Acute kidney injury (AKI) is common among hospitalized patients with Coronavirus Infectious Disease 2019 (COVID-19), with the occurrence of AKI ranging from 0.5% to 80%. The variability in the occurrence of AKI has been attributed to the difference in geographic locations, race/ethnicity, and severity of illness. AKI among hospitalized patients is associated with increased length of stay and in-hospital deaths. Even patients with AKI who survive to hospital discharge are at risk of developing chronic kidney disease or end-stage kidney disease. An improved knowledge of the pathophysiology of AKI in COVID-19 is crucial to mitigate and manage AKI and to improve the survival of patients who developed AKI during COVID-19. The goal of this article is to provide our current understanding of the etiology and the pathophysiology of AKI in the setting of COVID-19.
Acute kidney injury (AKI) has been reported to be a common complication among hospitalized patients with Coronavirus Disease 2019 (COVID-19), with the occurrence of AKI ranging from 0.5% to 80%.1, 2, 3, 4, 5 The understanding of the pathophysiology of AKI in the setting of COVID-19 is rapidly evolving; review of the current literature has demonstrated several etiologies: (1) prerenal azotemia, (2) proximal tubular injury, (3) glomerulopathy, (4) thrombotic microangiopathy, and (5) complications from the treatment of COVID-19. The pathogenesis of kidney injury in patients infected with severe acute respiratory virus-2.
Reference link- https://www.ackdjournal.org/article/S1548-5595(20)30150-6/fulltext
