ABSTRACT
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.
Subject(s)
Acute Kidney Injury/metabolism , COVID-19/metabolism , Cytokines/metabolism , Glomerulonephritis/metabolism , Thrombotic Microangiopathies/metabolism , Acute Kidney Injury/etiology , Acute Kidney Injury/pathology , Acute Kidney Injury/physiopathology , Anti-Bacterial Agents/adverse effects , Antiviral Agents/adverse effects , Apolipoprotein L1/genetics , Ascorbic Acid/adverse effects , Azotemia/metabolism , Azotemia/pathology , Azotemia/physiopathology , COVID-19/pathology , COVID-19/physiopathology , Disease Progression , Glomerulonephritis/pathology , Glomerulonephritis/physiopathology , Glomerulonephritis, Membranous/metabolism , Glomerulonephritis, Membranous/pathology , Glomerulonephritis, Membranous/physiopathology , Hospital Mortality , Humans , Kidney Tubules, Proximal/injuries , Length of Stay , Myoglobin/metabolism , Nephritis, Interstitial/metabolism , Nephritis, Interstitial/pathology , Nephritis, Interstitial/physiopathology , Nephrosis, Lipoid/metabolism , Nephrosis, Lipoid/pathology , Nephrosis, Lipoid/physiopathology , Renal Insufficiency, Chronic , Rhabdomyolysis/metabolism , SARS-CoV-2 , Severity of Illness Index , Thrombotic Microangiopathies/pathology , Thrombotic Microangiopathies/physiopathology , Vitamins/adverse effects , COVID-19 Drug TreatmentABSTRACT
In a stunningly short period of time, the unexpected coronavirus disease 2019 (COVID-19) pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has turned the unprepared world topsy-turvy. Although the rapidity with which the virus struck was indeed overwhelming, scientists throughout the world have been up to the task of deciphering the mechanisms by which SARS-CoV-2 induces the multisystem and multiorgan inflammatory responses that, collectively, contribute to the high mortality rate in affected individuals. In this issue of the JCI, Skendros and Mitsios et al. is one such team who report that the complement system plays a substantial role in creating the hyperinflammation and thrombotic microangiopathy that appear to contribute to the severity of COVID-19. In support of the hypothesis that the complement system along with neutrophils and platelets contributes to COVID-19, the authors present empirical evidence showing that treatment with the complement inhibitor compstatin Cp40 inhibited the expression of tissue factor in neutrophils. These results confirm that the complement axis plays a critical role and suggest that targeted therapy using complement inhibitors is a potential therapeutic option to treat COVID-19-induced inflammation.