Acute tubular injury (AKI) develops in up to 37% of hospitalized patients with COVID-19 and its pathophysiology has not been fully elucidated. In recent kidney biopsy and postmortem series, the most common pathology in patients with COVID-19 is ATI, but various pathologies have been described. 1-4 We report clinicopathologic characteristics and outcomes of 13 patients with COVID-19 with kidney injury and proteinuria. Methods are in Item S1; demographics and clinical characteristics are in Table S1. Twelve of the patients were men, median age was 52 years, 9 were Black, 2 were Hispanic, and 2 were White. All but 1 patient had 1 or more comorbid conditions, most commonly hypertension (85%), diabetes (46%), and obesity (54%). Twelve patients presented with pulmonary symptoms, 11 of whom had COVID-19 pneumonia diagnosed. Most had hypoxic respiratory failure and required supplemental oxygen (1 needed intubation). One patient presented with COVID-19 Guillain-Barré–like syndrome without pneumonia.

Patients presented with AKI on or during admission, superimposed on chronic kidney disease in 44%. Kidney injury was severe (peak serum creatinine level [Scr]> 3 mg/dL) in all patients except 1; 10 (77%) required dialysis during admission. Median peak and admission Scr were 8.9 and 3.9 mg/dL, respectively. One or more potential contributing factors to AKI, aside from pneumonia, were present in 6, including ARB or ACE inhibitor use in 5, vomiting in 2, and NSAID use in 1. All patients had proteinuria (median protein excretion, 5.5 g/d), including 11 (85%) with nephrotic-range proteinuria (NRP). Hypoalbuminemia was present in 75%, edema in 15%, nephrotic syndrome (NS) in 8%, and microhematuria in 77%.