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Objective: The triad of obesity, a high-protein diet from animal sources, and disturbed gut microbiota have been linked to poor clinical outcomes in patients with COVID-19. In this report, the effect of oxidative stress resulting from the Na + /K + -ATPase transporter signaling cascade is explored as a driver of this poor clinical outcome., Methods: Protein-protein interactions with the SARS-CoV-2 proteome were identified from the interactome data for Na + /K + -transporting ATPase subunit α-1 (ATP1A1), epidermal growth factor receptor, and ERB-B2 receptor tyrosine kinase 2, using the curated data from the BioGRID Database of Protein Interactions. Data for the gene expression pattern of inflammatory response were from the Gene Expression Omnibus database for cardiomyocytes post SARS-CoV-2 infection (number GSE151879)., Results: The ATP1A1 subunit of the Na + /K + -ATPase transporter is targeted by multiple SARS-CoV-2 proteins. Furthermore, receptor proteins associated with inflammatory response, including epidermal growth factor receptor and ERB-B2 receptor tyrosine kinase 2 (which interact with ATP1A1), are also targeted by some SARS-CoV-2 proteins. This heightened interaction likely triggers a cytokine release that increases the severity of the viral infection in individuals with obesity., Conclusions: The similarities between the effects of SARS-CoV-2 proteins and indoxyl sulphate on the Na + /K + -ATPase transporter signaling cascade suggest the possibility of an augmentation of gene changes seen with COVID-19 infection that can result in a hyperinduction of cytokine release in individuals with obesity., (© 2022 The Obesity Society.)

Viral infections in the immunocompetent host can cause both acute and chronic kidney disease either as a direct damage to the infected kidney cells or as a consequence of systemic immune responses that impact kidney function. Since identifying these entities in the 1970s and 80s, major breakthroughs in the understanding of the viral mechanisms have occurred. Viruses have evolved mechanisms to hijack signaling pathways of infected cells to evade antiviral immune responses by the host. Over time, the clinical presentations and management of these diseases have evolved along with our in-depth understanding of the various pathophysiological mechanisms causing these conditions. Similarly, both at the cellular and systemic levels, the host has evolved mechanisms to counter viral subversion strategies for mutual survival. Since the start of the current COVID-19 pandemic, numerous cases of acute kidney injury have been reported in the literature with various possible pathophysiological mechanisms. In this review, we summarize lessons learned from prior viral pandemics related to viral mechanisms utilized in the pathogenesis of numerous renal manifestations to attempt to utilize this knowledge in predicting post-COVID-19 kidney disease. [ABSTRACT FROM AUTHOR]