Introduction:
Although as of today, the hypothesis of bradykinin storm in COVID-19 cannot be directly confirmed, many theoretical assumptions and empirical data support its validity.

Aim:
The 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 study:
We 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 discussion:
We 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.

Conclusions:
This 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.