Patients with underlying health conditions or complicated chronic diseases are at a high risk of developing severe illnesses caused by coronavirus disease 2019 (COVID-19). Despite the recent development of novel antiviral drugs, a high proportion of patients still struggle with persistent health problems due to the post-COVID-19 syndrome. To reveal the impact of COVID-19 on people with disabilities and its contribution to causing disabilities, this chapter focuses on the pathogenesis of COVID-19-induced acute kidney injury (AKI) in chronic kidney disease (CKD) and that of post-COVID-19 syndrome, including pulmonary fibrosis and brain fog. In CKD, the kidney distribution of two proteins, angiotensin-converting enzyme 2 (ACE2) and transmembrane protease serine 2 (TMPRSS2), which aid in the entry of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) into cells and trigger the onset of a cytokine storm, is deeply associated with the development of COVID-19-induced AKI. In contrast, in post-COVID-19 pulmonary fibrosis or brain fog, in addition to leukocytes, such as lymphocytes and macrophages, mast cells are hyperactivated and contribute to enhanced immunological responses, leading to organ fibrosis or chronic neuroinflammation. Certain medications, including statins, nonsteroidal antiinflammatory drugs, antibiotics, and antihypertensive agents, are recognized for their ability to inhibit Kv1.3-channel activity and reduce the production of proinflammatory cytokines in leukocytes. Moreover, the latest generation of antihistamines, antibiotics, corticosteroids, and various food components effectively stabilize mast cells. The pharmacological characteristics of these medications or dietary components, along with the mechanisms underlying COVID-19-induced organ dysfunction or post-COVID-19 syndrome, offer opportunities for developing innovative therapeutic strategies by focusing on specific proteins and cellular targets.