IntroductionAlthough as of today, the hypothesis of bradykinin storm in COVID-19 cannot be directly confirmed, many theoretical assumptions and empirical data support its validity.AimThe purpose of this article is, using the example of a clinical case, to draw attention to the need for further study of the pathogenesis and clinical manifestations of COVID-19 and post-COVID-19 syndrome, considering the assessment of various theories, including bradykinin storm hypothesis.Case studyWe analysed the data from a young male patient with post-COVID-19 syndrome who referred to a consultant and expressed complaints of palpitation, blood pressure increase, muscle weakness, feeling of fear, hypochondria, sleep disturbances, and reduced working performance.Results and discussionWe found a high degree of autonomic dysregulation (predominantly sympathetic hyperactivation), anxiety, and sleep disorder. There was no hypertension, though ambulatory blood pressure monitoring allowed to determine the status of non-dipper. Patient's blood tests after COVID-19 revealed a decrease in the plasma level of aldosterone, a significant increase in both homocysteine blood level and free cortisol in urine, and mild transient isolated increase in free triiodothyronine. All abnormal blood test parameters turned to normal in 3 months after the onset of COVID-19. We assume that the clinical symptoms and changes in a number of laboratory parameters of the presented case may be associated with the effects of bradykinin storm.ConclusionsThis clinical case suggests continuing the discussion about the potential role of bradykinin storm in the clinical course of COVID-19 and post-COVID-19 syndrome.