Pathophysiology and Pathology of Acute Kidney Injury in Patients With COVID-19.

Jia H Ng, Vanesa Bijol, Matthew A Sparks, Meghan E Sise, Hassane Izzedine, Kenar D Jhaveri

Journal: Advances in chronic kidney disease 2021;27(5):365-376

PMID: 33308501

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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.

Address: Division of Kidney Diseases and Hypertension, Donald and Barbara Zucker School of Medicine at Hofstra/Northwell, Northwell Health, Great Neck, NY. Electronic address: [email protected].; Department of Pathology, Donald and Barbara Zucker School of Medicine at Hofstra/Northwell, Northwell Health, Great Neck, NY.; Division of Nephrology, Department of Medicine, Duke University School of Medicine, Durham, NC; Renal Section, Durham Veterans Affairs Health Care System, Durham, NC.; Division of Nephrology, Department of Medicine, Massachusetts General Hospital, Boston, MA.; Department of Nephrology, Peupliers Private Hospital, Ramsay Générale de Santé, Paris, France.; Division of Kidney Diseases and Hypertension, Donald and Barbara Zucker School of Medicine at Hofstra/Northwell, Northwell Health, Great Neck, NY.

DOI: 10.1053/j.ackd.2020.09.003

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MeSH Terms: Acute Kidney Injury, Anti-Bacterial Agents, Antiviral Agents, Apolipoprotein L1, Ascorbic Acid, Azotemia, COVID-19, 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, COVID-19 Drug Treatment