ascorbic-acid and Thrombotic-Microangiopathies

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.

Topics: Acute Kidney Injury; Anti-Bacterial Agents; Antiviral Agents; Apolipoprotein L1; Ascorbic Acid; Azotemia; COVID-19; COVID-19 Drug Treatment; Cytokines; Disease Progression; Glomerulonephritis; Glomerulonephritis, Membranous; Hospital Mortality; Humans; Kidney Tubules, Proximal; Length of Stay; Myoglobin; Nephritis, Interstitial; Nephrosis, Lipoid; Renal Insufficiency, Chronic; Rhabdomyolysis; SARS-CoV-2; Severity of Illness Index; Thrombotic Microangiopathies; Vitamins