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. 2021 Mar 9;5(1):e89–e103. doi: 10.1055/s-0041-1723784

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The Author(s). This is an open access article published by Thieme under the terms of the Creative Commons Attribution License, permitting unrestricted use, distribution, and reproduction so long as the original work is properly cited. ( https://creativecommons.org/licenses/by/4.0/ )

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Fig. 4 — Unique COVID-19 microangiopathy. ( A ) Normal endothelium. ( B ) SARS-CoV-2 enters the endothelial cells of capillaries via the ACE2R. Injured endothelial cells release HMW multimers of VWF which unfold in shear forces of the microvasculature. HMW multimers recruit platelets to the wounded endothelium. Unfolded HMW multimers consume circulating ADAMTS13 activity, allowing for increased platelet binding to uncleaved HMW multimers downstream. In turn, activated platelets aggregate activating coagulation and forming microvascular thrombi. In high shear stress, schistocytes are formed as a result of RBC shearing while forced through small vessels with thrombi. High D-dimers result from plasmin degradation of microthrombi. ACE2R, ACE2 receptor; ADAMTS13, a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13; COVID-19, coronavirus disease 2019; SARS-CoV-2, severe acute respiratory syndrome coronavirus 2. HMW, high molecular weight; VWF, von Willebrand factor.