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      Acute Kidney Injury in the 2019 Novel Coronavirus Disease

      , , *

      Kidney Diseases

      S. Karger AG

      2019 novel coronavirus disease, COVID-19, Acute kidney injury

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          Abstract

          Background: The 2019 novel coronavirus disease (CO­VID-19) is a newly defined serious infectious disease caused by the SARS-CoV-2 virus. The epidemic started in Wuhan, China, in December of 2019 and quickly spread to over 200 countries. It has affected 4,258,666 people, with 294,190 deaths worldwide by May 15, 2020. COVID-19 is characterized by acute respiratory disease, with 80% of patients presenting mild like flu-like symptoms; however, 20% of patients may have a severe or critical clinical presentation, which likely causes multiple organ injuries (e.g., kidney, heart, blood, and nervous system). Among them, acute kidney injury (AKI) is a critical complication due to its high incidence and mortality rate. Here we present a review of the current understanding of AKI in COVID-19. Summary: CO­VID-19 is a catastrophic contagious disease caused by the coronavirus, and the AKI induced by COVID-19 significantly increases the mortality rate. In this review, we summarize the clinical characteristics of COVID-19 induced AKI by focusing on its epidemiology, pathogenesis, clinical diagnosis, and treatment. Key Messages: Multiple studies have shown that COVID-19 may involve the kidneys and cause AKI. This article reviews the characteristics of COVID-19-induced AKI largely based on up-to-date studies in the hope that it will be helpful in the current global fight against and treatment of COVID-19.

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          Most cited references 13

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          Angiotensin-converting enzyme 2, angiotensin-(1-7) and Mas: new players of the renin-angiotensin system.

          Angiotensin (Ang)-(1-7) is now recognized as a biologically active component of the renin-angiotensin system (RAS). Ang-(1-7) appears to play a central role in the RAS because it exerts a vast array of actions, many of them opposite to those attributed to the main effector peptide of the RAS, Ang II. The discovery of the Ang-converting enzyme (ACE) homolog ACE2 brought to light an important metabolic pathway responsible for Ang-(1-7) synthesis. This enzyme can form Ang-(1-7) from Ang II or less efficiently through hydrolysis of Ang I to Ang-(1-9) with subsequent Ang-(1-7) formation by ACE. In addition, it is now well established that the G protein-coupled receptor Mas is a functional binding site for Ang-(1-7). Thus, the axis formed by ACE2/Ang-(1-7)/Mas appears to represent an endogenous counterregulatory pathway within the RAS, the actions of which are in opposition to the vasoconstrictor/proliferative arm of the RAS consisting of ACE, Ang II, and AT(1) receptor. In this brief review, we will discuss recent findings related to the biological role of the ACE2/Ang-(1-7)/Mas arm in the cardiovascular and renal systems, as well as in metabolism. In addition, we will highlight the potential interactions of Ang-(1-7) and Mas with AT(1) and AT(2) receptors.
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            Kidney disease: improving global outcomes (KDIGO) acute kidney injury work group KDIGO clinical practice guideline for acute kidney injury

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              In-vitro renal epithelial cell infection reveals a viral kidney tropism as a potential mechanism for acute renal failure during Middle East Respiratory Syndrome (MERS) Coronavirus infection

              Background The Middle East Respiratory Syndrome Coronavirus (MERS-CoV) causes symptoms similar to Severe Acute Respiratory Syndrome Coronavirus (SARS-CoV), yet involving an additional component of acute renal failure (ARF) according to several published case reports. Impairment of the kidney is not typically seen in Coronavirus infections. The role of kidney infection in MERS is not understood. Findings A systematic review of communicated and peer-reviewed case reports revealed differences in descriptions of kidney involvement in MERS versus SARS patients. In particular, ARF in MERS patients occurred considerably earlier after a median time to onset of 11 days (SD ±2,0 days) as opposed to 20 days for SARS, according to the literature. In-situ histological staining of the respective cellular receptors for MERS- and SARS-Coronavirus showed highly similar staining patterns with a focus of a receptor-specific signal in kidney epithelial cells. Comparative infection experiments with SARS- and MERS-CoV in primary human kidney cells versus primary human bronchial epithelial cells showed cytopathogenic infection only in kidney cells, and only if infected with MERS-CoV. Kidney epithelial cells produced almost 1000-fold more infectious MERS-CoV progeny than bronchial epithelial cells, while only a small difference was seen between cell types when infected with SARS-CoV. Conclusion Epidemiological studies should analyze kidney impairment and its characteristics in MERS-CoV. Virus replication in the kidney with potential shedding in urine might constitute a way of transmission, and could explain untraceable transmission chains leading to new cases. Individual patients might benefit from early induction of renoprotective treatment.
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                Author and article information

                Journal
                KDD
                KDD
                10.1159/issn.2296-9357
                Kidney Diseases
                S. Karger AG
                2296-9381
                2296-9357
                2020
                September 2020
                18 June 2020
                : 6
                : 5
                : 318-323
                Affiliations
                Institute of Nephrology, Zhong Da Hospital, Southeast University School of Medicine, Nanjing, China
                Author notes
                *Bi-Cheng Liu, Institute of Nephrology, Zhong Da Hospital, Southeast University School of Medicine, Dingjiaqiao Rd. 87, Nanjing, Jiangsu 210009 (China), liubc64@163.com
                Article
                509086 PMC7360511 Kidney Dis 2020;6:318–323
                10.1159/000509086
                PMC7360511
                32742978
                © 2020 The Author(s) Published by S. Karger AG, Basel

                This article is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License (CC BY-NC-ND). Usage and distribution for commercial purposes as well as any distribution of modified material requires written permission. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                Page count
                Pages: 6
                Categories
                Review Article

                Cardiovascular Medicine, Nephrology

                COVID-19, 2019 novel coronavirus disease, Acute kidney injury

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