Acute Kidney Injury Due to Collapsing Glomerulopathy Following COVID-19 Infection

INTRODUCTION A 46-year-old West African man presented to our hospital’s emergency room on March 15, 2020, with severe acute kidney injury. He reported that 2 to 3 weeks before his hospital presentation he had had subjective fever, myalgias, sore throat, and cough, which he had treated with multiple doses of ibuprofen. These complaints resolved 1 week before this hospital presentation, but he subsequently developed worsening abdominal pain, nausea, and anorexia that persisted for the following week, leading to his hospital presentation. He described lightheadedness when rising from a recumbent position. He reported decreased urine output but denied gross hematuria, frothy urine, or flank pain. He denied any new lower extremity edema or orthopnea, vomiting, diarrhea, change in mentation, persistent respiratory infectious symptoms, recent travel, or sick contacts. Other than his recent use of ibuprofen, he denied any other medication, vitamin supplementation, or herbal remedy. His medical history included obesity and obstructive sleep apnea for which he used nocturnal continuous positive airway pressure therapy. Baseline serum creatinine was 1.1 mg/dl (estimated glomerular filtration rate by Chronic Kidney Disease Epidemiology Collaboration equation, 93 ml/min per 1.73 m) on routine laboratory testing 16 months prior. He had no family history of kidney disease. He was born in Nigeria, worked as a nurse, lived with his wife and children in New York City, and did not use tobacco or illicit drugs. CASE PRESENTATION On initial presentation, vital signs were notable for blood pressure 144/100 mm Hg, heart rate 76 beats per minute, respiratory rate 16 breaths per minute, and SpO2 94% breathing ambient air while lying flat in bed. Body mass index was 44 kg/m. He had mild tenderness to palpation in the epigastrium and periumbilical region and trace lower extremity edema; the remainder of the examination was unremarkable. Laboratory tests were notable for severe acute kidney injury (presenting serum creatinine, 12.5 mg/dl) with nephrotic range proteinuria, hypoalbuminemia, elevated lactate dehydrogenase, and elevated inflammatory markers. Initial laboratory assessment and selected trends are shown in Table 1. Imaging studies included a chest X-ray showing mild pulmonary vascular congestion, a renal ultrasound with Doppler showing a 14.3 cm right kidney and 14.1 cm left kidney with bilaterally increased echogenicity and normal arterial and venous Doppler flow, a computed tomography scan of the abdomen and pelvis without iodinated contrast showing mild hepatic steatosis and normal-sized spleen, and a nuclear renal scan with dimercaptosuccinic acid showing equal perfusion to both kidneys without cortical defects. The patient was initially treated with several liters of isotonic fluid; however, his kidney function did not improve and he remained oliguric with orthopnea and persistent nausea. Therefore, a tunneled dialysis catheter was placed and he began intermittent hemodialysis on hospital day 4. Serologic screens were negative for HIV antibody, hepatitis C antibody, hepatitis B surface antigen and core antibody, anti-nuclear antibody, anti-