Kallikrein-kinin blockade in patients with covid-19 to prevent acute respiratory distress syndrome

Frank L. van de Veerdonk, Mihai G. Netea, Marcel van Deuren, Jos W.M. van der Meer, Quirijn de Mast, Roger J. Brüggemann, Hans van der Hoeven

Onderzoeksoutput: Bijdrage aan tijdschriftArtikelpeer review

209 Citaten (Scopus)


COVID-19 patients can present with pulmonary edema early in disease. We propose that the this is due to a local vascular problem because of activation of bradykinin 1 receptor (B1R) and B2R on endothelial cells in the lungs. SARS-CoV-2 enters the cell via ACE2 that next to its role in RAS is needed to inactivate des-Arg9 bradykinin, the potent ligand of the bradykinin receptor type 1 (B1). Without ACE2 acting as a guardian to inactivate the ligands of B1, the lung environment is prone for local vascular leakage leading to angioedema. Here we hypothesize that a bradykinin-dependent local lung angioedema via B1 and B2 receptors is an important feature of COVID-19. We propose that blocking the B2 receptor and inhibiting kallikrein activity might have an ameliorating effect on early disease caused by COVID-19 and might prevent acute respiratory distress syndrome (ARDS). In addition, this pathway might indirectly be responsive to anti-inflammatory agents.

Originele taal-2Engels
StatusGepubliceerd - 2020
Extern gepubliceerdJa


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