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Evidence for secondary thrombotic microangiopathy in COVID-19

Joseph M Sweeney1, Mohammad Barouqa2, Gregory J Krause3,4

  • 1Department Physiology and Biophysics. Albert Einstein College of Medicine, Bronx, NY.

Medrxiv : the Preprint Server for Health Sciences
|October 27, 2020
PubMed

Insights

COVID-19 can cause coagulopathy, resembling thrombotic microangiopathy (TMA). Lower ADAMTS13 activity and higher hemolysis markers predict poor outcomes in hospitalized patients.

Area of Science:

  • Hematology
  • Infectious Diseases
  • Critical Care Medicine

Background:

  • The mechanisms underlying coagulopathy in COVID-19 remain unclear.
  • Investigating endothelial activation, hemolysis, and coagulation markers is crucial for understanding disease severity and mortality.
  • COVID-19's impact on organ damage requires further elucidation.

Approach:

  • A retrospective study analyzed 181 hospitalized COVID-19 patients, balancing survivors and non-survivors.
  • Key markers assessed included ADAMTS13 activity, lactate dehydrogenase (LDH), schistocytes, and von Willebrand Factor (vWF).
  • Associations between these markers, disease severity, and mortality were examined.

Key Points:

  • Non-survivors exhibited significantly lower ADAMTS13 activity and higher LDH, schistocytes, and vWF levels compared to survivors.
  • Survival rates were markedly lower for patients with initial ADAMTS13 activity below 43% (30%) versus those with activity at or above 43% (60%).
  • Schistocytes on admission may indicate a need for thrombotic microangiopathy (TMA) work-up.

Conclusions:

  • COVID-19 can present as a TMA-like condition in a subset of hospitalized patients.
  • Findings highlight the potential link between endothelial dysfunction, coagulation activation, and COVID-19 severity.
  • Further research is warranted to explore TMA treatments' efficacy in COVID-19 patients.

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