Case Presentation: A 67 year-old woman presented with acute cough, fever, and hypoxia. SARS-CoV2 testing was positive, and she was treated with dexamethasone and remdesivir. Over the next two days, her serum creatinine increased from 0.6 to 3.0 mg/dL, platelet count decreased from 281 to 48 k/L, and hemoglobin decreased from 13.1 to 11.3 g/dL. She had serum LDH of 2300 U/L, undetectable haptoglobin, and elevated indirect bilirubin. Peripheral smear demonstrated frequent schistocytes. ADAMTS13 activity was within normal limits. The patient’s renal failure progressed and she was initiated on hemodialysis on hospital day 5 with creatinine of 7.1 mg/dL and uremia. Urgent renal biopsy was performed and pathology showed acute thrombotic microangiopathy (TMA) and glomerular immune deposition with IgM kappa. Plasma exchange was initiated for TMA. Her renal function improved, and she was discharged off of hemodialysis. Serum creatinine returned to baseline 3 weeks after initial presentation.

Discussion: Acute kidney injury, anemia, and thrombocytopenia are common findings in patients hospitalized with COVID-19. However, in this case, the simultaneous acute development of these abnormalities lead to consideration of microangiopathic hemolytic anemia (MAHA) and an intriguing differential diagnosis. MAHA can generally be identified by the presence of schistocytes on a peripheral blood smear in a patient with hemolytic anemia and acute thrombocytopenia. TMA describes a subset of MAHA with microvasculature thrombosis and endothelial abnormalities on pathology. In this setting, there should be immediate consideration of thrombotic thrombocytopenic purpura (TTP) given the importance of early initiation of therapy. The PLASMIC score can be used to estimate the probability of TTP, which was low in this patient. Other primary TMA syndromes include drug-induced TMA, hemolytic uremic syndrome (HUS) due to shiga toxin, and atypical HUS.In this case, severe acute renal failure due to TMA developed in a patient with COVID-19. The TMA may have been directly due to COVID-19 (secondary HUS) or due to unmasking of a complement pathway mutation (aHUS). Genetic testing has not yet been performed. To our knowledge, this is the first reported case of renal failure due to newly diagnosed TMA in a patient with COVID-19 who survived to hospital discharge. One published case describes renal failure due to TMA in a critically ill patient with COVID-19 who died soon after diagnosis, and another describes relapse of known aHUS in the setting of COVID-19. While clinically significant TMA is rarely reported in the setting of COVID-19, there is evidence of pathologic complement activation in COVID-19. In fact, the complement inhibitor eculizumab, which is used in treatment of aHUS, has been successfully used in severe COVID-19 without TMA. Our patient did not receive eculizumab due to limited data supporting use in the setting of COVID-19 at the time.

Conclusions: In this report, we describe a case of acute renal failure due to biopsy-proven TMA in the setting of COVID-19. The rapid development of acute kidney injury and severe thrombocytopenia in this patient prompted further evaluation for MAHA, leading to the unifying diagnosis. She was treated with plasma exchange and temporary hemodialysis, with complete recovery of her renal function within weeks. Hospitalists should consider this rare, but treatable, condition in patients with COVID-19 who develop thrombocytopenia and acute kidney injury.