Coronavirus disease of 2019 (COVID-19) is a disease caused by the novel coronavirus SARS-CoV-2, which is characterized by a multitude of clinical abnormalities, including hypercoagulability. Although thrombosis is commonly observed in sepsis, the hypercoagulable state associated with COVID-19 is much more dramatic and may not be related to either the severity of the disease or the D-dimer levels. It may be due to a prothrombotic state induced by the disease itself. We report three cases of arterial thrombosis with a significant clot burden requiring urgent medical and surgical intervention. It is now a common practice to initiate anticoagulation for deep venous thrombosis (DVT) prophylaxis based on the D-dimer level in hospitalized patients with COVID-19. However, in our clinical experience, D-dimer levels did not correlate well with the clot burden or the risk for future thrombosis.

A 30-year-old male presented with severe, warm autoimmune hemolysis 17 months subsequent to a matched, unrelated peripheral hematopoietic stem cell transplant. The patient responded poorly to conventional therapy with steroids and immunoglobulin, prompting the initiation of rituximab. On account of persistent, severe hemolysis, therapeutic plasma exchange was employed as a bridge until the rituximab therapy became effective. Immediately following plasmapheresis, the patient demonstrated clinical improvement followed by attenuation of the hemolysis and improved reticulocytosis. The hemoglobin concentration and reticulocyte index demonstrated further improvement following subsequent doses of rituximab and continued following the cessation of plasmapheresis. This case suggests the utility of plasmapheresis and rituximab in severe, life-threatening cases of warm autoimmune hemolytic anemia refractory to conventional therapy.

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Acute kidney injury (AKI) has been seen in patients hospitalized with a SARS-CoV-2 (COVID-19) infection, but the pathophysiology of glomerular injury is not yet fully understood. We present a case of COVID-19related "glomerular endotheliosis" in which a 51-year-old female with a 13-year history of class IV lupus nephritis was admitted for COVID-19 pneumonia. Her lupus nephritis had been in complete renal remission for the past 10 years with a baseline serum creatinine level of 1.3 mg/dL and no proteinuria. Her serological workup, including complement levels, was unremarkable. Due to the worsening renal function and persistent proteinuria, she underwent a kidney biopsy that revealed diffuse glomerular endothelial cell swelling, also known as glomerular endotheliosis. Her clinical course unfortunately deteriorated and she succumbed to acute respiratory distress syndrome. As circulating anti-angiogenic factors may contribute to the pathogenesis of endothelial dysfunction leading to glomerular endotheliosis, we propose that a similar circulating antiangiogenic factor may have been triggered by COVID-19 and played a role in our patient's progressive renal failure.