Thrombotic Microangiopathy Triggered by COVID-19: Case Reports
Julia Korotchaeva1, Natalia Chebotareva1, Elena Andreeva1
1Nephrology Sechenov First Moscow State Medical University, Moscow, Russian Federation.
Nephron
|November 22, 2021
Summary
Severe kidney injury in COVID-19 patients can stem from SARS-CoV-2-induced thrombotic microangiopathy (TMA). This condition involves abnormal complement activation and requires differentiating from disseminated intravascular coagulation.
Area of Science:
- Nephrology
- Hematology
- Immunology
Background:
- COVID-19, caused by SARS-CoV-2, is linked to thrombotic microangiopathy (TMA).
- TMA is a significant cause of acute kidney injury in COVID-19 patients.
- Complement pathway activation plays a key role in SARS-CoV-2-related TMA.
Observation:
- This study details three cases of severe kidney injury due to SARS-CoV-2-triggered TMA.
- Atypical hemolytic uremic syndrome was diagnosed in the absence of other causes, linked to aberrant complement activation.
- Elevated D-dimer levels and activated coagulation factors in COVID-19 necessitate careful distinction between TMA and disseminated intravascular coagulation.
Findings:
- SARS-CoV-2 infection can precipitate TMA through alternative and lectin complement pathway activation.
- Complement dysregulation is a critical mechanism underlying COVID-19-associated TMA and acute kidney injury.
- Distinguishing TMA from disseminated intravascular coagulation is essential due to overlapping clinical and laboratory findings.
Implications:
- Anticomplement therapies, such as eculizumab, may be beneficial for refractory COVID-19 cases with progressive TMA.
- Further controlled clinical trials are necessary to establish the efficacy of anticomplement agents in managing SARS-CoV-2-related TMA.
- Understanding the role of complement activation in COVID-19 pathogenesis can guide therapeutic strategies for kidney protection.
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