Hypotheses for the pathogenesis of acute kidney injury after COVID-19 vaccination. First, vaccination triggers the activation of antigen-presenting cells (APCs) and B cells. These cells then stimulate T cells through antigen presentation and cytokine production, which has an impact on the immune and complement systems. This process may result in the formation of a cellular inflammatory cytokine storm, dysregulation of neutrophil extracellular traps (NETs) and activation of the membrane attack complex (MAC). Besides, SARS-CoV-2 is capable of infecting renal tissue by utilizing angiotensin-converting enzyme 2 (ACE2), CD147 and glucose regulatory protein 78 (GRP78) in conjunction with furin-like cleavage on transmembrane protease serine 2 (TMPRESS2) and spike protein (S), damaging proximal tubular cells and podocytes. What’s more, the activation of platelets, endothelial cell damage and abnormal coagulation can be caused by an abnormal immune system or direct viral damage. AKI may also be attributed to infection or drug-induced rhabdomyolysis, underlying chronic or autoimmune disease, genetic predisposition and elevated levels of ANCA antibodies.