Thrombotic Microangiopathy Following COVID-19 Infection

Introduction: The relationship between COVID-19 infection and the activation of a wide spectrum of pro-inflammatory and pro-thrombotic mechanisms such as antiphospholipid syndrome (APS) and Thrombotic Microangiopathy (TMA) is not yet well understood. However, there is emerging evidence on the link between COVID-19 and TMA. Here, we report a case of a biopsy-proven chronic TMA following COVID-19 infection. Case Description: A 48-year-old Hispanic female with a past medical history of diabetes, and hypothyroidism, who was recently discharged from the hospital following a COVID-19 infection (complicated by ICU admission requiring intubation about a month ago), presented with severe abdominal pain. No prior history of miscarriage in the past;the patient has two kids with uneventful pregnancies. Denies any family history of autoimmune disease. Initial workups indicated that splenic and renal infarcts concerning primary antiphospholipid syndrome were further supported by positive serological testing confirming the presence of positive Antineutrophil antibody, Cardiolipin antibody, B2glycoprotein, and Lupus anticoagulant. In addition, the urinalysis showed active urinary sediment with dysmorphic RBCs and nephrotic range proteinuria. The patient had a kidney biopsy which was consistent with chronic TMA and was initiated on anticoagulation therapy with warfarin for antiphospholipid antibody syndrome. Discussion: The possibility of occurrence of TMA following COVID-19 infection and the possible association between markers of endothelial activation, intravascular hemolysis, coagulation and organ damage in infection should be considered. This understanding is clinically relevant as it may necessitate the need for early APS antibody and TMA panel testing and initiation of anticoagulation in the amplified hypercoagulable state in COVID-19, especially in preventing life-threatening thrombosis.