• Adrian Post, Edwin S G den Deurwaarder, BakkerStephan J LSJLDepartment of Internal Medicine, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands., Robbert J de Haas, Matijs van Meurs, Ron T Gansevoort, and Stefan P Berger.
• Department of Internal Medicine, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands. Electronic address: a.post01@umcg.nl.
• Am. J. Kidney Dis. 2020 Sep 1; 76 (3): 431-435.

AbstractCoronavirus disease 2019 (COVID-19) is a contagious life-threatening infection caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Recent findings indicate an increased risk for acute kidney injury during COVID-19 infection. The pathophysiologic mechanisms leading to acute kidney injury in COVID-19 infection are unclear but may include direct cytopathic effects of the virus on kidney tubular and endothelial cells, indirect damage caused by virus-induced cytokine release, and kidney hypoperfusion due to a restrictive fluid strategy. In this report of 2 cases, we propose an additional pathophysiologic mechanism. We describe 2 cases in which patients with COVID-19 infection developed a decrease in kidney function due to kidney infarction. These patients did not have atrial fibrillation. One of these patients was treated with therapeutic doses of low-molecular-weight heparin, after which no further deterioration in kidney function was observed. Our findings implicate that the differential diagnosis of acute kidney injury in COVID-19-infected patients should include kidney infarction, which may have important preventive and therapeutic implications.Copyright © 2020 The Authors. Published by Elsevier Inc. All rights reserved.

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