ASN's Mission

ASN leads the fight to prevent, treat, and cure kidney diseases throughout the world by educating health professionals and scientists, advancing research and innovation, communicating new knowledge, and advocating for the highest quality care for patients.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005

email@asn-online.org

202-640-4660

The Latest on Twitter

Kidney Week

Abstract: PO0789

Thrombotic Microangiopathy (TMA) in a Patient with COVID-19

Session Information

Category: Trainee Case Report

  • 000 Coronavirus (COVID-19)

Authors

  • Flores Chang, Bessy Suyin, Donald and Barbara Zucker School of Medicine at Hofstra/Northwell, Hempstead, New York, United States
  • Parikh, Rushang, Donald and Barbara Zucker School of Medicine at Hofstra/Northwell, Hempstead, New York, United States
  • Wanchoo, Rimda, Donald and Barbara Zucker School of Medicine at Hofstra/Northwell, Hempstead, New York, United States
  • Bijol, Vanesa, Donald and Barbara Zucker School of Medicine at Hofstra/Northwell, Hempstead, New York, United States
  • Jhaveri, Kenar D., Donald and Barbara Zucker School of Medicine at Hofstra/Northwell, Hempstead, New York, United States
Introduction

We describe a patient with COVID-19 and clinically significant kidney biopsy proven TMA

Case Description

69-year-old Caucasian female with medical history of asthma came to the ED with productive cough, fever and dyspnea for 2 weeks. She was afebrile, tachypneic and hypoxic. Initial laboratories showed a normal WBC, hemoglobin level and platelet count. Inflammatory markers were elevated. SARS-CoV-2 infection was confirmed by PCR assay. CXR showed bilateral diffuse patchy opacities. Treated with hydroxychloroquine, enoxaparin and oxygen was started. Patient received anakinra and tocilizumab. On day 12, the patient developed thrombocytopenia, anemia and worsening kidney function concerning for microangiopathic hemolytic anemia. Due to worsening hypoxemia, patient received convalescent plasma. On day 17, she was intubated due to worsening respiratory failure. Findings suggestive of hemolysis were present. Urinalysis showed hematuria and proteinuria. Patient’s kidney function worsened requiring initiation of CRRT. On day 20, the patient underwent a kidney biopsy that revealed severe acute TMA with cortical necrosis. Beta 2 glycoprotein-1 IgM levels were elevated, anti-phospholipid antibodies were absent. A disintegrin and ADAMTS13 level were not low. C3,C4 were in normal range. Heparin induced antibody testing was negative. Coagulation parameters were normal. Kidney doppler was unremarkable. No other systemic findings of macro thrombi were found. Low factor H complement antigen, elevated plasma CBb complement and plasma SC5b-9 complement levels suggesting an activation of the alternative complement pathway were found. Genetic testing was not done. Plasma exchange was not performed, but received a single dose of eculizumab on day 21. Unfortunately, she died on day 23.

Discussion

Coagulopathy associated with SARS-CoV-2 has been widely reported. Profound hypoxia, inflammation, disseminated intravascular coagulation(DIC) have all been implicated as potential causes, but were not present in our patient. To the best of our knowledge, we report the first case of TMA associated with SARS-CoV-2 with presence of diffuse cortical necrosis and widespread microthrombi in kidney biopsy. It is not clear if the virus played a direct pathogenic role or unmasked a latent complement defect leading to widespread endothelial damage and micro thrombi