Abstract

Both SARS-CoV-2 infection and COVID-19 vaccination have been associated with renal complications. In the context of SARS-CoV-2 infection, kidney injury is primarily attributed to a complex interplay of systemic immune dysregulation and vascular damage. Severe infection triggers a cytokine-mediated inflammatory response characterized by elevated levels of pro-inflammatory mediators, resulting in systemic hemodynamic instability, increased capillary permeability, and renal hypoperfusion, ultimately leading to acute tubular injury. In addition, virus-induced endothelial activation promotes a prothrombotic state, microvascular injury, and further impairment of renal perfusion. Collectively, these processes converge to produce acute kidney injury (AKI) and, in severe or prolonged cases, may contribute to chronic tubulointerstitial damage and progressive renal dysfunction. In contrast, renal manifestations following COVID-19 vaccination are relatively uncommon and are thought to arise primarily from immune-mediated dysregulation rather than direct cytopathic effects. Reported cases include minimal change disease, IgA nephropathy, focal segmental glomerulosclerosis (FSGS), acute interstitial nephritis and other glomerulopathies, which present as either new-onset disease or relapses. These lesions are thought to result from transient immune activation following vaccination, including T-cell stimulation and altered humoral responses, which may trigger or unmask an underlying susceptibility to renal injury. Careful post-vaccination monitoring in high-risk populations may be warranted, and further molecular and population-level studies are needed to elucidate the underlying mechanisms and refine risk assessment.

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