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      Collapsing Glomerulopathy Affecting Native and Transplant Kidneys in Individuals with COVID-19

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          Abstract

          Since the emergency of novel coronavirus COVID-19 (SARS-CoV-2) in December 2019, infections have spread rapidly across the world. The reported incidence of acute kidney injury (AKI) in the context of COVID-19 is variable, and its mechanism is not well understood. Data are emerging about possible mechanisms of AKI including virus-induced cytopathic effect and cytokine storm-induced injury. To date, there have been few reports of kidney biopsy findings in the context of AKI in COVID-19 infection. This article describes 2 cases of collapsing glomerulopathy, 1 in a native kidney and, for the first time, 1 in a kidney transplant. Both individuals were black, and both presented without significant respiratory compromise. Indeed, the 2 patients we describe remained systemically well for the majority of their inpatient stay, which would support the hypothesis that for these patients, AKI was caused by a cytopathic viral effect, rather than that of a cytokine storm or acute tubular necrosis caused by prolonged hypovolaemia or the effect of medication known to exacerbate AKI. Here, we report 2 cases of AKI with collapsing glomerulopathy in COVID-19, one of which is in a kidney transplant recipient, not previously described elsewhere.

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          Collapsing glomerulopathy.

          Collapsing glomerulopathy (CG) has become an important cause of ESRD. First delineated from other proteinuric glomerular lesions in the 1980s, CG is now recognized as a common, distinct pattern of proliferative parenchymal injury that portends a rapid loss of renal function and poor responses to empiric therapy. Notwithstanding, the rise in disorders that are associated with CG, the identification of the first susceptibility genes for CG, the remarkable increase in murine modeling of CG, and promising preclinical testing of new therapeutic strategies suggest that the outlook for CG as a poorly understood and therapeutically resistant renal disease is set to change in the future. This focused review highlights recent advances in research into the pathogenesis and treatment of CG.
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            Renin-angiotensin system at the heart of COVID-19 pandemic

            Significant aspects of COVID-19 pandemic remain obscure. Angiotensin converting enzyme 2 (ACE2), a component of the renin-angiotensin system, whose expression dominates on lung alveolar epithelial cells, is the human cell receptor of SARS-CoV-2, the causative agent of COVID-19. We strongly encourage the concept that thorough considerations of receptor-ligand interactions should be kept at the heart of scientific debate on infection. In this idea, the whole renin-angiotensin system has to be evaluated. We hypothesize that factors related to ethnicity, environment, behaviors, associated illness, and medications involving this complex system are probably responsible for situations regarded as anomalous from both an epidemiological and a clinical point of view, but, taken together, such factors may explain most of the aspects of current outbreak. We decided to use the analogy of a play and speculate about the possible impact in this tragedy of 1) air pollution via the interference of nitrogen dioxide on ACE2 expression; 2) the dual role of nicotine; 3) the hypothetical involvement of ACE2 polymorphisms, the relationships of which with ethnic factors and susceptibility to cardiovascular disease seems intriguing; 4) the impact on the severity of infection of hypertension and related medications acting on the renin/angiotensin system, and, finally, 5) the possible helpful role of chloroquine, thanks to its capacity of modifying ACE2 affinity to the viral spike protein by altering glycosylation. This hypothesis paper is an urgent call for the development of research programs that aim at questioning whether the putative protagonists of this tragedy are real-life actors in COVID-19.
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              Is Open Access

              Genetic associations between genes in the renin-angiotensin-aldosterone system and renal disease: a systematic review and meta-analysis

              Background Chronic kidney disease (CKD) is defined by abnormalities in kidney structure and/or function present for more than 3 months. Worldwide, both the incidence and prevalence rates of CKD are increasing. The renin-angiotensin-aldosterone system (RAAS) regulates fluid and electrolyte balance through the kidney. RAAS activation is associated with hypertension, which is directly implicated in causation and progression of CKD. RAAS blockade, using drugs targeting individual RAAS mediators and receptors, has proven to be renoprotective. Objectives To assess genomic variants present within RAAS genes, ACE, ACE2, AGT, AGTR1, AGTR2 and REN, for association with CKD. Design and data sources A systematic review and meta-analysis of observational research was performed to evaluate the RAAS gene polymorphisms in CKD using both PubMed and Web of Science databases with publication date between the inception of each database and 31 December 2018. Eligible articles included case–control studies of a defined kidney disease and included genotype counts. Eligibility criteria Any paper was removed from the analysis if it was not written in English or Spanish, was a non-human study, was a paediatric study, was not a case–control study, did not have a renal disease phenotype, did not include data for the genes, was a gene expression-based study or had a pharmaceutical drug focus. Results A total of 3531 studies were identified, 114 of which met the inclusion criteria. Genetic variants reported in at least three independent publications for populations with the same ethnicity were determined and quantitative analyses performed. Three variants returned significant results in populations with different ethnicities at p<0.05: ACE insertion, AGT rs699-T allele and AGTR1 rs5186-A allele; each variant was associated with a reduced risk of CKD development. Conclusions Further biological pathway and functional analyses of the RAAS gene polymorphisms will help define how variation in components of the RAAS pathway contributes to CKD.
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                Author and article information

                Journal
                NEF
                Nephron
                10.1159/issn.1660-8151
                Nephron
                S. Karger AG
                1660-8151
                2235-3186
                07 September 2020
                :
                :
                : 1-6
                Affiliations
                aNottingham Renal and Transplant Unit, Nottingham University Hospitals NHS Trust, Nottingham, United Kingdom
                bHistopathology Department, Nottingham City Hospital, Nottingham University Hospitals NHS Trust, Nottingham, United Kingdom
                Author notes
                *Mark Jesky, Nottingham Renal and Transplant Unit, Nottingham University Hospitals, Hucknall Road, Nottingham NG5 1PB (UK), mark.jesky@nuh.nhs.uk
                Article
                509938 Nephron
                10.1159/000509938
                32894838
                © 2020 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. 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
                Figures: 1, Tables: 2, Pages: 6
                Product
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/509938
                Self URI (journal page): https://www.karger.com/Tap/Home/278492
                Categories
                Clinical Practice: Case Report

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