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      Subclinical Acute Kidney Injury in COVID-19 Patients: A Retrospective Cohort Study

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          Dear Editor, We read with great interest the recent article “COVID-19 Infection in a Patient with End-Stage Kidney Disease” by Fu et al. [1]. Previous studies have reported that ∼10% of infected patients may develop acute kidney injury (AKI), which is a strong prognostic factor increasing risk of death [2, 3, 4]. We agree with the authors that SARS-CoV2 affects the kidney function and special care of renal function should be taken into account in COVID-19 patients. However, the current definition of AKI does not provide a measurement of loss of kidney function because serum creatinine level is not a sensitive marker of early tubular injury (elevation of serum creatinine requires damage/dysfunction of >50% of the nephron mass), whereas biomarkers of tubular injury provide information on early kidney injury and response to noxious stimuli [5]. All COVID-19 infection patients without a prior history of chronic kidney disease included in our study (n = 32) were consecutively admitted to our hospital in February, who were confirmed, classified as 3 subtypes (common, severe, and critical), and discharged from our hospital based on the guidelines for the diagnosis and treatment of novel coronavirus disease (version 6) [6]. Most of these patients had mean levels of estimated glomerular filtration rate (eGFR) within the normal range, whereas 31.3% (n = 10) had proteinuria, 9.4% (n = 3) had macroalbuminuria, and 12.5% (n = 4) had microalbuminuria (Table 1). The proportion of patients with increased urinary levels of β2-microglobulin (β2MG), α1-microglobulin (α1MG), retinol binding protein (RBP), and N-acetyl-β-d-glucosaminidase (NAG) levels were 20, 20, 10, and 10%, respectively. On the first day of hospital admission, there were no significant differences in mean levels of serum creatinine, blood urea nitrogen, and eGFR among the common, severe, and critical subtypes. However, the proportion of albuminuria as well as the levels of urinary β2MG-creatinine ratio, α1MG-creatinine ratio, RBP-creatinine ratio, and NAG-creatinine ratio significantly increased according to the severity of disease. During the hospital stay, the proportion of proteinuria (dipstick >1+) in critically ill COVID-19 patients was significantly higher than that observed in common COVID-19 patients on the first check and gradually improved during the patients' hospital admission (Fig. 1). No significant differences were observed in the mean levels of eGFR both on the first day of admission and during the hospital stay amongst the 3 patient subtypes. Furthermore, Kaplan-Meier survival curves showed that patients with elevated urinary β2MG and α1MG levels had significantly lower rates of hospital discharge compared to those with normal urinary β2MG and α1MG levels. In conclusion, we suggest that COVID-19 infection may induce early development of abnormal albuminuria and impair kidney tubular function. Because SARS-CoV-2 has been isolated from urinary samples of an infected patient and the receptor of this virus is the angiotensin converting enzyme II which is expressed on podocytes and proximal straight tubule cells [4, 7]. Notably, podocytes and proximal straight tubule cells are particularly vulnerable to viral attacks, and our findings suggested that the excretion of these urinary biomarkers may be related to the severity of the infection. Therefore, more careful medical surveillance of urinary biomarkers of early AKI is required in COVID-19-infected patients because early detection and treatment can slow or prevent progression of kidney disease. Disclosure Statement The authors have no conflicts of interest to declare. Funding Sources This work was supported by grants from the National Natural Science Foundation of China (81500665), High Level Creative Talents from Department of Public Health in Zhejiang Province and Project of New Century 551 Talent Nurturing in Wenzhou. G.T. is supported in part by grants from the School of Medicine, University of Verona, Verona, Italy. C.D.B. is supported in part by the Southampton NIHR Biomedical Research Centre (IS-BRC-20004), UK. Author Contributions Dan-Qin Sun and Ming-Hua Zheng conceived and designed the study; Ting-Yao Wang and Yong-Ping Chen collected the data; Dan-Qin Sun and Ting-Yao Wang analyzed and interpreted the data; Dan-Qin Sun and Kenneth I. Zheng drafted the manuscript; Giovanni Targher and Christopher D. Byrne reviewed and edited the manuscript. All authors contributed to the manuscript for important intellectual content and approved the submission.

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          COVID-19 Infection in a Patient with End-Stage Kidney Disease

          Since December 2019, the epidemic of coronavirus disease 2019 (COVID-19) has spread very rapidly in China and worldwide. In this article, we report on a 75-year-old man infected with 2019 novel coronavirus who has end-stage kidney disease (ESKD). COVID-19 patients with ESKD need isolation dialysis, but most of them cannot be handled in time due to limited continuous renal replacement therapy (CRRT) machines. CRRT provided benefits for this patient by removing potentially damaging toxins and stabilizing his metabolic and hemodynamic status. With the control of uremia and fluid status, this patient ended up with an uneventful post-CRRT course, absence of clinical symptoms, and negative PCR tests. Greater efforts are needed to decrease the mortality of COVID-19-infected ESKD patients.
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            Potential risk of the kidney vulnerable to novel coronavirus 2019 infection

            to the editor: In December 2019, an outbreak of acute respiratory illness, since named coronavirus disease 2019 (COVID-19) by the World Health Organization, emerged in Wuhan, Hubei, China. As of March 28, 2020, there had been 512,701 confirmed cases and 23,495 deaths documented globally (12a). COVID-19 has become a global health threat. Through the efforts of experts and scientists all over the world, our understanding of COVID-19 has grown considerably. Researchers performed deep sequencing analysis from lower respiratory tract samples and identified a novel coronavirus that has since been named novel coronavirus 2019 [2019-nCoV; now severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)]. It has been confirmed as the cause of COVID-19 (14). This is the third epidemic caused by a coronavirus in the 21st century, after SARS (caused by SARS-CoV) and Middle East respiratory syndrome (MERS). Studies have shown that both 2019-nCoV and SARS-CoV shared the same cell entry receptor, angiotensin-converting enzyme 2 (ACE2) (5, 13). In this way, ACE2 expression patterns in different organs, tissues, and cell types could uncover the potential risk to 2019-nCoV infection. ACE2 is expressed in humans in the epithelia of the lung, small intestine, heart, liver, and kidney (8). In autopsy samples obtained from patients with SARS, immunohistochemical examination revealed SARS-CoV virions, RNA, and antigen in the lung and other organs, including the kidney (4). One in vitro study (11) established that SARS-CoV with proximal tubular epithelial cells showed persistent and productive infection, which was partly correlated with ACE2 expression. Using state-of-art single cell techniques, Zou et al. (15) stratified organs into high and low risk according to the expression level of ACE2. In their analysis, the kidney should be listed as high risk. These findings indicate the possibility of 2019-nCoV infection of kidney cells. Clinical manifestations of COVID-19 in parts of China have been recently reported (1, 6, 12). In accordance with ACE2 expression in organs, besides respiratory symptoms, nonrespiratory symptoms such as fatigue, myalgia, and diarrhea have also been reported. Acute kidney injury (AKI) has been reported as one of the complications that occur during the progression of COVID-19 in both patients comorbid with kidney disease and those who are not (6, 12). One study (12) of 138 patients with COVID-19 reported that ~4% of patients with COVID-19 had AKI (12). Huang et al. (6) reported on 41 patients with COVID-19, among whom 10% had elevated creatinine (>133 μmol/L) on admission and 7% had AKI. Laboratory tests showed that the level of blood urea and creatine increased progressively in the progression of COVID-19. The incidence of AKI in patients with COVID-19 is similar to that found in patients with SARS; one retrospective analysis showed 6% of patients SARS to have AKI (2). In an analysis of 536 patients with SARS, 6.7% developed acute renal impairment, and the involvement of the kidney in SARS cases has been associated with a high (91.7%) mortality rate (3). Similarly, patients with COVID-19 who received care in intensive care units were more likely to have AKI than patients that did not receive care in intensive care units (12). All these findings indicate that AKI could be one of the risk factors for mortality in patients with COVID-19. The pathophysiological mechanisms of AKI could be multifactorial, including direct infection with 2019-nCoV, immune and inflammatory responses induced by viral infection, and systemic toxic reaction resulting from respiratory failure. These mechanisms may be closely associated with death in severe cases of COVID-19. Since the routes of transmission have contributed greatly to the rapid spread of 2019-nCoV, this reminds us that urine samples should be tested to exclude a potential alternative route of transmission except respiratory droplets and direct contact (7, 10). Special care of renal function should be taken into account when treating patients with COVID-19. Such information calls for patient care regarding renal function of patients currently under emergency and potential postcure treatment for kidney recovery. We suggest that epidemiological studies should analyze kidney impairment and its characteristics in 2019-nCoV. This work might shed light on further investigations of the pathogenesis, route of 2019-nCoV infection, and production of effective antiviral agents and vaccines. GRANTS This work was supported by Hunan Provincial People’s Hospital RENSHU Funding Project RS201801. DISCLOSURES No conflicts of interest, financial or otherwise, are declared by the author(s). AUTHOR CONTRIBUTIONS F.Z. drafted manuscript; Y. L. edited and revised manuscript, F.Z. and Y. L. approved final version of manuscript.
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              Molecular nephrology: types of acute tubular injury


                Author and article information

                Nephron Clin Pract
                Nephron Clin Pract
                Nephron. Clinical Practice
                S. Karger AG (Allschwilerstrasse 10, P.O. Box · Postfach · Case postale, CH–4009, Basel, Switzerland · Schweiz · Suisse, Phone: +41 61 306 11 11, Fax: +41 61 306 12 34, )
                26 May 2020
                : 1-4
                [1 ] aDepartment of Nephrology, The Affiliated Wuxi No. 2 People's Hospital of Nanjing Medical University, Wuxi, China
                [2 ] bDepartment of Nephrology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China
                [3 ] cNAFLD Research Center, Department of Hepatology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China
                [4 ] dSection of Endocrinology, Diabetes and Metabolism, Department of Medicine, University and Azienda Ospedaliera Universitaria Integrata of Verona, Verona, Italy
                [5 ] eSouthampton National Institute for Health Research Biomedical Research Centre, University Hospital Southampton, Southampton General Hospital, Southampton, United Kingdom
                [6 ] fInstitute of Hepatology, Wenzhou Medical University, Wenzhou, China
                [7 ] gKey Laboratory of Diagnosis and Treatment for The Development of Chronic Liver Disease in Zhejiang Province, Wenzhou, China
                Author notes
                *Dr. Ming-Hua Zheng, NAFLD Research Center, Department of Hepatology, The First Affiliated Hospital of Wenzhou Medical University, No. 2 Fuxue Lane, Wenzhou 325000 (China), zhengmh@

                Dan-Qin Sun and Ting-Yao Wang are co-first authors.

                Copyright © 2020 by S. Karger AG, Basel

                This article is made available via the PMC Open Access Subset for unrestricted re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the COVID-19 pandemic or until permissions are revoked in writing. Upon expiration of these permissions, PMC is granted a perpetual license to make this article available via PMC and Europe PMC, consistent with existing copyright protections.

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                Figures: 1, Tables: 1, References: 7, Pages: 4
                Clinical Practice: Letter to the Editor


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