No Evidence for Classic Thrombotic Microangiopathy in COVID-19.
Tanja FalterHeidi RossmannPhilipp MengeJan GoetjeSteffen GroenwoldtArndt WeinmannVisvakanth SivanathanAndreas SchulzNiels A W LemmermannSven DanckwardtKarl J LacknerPeter Robert GalleInge ScharrerBernhard LämmleMartin Franz SprinzlPublished in: Journal of clinical medicine (2021)
DIC occurred in 7/65 COVID-19 patients but fibrinogen and platelet consumption were compensated in almost all. ADAMTS13 assays excluded TTP and hallmarks of classic TMA were absent in all investigated patients. We hypothesize that the lacking erythrocyte fragmentation and only mild platelet consumption in severe COVID-19 are due to a microangiopathy predominantly localized to the alveolar microcirculation with a low blood pressure gradient.