Renal complications in coronavirus disease 2019: a systematic review
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(2020) 40:31
`R E V I E W
Inflammation and Regeneration
Open Access
Renal complications in coronavirus disease 2019: a systematic review Taichiro Minami1,2*, Yasunori Iwata2 and Takashi Wada2
Abstract The world today is facing a pandemic caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), which mainly causes a respiratory disease known as coronavirus disease 2019 (COVID-19). Therefore, its pathogenesis and complications should be identified and understood. SARS-CoV-2 infects the host using the angiotensin-converting enzyme 2 (ACE2) as its receptor, which is expressed in several organs including the lungs, heart, kidneys, and intestines. Kidney complications are relatively common, and acute kidney injury (AKI) is a lifethreatening complication in patients with COVID-19. In this review, the renal histological patterns of COVID-19 are described in detail, and its potential mechanisms associated with AKI are discussed. Keywords: COVID-19, Renal complication, AKI
Background In the late 2019, a novel coronavirus (severe acute respiratory syndrome coronavirus 2 [SARS-CoV-2]) was identified as the cause of a cluster of pneumonia cases in Wuhan, China. This outbreak has led to a worldwide pandemic within a short period of time, and as of June 21, 2020, there are more than 8.7 million confirmed cases with 460,000 deaths in 216 countries, areas, or territories according to the World Health Organization. Although lung infection and acute respiratory failure are the main characteristics of coronavirus disease 2019 (COVID-19), other organs such as the heart, small intestines, and kidneys are also reportedly involved. Acute kidney injury (AKI) is defined as increased serum creatinine level (by 0.3 mg/dL within 48 h or > 1.5 times from its baseline level) or decreased urine output (< 0.5 mL/kg/h for 6 h) according to the Kidney Disease Improving Global Outcomes guideline. AKI is one of the important complications of COVID-19, occurring in 0.5–7% of cases and in 2.9–23% of intensive care unit (ICU) patients [1–3]. A single-center prospective cohort study of 701 * Correspondence: [email protected] 1 Renal Division, Department of Medicine, Brigham and Women’s Hospital, 4 Blackfan Street, Boston, MA, USA 2 Department of Nephrology and Laboratory Medicine, Kanazawa University, Kanazawa, Ishikawa, Japan
inpatients with COVID-19 in China reported that 43.9% of patients had proteinuria and 26.7% had hematuria on admission and 5.1% developed AKI during hospitalization [4]. An Italian study involving > 2000 inpatients with COVID-19 reported the AKI incidence of 27.8% [5]. When compared with the AKI occurrence in severe acute respiratory syndrome (SARS), no significant difference was observed in the incidence, peak creatinine levels, and histological findings (Table 1). Understanding the COVID-19 pathogenesis is evolving. This review focuses on the potential AKI mechanism in COVID-19, especially the direct viral cytotoxicity to kidney host cells. Pathological features of kidney diseases in COVID-19
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