Organ Working Group Organs Lesion Modifier(S)

Total Page:16

File Type:pdf, Size:1020Kb

Organ Working Group Organs Lesion Modifier(S) Nomenclature file from goRENI, version 3.15 as of 18-Dec-2019 Organ Working Group Organs Lesion Modifier(s) Synonym/other term Status Respiratory System Nasal cavity Cleft palate Published Respiratory System Nasal cavity Deviation, nasal septum Modified after publication Respiratory System Nasal cavity Perforation, septum Modified after publication Respiratory System Nasal cavity Atrophy Published Respiratory System Nasal cavity Degeneration Published Respiratory System Nasal cavity Eosinophilic globules Hyaline droplets; Modified Eosinophilic inclusions; after Hyaline droplet publication accumulation Respiratory System Nasal cavity Corpora amylacea Published Respiratory System Nasal cavity Amyloid Published Respiratory System Nasal cavity Necrosis Published Respiratory System Nasal cavity Erosion/ulcer Modified after publication Respiratory System Nasal cavity Regeneration Published Respiratory System Nasal cavity Inflammation Acute; Chronic; Chronic Rhinitis Modified active; Granulomatous; after Lymphocytic or eosinophilic publication Organ Working Group Organs Lesion Modifier(s) Synonym/other term Status Respiratory System Nasal cavity; Paranasal Infiltrate Type of inflammatory cell Infiltration; Infiltrate Added after sinus; Nasopharynx; Larynx; that represents the inflammatory cell; Cell publication Trachea; Bronchi; Lung: predominant cell type in the infiltration Bronchioles; Lung: Terminal infiltrate: Lymphocyte; bronchioles; Lung: Alveoli; Plasma cell; Mast cell; Pleura Monocyte/macrophage; Mononuclear; Neutrophil; Eosinophil; Basophil; Mixed Respiratory System Nasal cavity Congestion Hyperemia Published Respiratory System Nasal cavity Edema Published Respiratory System Nasal cavity Hemorrhage Published Respiratory System Nasal cavity Angiectasis Published Respiratory System Nasal cavity Thrombus Modified after publication Respiratory System Nasal cavity; Paranasal Metaplasia, squamous cell Published sinus; Nasopharynx Respiratory System Nasal cavity Metaplasia, respiratory, Published olfactory/glandular epithelium Respiratory System Nasal cavity Hyperplasia, squamous cell Published Respiratory System Nasal cavity Hyperplasia, transitional Published epithelium Respiratory System Nasal cavity; Paranasal Hyperplasia, respiratory Published sinus; Nasopharynx epithelium Respiratory System Nasal cavity; Paranasal Hyperplasia/metaplasia, Hyperplasia, goblet cell; Published sinus; Nasopharynx mucous cell Metaplasia, mucous cell; Metaplasia, goblet cell Organ Working Group Organs Lesion Modifier(s) Synonym/other term Status Respiratory System Nasal cavity Hyperplasia, olfactory Published epithelium Respiratory System Nasal cavity; Paranasal Hyperplasia, basal cell Published sinus; Nasopharynx Respiratory System Nasal cavity; Paranasal Hyperplasia, Published sinus; Nasopharynx neuroendocrine cell Respiratory System Nasal cavity; Paranasal Hyperplasia, atypical Modified sinus; Nasopharynx after publication Respiratory System Nasal cavity; Paranasal Papilloma, squamous cell Published sinus; Nasopharynx Respiratory System Nasal cavity; Paranasal Adenoma Published sinus; Nasopharynx Respiratory System Nasal cavity; Paranasal Carcinoma, squamous cell Published sinus; Nasopharynx Respiratory System Nasal cavity; Paranasal Carcinoma, adenosquamous Published sinus; Nasopharynx Respiratory System Nasal cavity; Paranasal Adenocarcinoma Published sinus; Nasopharynx Respiratory System Nasal cavity; Paranasal Carcinoma, neuroepithelial Neuroepithelioma, Published sinus; Nasopharynx olfactory; Neuroblastoma, olfactory; Esthesioneuroblastoma; Carcinoma, olfactory Respiratory System Larynx; Trachea; Bronchi; Degeneration Published Lung: Bronchioles Respiratory System Larynx; Trachea; Bronchi; Necrosis Published Lung: Bronchioles Respiratory System Larynx; Trachea; Bronchi; Erosion/ulcer Modified Lung: Bronchioles after publication Organ Working Group Organs Lesion Modifier(s) Synonym/other term Status Respiratory System Larynx; Trachea; Bronchi Ectasia, submucosal gland Modified after publication Respiratory System Larynx; Trachea; Bronchi; Regeneration Published Lung: Bronchioles Respiratory System Larynx; Trachea; Bronchi; Inflammation Acute; Granulomatous; Laryngitis; Tracheitis; Modified Lung: Bronchioles Chronic; Chronic active Bronchitis after publication Respiratory System Larynx; Trachea; Bronchi; Bronchiectasis Published Lung: Bronchioles Respiratory System Larynx Epithelial alteration Published Respiratory System Larynx; Trachea; Bronchi; Metaplasia, squamous cell Published Lung: Bronchioles Respiratory System Larynx; Trachea; Bronchi; Hyperplasia, squamous cell Published Lung: Bronchioles Respiratory System Larynx; Trachea; Bronchi; Hyperplasia, respiratory Modified Lung: Bronchioles epithelium after publication Respiratory System Larynx; Trachea; Bronchi; Hyperplasia, mucous cell Metaplasia, mucous cell; Published Lung: Bronchioles Metaplasia/hyperplasia, goblet cell Respiratory System Larynx; Trachea; Bronchi; Hyperplasia, Hyperplasia, pulmonary Published Lung: Bronchioles neuroendocrine cell neuroendocrine cell (PNEC) Respiratory System Larynx; Trachea; Bronchi; Hyperplasia, atypical Modified Lung: Bronchioles after publication Respiratory System Larynx; Trachea; Bronchi; Papilloma Published Lung: Bronchioles Organ Working Group Organs Lesion Modifier(s) Synonym/other term Status Respiratory System Larynx; Trachea; Bronchi; Tumor, neuroendocrine cell, Papilloma, neuroendocrine; Published Lung: Bronchioles benign Papilloma, pulmonary neuroendocrine cells (PNEC) Respiratory System Larynx; Trachea; Bronchi; Carcinoma, squamous cell Carcinoma, epidermoid Published Lung: Bronchioles Respiratory System Larynx; Trachea; Bronchi; Adenocarcinoma Published Lung: Bronchioles Respiratory System Larynx; Trachea; Bronchi; Tumor, neuroendocrine cell, Carcinoma, clear cell; Published Lung: Bronchioles malignant Carcinoma, neuroendocrine Respiratory System Lung: Terminal bronchioles; Cyst, congenital Modified Lung: Alveoli; Pleura after publication Respiratory System Lung: Terminal bronchioles; Hypoplasia Modified Lung: Alveoli after publication Respiratory System Lung: Terminal bronchioles; Degeneration Modified Lung: Alveoli after publication Respiratory System Lung: Terminal bronchioles; Necrosis Modified Lung: Alveoli after publication Respiratory System Lung: Terminal bronchioles; Regeneration Published Lung: Alveoli Respiratory System Lung: Terminal bronchioles; Macrophages, increased Alveolar histiocytosis; Modified Lung: Alveoli Alveolar phospholipidosis after publication Organ Working Group Organs Lesion Modifier(s) Synonym/other term Status Respiratory System Lung: Terminal bronchioles; Alveolar lipoproteinosis Published Lung: Alveoli Respiratory System Lung: Terminal bronchioles; Pigment/foreign material Modified Lung: Alveoli; Pleura after publication Respiratory System Lung: Terminal bronchioles; Inflammation Acute alveolar/interstitial; Bronchiolitis; Pneumonitis; Modified Lung: Alveoli; Pleura Chronic interstitial; Acute Pneumonia; Pleuritis after bronchioloalveolar; Chronic publication bronchioloalveolar; Granulomatous Respiratory System Lung: Terminal bronchioles; Fibrosis Modified Lung: Alveoli; Pleura after publication Respiratory System Pleura Pyothorax Suppurative pleuritis; Published Pleurisy Respiratory System Lung: Alveoli Ectasia, acinus Modified after publication Respiratory System Lung: Alveoli Alveolar emphysema Published Respiratory System Lung: Terminal bronchioles; Atelectasis Published Lung: Alveoli Respiratory System Lung: Terminal bronchioles; Hemorrhage Modified Lung: Alveoli; Pleura after publication Respiratory System Lung: Terminal bronchioles; Congestion Modified Lung: Alveoli after publication Organ Working Group Organs Lesion Modifier(s) Synonym/other term Status Respiratory System Lung: Terminal bronchioles; Edema Modified Lung: Alveoli after publication Respiratory System Lung: Terminal bronchioles; Embolus Modified Lung: Alveoli after publication Respiratory System Lung: Terminal bronchioles; Hypertrophy, media, artery Modified Lung: Alveoli after publication Respiratory System Lung: Terminal bronchioles; Mineralization Published Lung: Alveoli; Pleura Respiratory System Pleura Effusion, noninflammatory Hydrothorax; Hemothorax; Modified Chylothorax after publication Respiratory System Lung: Terminal bronchioles; Metaplasia, mucous cell Metaplasia, goblet cell Modified Lung: Alveoli after publication Respiratory System Lung: Terminal bronchioles; Metaplasia, squamous cell Modified Lung: Alveoli after publication Respiratory System Lung: Terminal bronchioles; Hyperplasia, bronchiolo- Alveolar; Bronchiolar Hyperplasia, Modified Lung: Alveoli alveolar (bronchiolization); Mixed bronchiolar/alveolar; after Hyperplasia, type II cell; publication Bronchiolization Respiratory System Pleura Hyperplasia, mesothelium Published Respiratory System Lung: Alveoli Cyst, keratinizing Modified after publication Organ Working Group Organs Lesion Modifier(s) Synonym/other term Status Respiratory System Lung: Alveoli Epithelioma, cystic, Tumor, squamous cell, Modified keratinizing keratinizing, cystic, benign; after Epithelioma, squamous; publication Cyst, squamous Respiratory System Lung: Alveoli Epithelioma, nonkeratinizing Tumor, squamous cell, Modified nonkeratinizing, benign after publication Respiratory System Lung: Terminal bronchioles; Adenoma, bronchiolo- Solid; Papillary; Mixed; Adenoma, type II cell; Modified Lung: Alveoli alveolar Alveolar; Tubular Adenoma, pulmonary after publication Respiratory System Lung:
Recommended publications
  • This Thesis Has Been Submitted in Fulfilment of the Requirements for a Postgraduate Degree (E.G
    This thesis has been submitted in fulfilment of the requirements for a postgraduate degree (e.g. PhD, MPhil, DClinPsychol) at the University of Edinburgh. Please note the following terms and conditions of use: This work is protected by copyright and other intellectual property rights, which are retained by the thesis author, unless otherwise stated. A copy can be downloaded for personal non-commercial research or study, without prior permission or charge. This thesis cannot be reproduced or quoted extensively from without first obtaining permission in writing from the author. The content must not be changed in any way or sold commercially in any format or medium without the formal permission of the author. When referring to this work, full bibliographic details including the author, title, awarding institution and date of the thesis must be given. Endothelin‐1 antagonism in glomerulonephritis Elizabeth Louise Owen BSc. (Hons), MSc. A thesis submitted towards the degree of PhD The University of Edinburgh 2016 Declaration I declare that the work presented in this thesis is my own and has not previously been published or presented towards another higher degree except where clearly acknowledged as such in the text. ……………………………………… …………. Elizabeth Louise Owen Date Page | 2 Acknowledgements I would like to express my gratitude to my supervisor David Kluth for his support, guidance and efforts during my PhD; Bean, thankyou for your patience and input. Thankyou also to Jeremy Hughes and Simon Brown for your advice and input for the various aspects of labwork, presentations and general how to’s. Jason King, thanks for all your help in the lab, you were always my ‘go‐to‐guy’ for all things technical….and for your many cool pairs of trainers.
    [Show full text]
  • Renal Biopsy in Children with Nephrotic Syndrome at Tripoli Children Hospital
    RESULTS OF RENAL BIOPSY IN CHILDREN WITH NEPHROTIC SYNDROME AT TRIPOLI CHILDREN HOSPITAL Naziha R. Rhuma1, Mabruka Ahmed Zletni1, Mohamed Turki1, Omar Ahmed Fituri1, Awatif. El Boeshi2 1- Faculty of medicine, University of Tripoli, Libya. 2- Nephrology Unit, Children Hospital of Tripoli, Libya. ABSTRACT Nephrotic syndrome is an important renal disorder in children. The role of renal biopsy in children with nephrotic syndrome is controversial, especially in children with frequent relapses or steroid-dependent nephrotic syndrome. The aims of this study are to verify indications of renal biopsy in children with nephrotic syndrome, to identify pat- terns of glomerular disease and its corresponding outcomes. This is a descriptive study reviewed retrospectively a 25 renal biopsies from children with nephrotic syndrome who followed up in nephrology unit at Tripoli Children Hos- pital from Jun. 1995 to Jan. 2006. Children with either steroid resistant or steroid dependent who underwent renal biopsy were included. Twenty five of children (14 male and 11 female) with nephrotic syndrome were included. The mean age 5.2±4.6years (range was from 1-14 years). 14(56%) children were steroid resistant and 11(44%) children were steroid dependent. Minimal-change disease (MCD) accounted for 12(48%) children, focal and segmental scle- rosis (FSGS) was accounted for 10(40%) children and 3(12%) children accounted for other histopathological types. 7(87.5%) of children with FSGS had progressed to end stage renal disease. Steroid resistant was the main indication for renal biopsy in children with nephrotic syndrome. There was increased frequency of FSGS nephrotic syndrome among children with steroid resistant type with poor outcomes.
    [Show full text]
  • Childhood Nephrotic Syndrome -A Single Centre Experience in Althawra Central Hospital, Albaida- Libya During 2005-2016
    MOJ Surgery Case Report Open Access Childhood nephrotic syndrome -a single centre experience in Althawra central hospital, Albaida- Libya during 2005-2016 Abstract Volume 6 Issue 6 - 2018 The aim of this study is to determine response to treatment in terms of remission Mabrouka A M Bofarraj,1 Fatma S Ben and relapse, related risk factors, type of management and complications of nephrotic 2 1 syndrome among studied patients. Khaial, Najwa H Abduljawad, Rima Alshowbki1 Design: Retrospective, analytical study. 1Department of Pediatric Medicine, Al Thawra Central Teaching Hospital, Libya Setting: Pediatric nephrology clinic at Althawra Central Teaching Hospital-Albida, 2Department of Family and Community Medicine, Faculty of Participants/patients: All patients with idiopathic nephrotic syndrome (INS) were Medicine, Benghazi University, Libya evaluated during 2005- 2016. Patients divided into two groups, group I 46 (39%) is non-relapse and group II 72 (62.7%) is relapse group. Group II are sub divided into Correspondence: Mabrouka A M Bofarraj, Department of group A: frequent relapse steroid dependent (FRNS/SDNS) and group B: infrequent Pediatric Medicine, Al Thawra Central Teaching Hospital, Faculty relapse nephrotic syndrome (IRNS). of medicine, Omar Al Moukhtar University, Albaida-Libya, Tel 00218927445625, Email Results: Records of 118 children with INS were studied and 74 (62.7%) were boys, male to female ratio 1.7:1. There was no significance difference between group I and Received: October 24, 2018 | Published: November 23, 2018 group II in the following parameters; age group, sex, family history, initial hypertension and hematuria (p value = >0.05). Mean proteinuria was significantly higher in group II (p=0.001), while mean S.
    [Show full text]
  • ICD-10 International Statistical Classification of Diseases and Related Health Problems
    ICD-10 International Statistical Classification of Diseases and Related Health Problems 10th Revision Volume 2 Instruction manual 2010 Edition WHO Library Cataloguing-in-Publication Data International statistical classification of diseases and related health problems. - 10th revision, edition 2010. 3 v. Contents: v. 1. Tabular list – v. 2. Instruction manual – v. 3. Alphabetical index. 1.Diseases - classification. 2.Classification. 3.Manuals. I.World Health Organization. II.ICD-10. ISBN 978 92 4 154834 2 (NLM classification: WB 15) © World Health Organization 2011 All rights reserved. Publications of the World Health Organization are available on the WHO web site (www.who.int) or can be purchased from WHO Press, World Health Organization, 20 Avenue Appia, 1211 Geneva 27, Switzerland (tel.: +41 22 791 3264; fax: +41 22 791 4857; e-mail: [email protected]). Requests for permission to reproduce or translate WHO publications – whether for sale or for noncommercial distribution – should be addressed to WHO Press through the WHO web site (http://www.who.int/about/licensing/copyright_form). The designations employed and the presentation of the material in this publication do not imply the expression of any opinion whatsoever on the part of the World Health Organization concerning the legal status of any country, territory, city or area or of its authorities, or concerning the delimitation of its frontiers or boundaries. Dotted lines on maps represent approximate border lines for which there may not yet be full agreement. The mention of specific companies or of certain manufacturers’ products does not imply that they are endorsed or recommended by the World Health Organization in preference to others of a similar nature that are not mentioned.
    [Show full text]
  • Pathogenesis of Human Systemic Lupus Erythematosus: a Cellular Perspective Vaishali R
    Feature Review Pathogenesis of Human Systemic Lupus Erythematosus: A Cellular Perspective Vaishali R. Moulton,1,* Abel Suarez-Fueyo,1 Esra Meidan,1,2 Hao Li,1 Masayuki Mizui,3 and George C. Tsokos1,* Systemic lupus erythematosus (SLE) is a chronic autoimmune disease affecting Trends multiple organs. A complex interaction of genetics, environment, and hormones Recent work has identified patterns of leads to immune dysregulation and breakdown of tolerance to self-antigens, altered gene expression denoting resulting in autoantibody production, inflammation, and destruction of end- molecular pathways operating in organs. Emerging evidence on the role of these factors has increased our groups of SLE patients. knowledge of this complex disease, guiding therapeutic strategies and identi- Studies have identified local, organ- fying putative biomarkers. Recent findings include the characterization of specific factors enabling or ameliorat- ing SLE tissue damage, thereby dis- genetic/epigenetic factors linked to SLE, as well as cellular effectors. Novel sociating autoimmunity and end-organ observations have provided an improved understanding of the contribution of damage. tissue-specific factors and associated damage, T and B lymphocytes, as well Novel subsets of adaptive immune as innate immune cell subsets and their corresponding abnormalities. The effectors, and the contributions of intricate web of involved factors and pathways dictates the adoption of tailored innate immune cells including platelets therapeutic approaches to conquer this disease. and neutrophils, are being increasingly recognized in lupus pathogenesis. Studies have revealed metabolic cellu- SLE, a Devastating Disease for Young Women lar aberrations, which underwrite cell SLE afflicts mostly women [1] in which the autoimmune response is directed against practically and organ injury, as important contri- all organs, leading to protean clinical manifestations including arthritis, skin disease, blood cell butors to lupus disease.
    [Show full text]
  • Solid Tumour and Glomerulopathy
    QJ Med 1996; 89:361-367 Solid tumour and glomerulopathy P. PAI, J.M. BONE, I. McDICKEN and CM. BELL From the Regional Renal Unit, Royal Liverpool University Hospital, Liverpool, UK Received 11 October 1995 and in revised form 31 January 1996 Downloaded from https://academic.oup.com/qjmed/article/89/5/361/1578010 by guest on 01 October 2021 Summary We retrospectively examined the prevalence of solid centic GN and one case of focal segmental GN. tumours in patients with glomerulonephritis (GN) Bronchogenic (6) and gastrointestinal carcinoma followed in our regional renal unit between 1977 (CA) (5) were the commonest tumours encountered. and 1994. We identified 17 cases of what was Other tumours included breast CA (1), renal cell thought to be solid-tumour-related glomerulo- CA (1), prostatic CA (1), an epithelial thymoma and nephritis. Tumours and GN were diagnosed together a leiomyosarcoma of the lung. All MGN and mesang- in six cases, and within a year of each other in ial proliferative GN cases developed nephrotic range another four. In addition, there were seven other proteinuria, whereas all patients with rapidly pro- cases with a weaker temporal relationship (median gressive crescentic GN presented with acute renal duration between GN and cancer diagnosis, two failure. Four cases had received immunosuppressive and a half years) but which nonetheless could be therapy prior to tumour diagnosis. We discuss the tumour-related. In total, there were seven membran- validity of each case as tumour-related glomerulo- ous GN, four mesangial proliferative GN, five cres- nephritis. Introduction Since the first clinicopathological study to present an University Hospital serves a population of 2 million association between cancer and nephrotic syndrome people in the Mersey region of the Northwest of (NS) was suggested by Lee et a\.? the subject of England.
    [Show full text]
  • Glomerulonephritis
    Adolesc Med 16 (2005) 67–85 Glomerulonephritis Keith K. Lau, MDa,b, Robert J. Wyatt, MD, MSa,b,* aDivision of Pediatric Nephrology, Department of Pediatrics, University of Tennessee Health Sciences Center, Room 301, WPT, 50 North Dunlap, Memphis, TN 38103, USA bChildren’s Foundation Research Center at the Le Bonheur Children’s Medical Center, Room 301, WPT, 50 North Dunlap, Memphis, TN 38103, USA Early diagnosis of glomerulonephritis (GN) in the adolescent is important in initiating appropriate treatment and controlling chronic glomerular injury that may eventually lead to end-stage renal disease (ESRD). The spectrum of GN in adolescents is more similar to that seen in young and middle-aged adults than to that observed in prepubertal children. In this article, the authors discuss the clinical features associated with GN and the diagnostic evaluation required to determine the specific type of GN. With the exception of hereditary nephritis (Alport’s disease), virtually all types of GN are immunologically mediated with glomerular deposition of immunoglobulins and complement proteins. The inflammatory events leading to GN may be triggered by a number of factors. Most commonly, immune complexes deposit in the glomeruli or are formed in situ with the antigen as a structural component of the glomerulus. The immune complexes then initiate the production of proinflammatory mediators, such as complement proteins and cytokines. Subsequently, the processes of sclerosis within the glomeruli and fibrosis in the tubulointerstitial cells lead to chronic or even irreversible renal injury [1]. Less commonly, these processes occur without involvement of immune complexes—so-called ‘‘pauci-immune GN.’’ * Corresponding author.
    [Show full text]
  • Acute Poststreptococcal Glomerulonephritis: Immune Deposit Disease
    Acute poststreptococcal glomerulonephritis: immune deposit disease. A F Michael Jr, … , R A Good, R L Vernier J Clin Invest. 1966;45(2):237-248. https://doi.org/10.1172/JCI105336. Research Article Find the latest version: https://jci.me/105336/pdf Journal of Clinical Investigation Vol. 45, No. 2, 1966 Acute Poststreptococcal Glomerulonephritis: Immune Deposit Disease * ALFRED F. MICHAEL, JR.,t KEITH N. DRUMMOND,t ROBERT A. GOOD,§ AND ROBERT L. VERNIER || WITH THE TECHNICAL ASSISTANCE OF AGNES M. OPSTAD AND JOYCE E. LOUNBERG (From the Pediatric Research Laboratories of the Variety Club Heart Hospital and the Department of Pediatrics, University of Minnesota, Minneapolis, Minn.) The possible role of immunologic mechanisms in the kidney in acute glomerulonephritis have also acute poststreptococcal glomerulonephritis was revealed the presence of discrete electron dense suggested in 1908 by Schick (2), who compared masses adjacent to the epithelial surface of the the delay in appearance of serum sickness after glomerular basement membrane (11-18). injection of heterologous serum to the latent pe- The purpose of this paper is to describe immuno- riod between scarlet fever and onset of acute glo- fluorescent and electron microscopic observations merulonephritis. Evidence in support of this con- of the kidney in 16 children with acute poststrepto- cept is the depression of serum complement during coccal glomerulonephritis. This study demon- the early stages of the disease (3) and glomerular strates 1) the presence of discrete deposits of yG- localization of immunoglobulin. Immunofluores- and fl3c-globulins along the glomerular basement cent studies have revealed either no glomerular membrane and its epithelial surface that are similar deposition of a-globulin (4) or a diffuse involve- in size and location to the dense masses seen by ment of the capillary wall (5-9).
    [Show full text]
  • Fibrillary Glomerulonephritis and Immunotactoid Glomerulopathy
    PATHOPHYSIOLOGY of the RENAL BIOPSY www.jasn.org Fibrillary Glomerulonephritis and Immunotactoid Glomerulopathy Charles E. Alpers and Jolanta Kowalewska Department of Pathology, University of Washington, Seattle, Washington ABSTRACT extracellular accumulation of haphaz- Fibrillary glomerulonephritis is a now widely recognized diagnostic entity, occur- ardly arranged fibrils measuring ap- ring in approximately 1% of native kidney biopsies in several large biopsy series proximately 16 nm in thickness. Podo- obtained from Western countries. The distinctive features are infiltration of glo- cyte foot processes were diffusely merular structures by randomly arranged fibrils similar in appearance but larger effaced. There was no evidence of than amyloid fibrils and the lack of staining with histochemical dyes typically fibrillary deposits in the tubular base- reactive with amyloid. It is widely but not universally recognized to be distinct from ment membranes or interstitium. The immunotactoid glomerulopathy, an entity characterized by glomerular deposits of diagnosis of fibrillary glomerulone- immunoglobulin with substructural organization as microtubules and with clinical phritis was established on the basis of associations with lymphoplasmacytic disorders. The pathophysiologic basis for the ultrastructural findings in conjunc- organization of the glomerular deposits as fibrils or microtubules in these entities tion with the negative Congo Red stain remains obscure. and typical histologic and immunohis- J Am Soc Nephrol 19: 34–37, 2008. doi:
    [Show full text]
  • Nephrotic Syndrome in Outpatient Practice
    МИНИСТЕРСТВО ЗДРАВООХРАНЕНИЯ РЕСПУБЛИКИ БЕЛАРУСЬ БЕЛОРУССКИЙ ГОСУДАРСТВЕННЫЙ МЕДИЦИНСКИЙ УНИВЕРСИТЕТ КАФЕДРА ПОЛИКЛИНИЧЕСКОЙ ТЕРАПИИ Е. С. АЛЕКСЕЕВА, В. В. ДРОЩЕНКО, Е. В. ЯКОВЛЕВА НЕФРОТИЧЕСКИЙ СИНДРОМ В АМБУЛАТОРНОЙ ПРАКТИКЕ NEPHROTIC SYNDROME IN OUTPATIENT PRACTICE Учебно-методическое пособие Минск БГМУ 2019 1 УДК 616.61-008.6-039.57(075.8)-054.6 ББК 56.9я73 А46 Рекомендовано Научно-методическим советом университета в качестве учебно-методического пособия 21.06.2019 г., протокол № 10 Р е ц е н з е н т ы: канд. мед. наук, доц. 2-й каф. внутренних болезней Белорусского государственного медицинского университета О. А. Паторская; канд. мед. наук, доц. зав. каф. общей врачебной практики Белорусской медицинской академии последипломного образования И. В. Патеюк Алексеева, Е. С. А46 Нефротический синдром в амбулаторной практике = Nephrotic syndrome in outpatient practice : учебно-методическое пособие / Е. С. Алексеева, В. В. Дрощенко, Е. В. Яковлева. – Минск : БГМУ, 2019. – 26 с. ISBN 978-985-21-0408-1. Представлены сведения о критериях и патофизиологии нефротического синдрома, рассмотрены вопросы дифференциальной диагностики и лечения. Предназначено для студентов 5-го и 6-го курсов и медицинского факультета иностранных уча- щихся, обучающихся на английском языке. УДК 616.6-008.6-039.57(075.8)-054.6 ББК 56.9я73 ISBN 978-985-21-0408-1 © Алексеева Е. С., Дрощенко В. В., Яковлева Е. В., 2019 © УО «Белорусский государственный медицинский университет», 2019 2 ABBREVIATIONS ACE — Angiotensin-converting enzyme ApoB — Apolipoprotein B ANA — Antinuclear
    [Show full text]
  • Characterization of Iga Deposition in the Kidney of Patients with Iga Nephropathy and Minimal Change Disease
    Journal of Clinical Medicine Article Characterization of IgA Deposition in the Kidney of Patients with IgA Nephropathy and Minimal Change Disease Won-Hee Cho 1, Seon-Hwa Park 2, Seul-Ki Choi 2, Su Woong Jung 2, Kyung Hwan Jeong 3, Yang-Gyun Kim 2 , Ju-Young Moon 2, Sung-Jig Lim 4 , Ji-Youn Sung 5, Jong Hyun Jhee 6, Ho Jun Chin 7,8, Bum Soon Choi 9 and Sang-Ho Lee 2,* 1 Department of Medicine, Graduate School, Kyung Hee University, Seoul 02447, Korea; [email protected] 2 Division of Nephrology, Department of Internal Medicine, Kyung Hee University Hospital at Gangdong, Seoul 05278, Korea; [email protected] (S.-H.P.); [email protected] (S.-K.C.); [email protected] (S.W.J.); [email protected] (Y.-G.K.); [email protected] (J.-Y.M.) 3 Division of Nephrology, Department of Internal Medicine, Kyung Hee University Medical Center, Seoul 02447, Korea; [email protected] 4 Department of Pathology, Kyung Hee University Hospital at Gangdong, Kyung Hee University, Seoul 05278, Korea; [email protected] 5 Department of Pathology, Kyung Hee University Hospital, Kyung Hee University College of Medicine, Seoul 02447, Korea; [email protected] 6 Division of Nephrology, Department of Internal Medicine, Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul 06273, Korea; [email protected] 7 Department of Internal Medicine, Seoul National University Bundang Hospital, Seongnam 13620, Korea; [email protected] 8 Department of Internal Medicine, College of Medicine, Seoul National University, Seoul 03080, Korea 9 Division of Nephrology, Department of Internal Medicine, College of Medicine, The Catholic University of Korea, Seoul 06591, Korea; [email protected] * Correspondence: [email protected] Received: 5 July 2020; Accepted: 9 August 2020; Published: 12 August 2020 Abstract: Approximately 5% of patients with IgA nephropathy (IgAN) exhibit mild mesangial lesions with acute onset nephrotic syndrome and diffuse foot process effacement representative of minimal change disease (MCD).
    [Show full text]
  • A Narrative Review on C3 Glomerulopathy: a Rare Renal Disease
    International Journal of Molecular Sciences Review A Narrative Review on C3 Glomerulopathy: A Rare Renal Disease Francesco Paolo Schena 1,2,*, Pasquale Esposito 3 and Michele Rossini 1 1 Department of Emergency and Organ Transplantation, Renal Unit, University of Bari, 70124 Bari, Italy; [email protected] 2 Schena Foundation, European Center for the Study of Renal Diseases, 70010 Valenzano, Italy 3 Department of Internal Medicine, Division of Nephrology, Dialysis and Transplantation, University of Genoa and IRCCS Ospedale Policlinico San Martino, 16132 Genova, Italy; [email protected] * Correspondence: [email protected] Received: 5 December 2019; Accepted: 10 January 2020; Published: 14 January 2020 Abstract: In April 2012, a group of nephrologists organized a consensus conference in Cambridge (UK) on type II membranoproliferative glomerulonephritis and decided to use a new terminology, “C3 glomerulopathy” (C3 GP). Further knowledge on the complement system and on kidney biopsy contributed toward distinguishing this disease into three subgroups: dense deposit disease (DDD), C3 glomerulonephritis (C3 GN), and the CFHR5 nephropathy. The persistent presence of microhematuria with or without light or heavy proteinuria after an infection episode suggests the potential onset of C3 GP. These nephritides are characterized by abnormal activation of the complement alternative pathway, abnormal deposition of C3 in the glomeruli, and progression of renal damage to end-stage kidney disease. The diagnosis is based on studying the complement system, relative genetics, and kidney biopsies. The treatment gap derives from the absence of a robust understanding of their natural outcome. Therefore, a specific treatment for the different types of C3 GP has not been established.
    [Show full text]