). While most patients with COVID-19 have moderate symptoms, some have severe symptoms, such as septic shock and ARDS. Also, it has been proven that some patients have severe symptoms, such as the failure of several organs. The kidneys are often affected either directly or indirectly. The major signs of kidney involvement are proteinuria and AKI. It is hypothesized that multiple mechanisms contribute to kidney injury in COVID-19. Direct infection of podocytes and proximal tubular cells in the kidneys may lead to acute tubular necrosis and collapsing glomerulopathy. SARS-CoV2 may also trigger a cascade of immunological responses that lead to AKI, including cytokine storm (CS), macrophage activation syndrome, and Toll-like receptor type-4 activation (TLR-4). Other proposed processes of AKI include interactions between organs, endothelial failure, hypercoagulability, rhabdomyolysis, and sepsis. Furthermore, ischemic damage to the kidney might result from the decreased oxygen supply. This article focuses on kidney injury's epidemiology, etiology, and pathophysiological processes. Specifically, it focuses on the CS and the role of TLR-4 in this process. To effectively manage and treat acute kidney damage and AKI in COVID-19, it is crucial to understand the underlying molecular pathways and pathophysiology.
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Almazmomi, M. A., & Alsieni, M. (2022). Targeting TLR-4 Signaling to Treat COVID-19-induced Acute Kidney Injury. Journal of Pharmacology and Pharmacotherapeutics, 13(4), 316–329. https://doi.org/10.1177/0976500X221147798