Acute Abdominal Pain in a COVID-19 Patient

Discussion

What began as a series of cases of viral pneumonia initially described in Wuhan, Hubei, China, rapidly spread to emerge as a global pandemic. The virus was identified as SARS-CoV-2 and is the cause of coronavirus disease 2019 (COVID-19). Kidney injury has been associated with this infection, although the exact mechanism of injury remains unclear. Increased severity of illness has been associated with the development of coagulopathy (1). Laboratory abnormalities including leukopenia, lymphopenia, elevated prothrombin time, and d-dimer have been found in patients who are critically ill (2). A case series from Wuhan described patients with COVD-19 testing positive for anti-cardiolipin IgA and anti–β₂-glycoprotein I IgA and IgG antibodies (3). Although not specific to this infection, it is hypothesized to be associated with the development of both micro- and macrovascular thrombi. A small study observed a mortality benefit in patients with severe sepsis receiving anticoagulation with low mol wt heparin (low mol wt heparin 40% versus controls 64%) (4). These preliminary data have led international societies to recommend anticoagulation in patients who are critically ill and infected with SARS-CoV-2.

Literature has described both microvascular and macrovascular coagulopathy to be associated with severe COVID-19 infection (1); however, abnormal coagulation with the development of clots has not been described in patients with relatively mild disease. Whereas venous thromboembolism and pulmonary embolism have been reported (5), no reports of renal artery thrombosis or renal infarction have been described. Our patient with relatively mild COVID-19 had derangements in coagulation markers and had a renal artery thrombus with renal infarction. Further studies are warranted to evaluate whether renal infarctions are playing a role in the AKI and whether prophylactic anticoagulation could have benefit in renal outcomes.