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Of note, there are at least five other mechanisms besides secondary neuroinflammation by which COVID can affect the CNS (direct viral invasion of neural tissue, autoimmunity, reactivation of herpesviruses, neurovascular dysfunction, the sequelae of hypoxic, and other metabolic disturbances), which may occur exclusively or in combination in some individuals with varying frequency and timing (for review, see [88])

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These metabolites significantly differed between septic mice with and without signs of acute kidney injury (AKI), as defined by Kidney Disease Improving Global Outcomes (KDIGO), as creatinine levels tripled the average of sham mice