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De novo glomerular diseases after renal transplantation: How is it different from recurrent glomerular diseases?
The glomerular diseases after renal transplantation can occur de novo, i.e., with no relation to the native kidney disease, or more frequently occur as a recurrence of the original disease in the native kidney. There may not be any difference in clinical features and histological pattern between de...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Baishideng Publishing Group Inc
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5743866/ https://www.ncbi.nlm.nih.gov/pubmed/29312858 http://dx.doi.org/10.5500/wjt.v7.i6.285 |
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author | Abbas, Fedaey El Kossi, Mohsen Jin, Jon Kim Sharma, Ajay Halawa, Ahmed |
author_facet | Abbas, Fedaey El Kossi, Mohsen Jin, Jon Kim Sharma, Ajay Halawa, Ahmed |
author_sort | Abbas, Fedaey |
collection | PubMed |
description | The glomerular diseases after renal transplantation can occur de novo, i.e., with no relation to the native kidney disease, or more frequently occur as a recurrence of the original disease in the native kidney. There may not be any difference in clinical features and histological pattern between de novo glomerular disease and recurrence of original glomerular disease. However, structural alterations in transplanted kidney add to dilemma in diagnosis. These changes in architecture of histopathology can happen due to: (1) exposure to the immunosuppression specifically the calcineurin inhibitors (CNI); (2) in vascular and tubulointerstitial alterations as a result of antibody mediated or cell-mediated immunological onslaught; (3) post-transplant viral infections; (4) ischemia-reperfusion injury; and (5) hyperfiltration injury. The pathogenesis of the de novo glomerular diseases differs with each type. Stimulation of B-cell clones with subsequent production of the monoclonal IgG, particularly IgG3 subtype that has higher affinity to the negatively charged glomerular tissue, is suggested to be included in PGNMID pathogenesis. De novo membranous nephropathy can be seen after exposure to the cryptogenic podocyte antigens. The role of the toxic effects of CNI including tissue fibrosis and the hemodynamic alterations may be involved in the de novo FSGS pathophysiology. The well-known deleterious effects of HCV infection and its relation to MPGN disease are frequently reported. The new concepts have emerged that demonstrate the role of dysregulation of alternative complement pathway in evolution of MPGN that led to classifying into two subgroups, immune complex mediated MPGN and complement-mediated MPGN. The latter comprises of the dense deposit disease and the C3 GN disease. De novo C3 disease is rather rare. Prognosis of de novo diseases varies with each type and their management continues to be empirical to a large extent. |
format | Online Article Text |
id | pubmed-5743866 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Baishideng Publishing Group Inc |
record_format | MEDLINE/PubMed |
spelling | pubmed-57438662018-01-08 De novo glomerular diseases after renal transplantation: How is it different from recurrent glomerular diseases? Abbas, Fedaey El Kossi, Mohsen Jin, Jon Kim Sharma, Ajay Halawa, Ahmed World J Transplant Review The glomerular diseases after renal transplantation can occur de novo, i.e., with no relation to the native kidney disease, or more frequently occur as a recurrence of the original disease in the native kidney. There may not be any difference in clinical features and histological pattern between de novo glomerular disease and recurrence of original glomerular disease. However, structural alterations in transplanted kidney add to dilemma in diagnosis. These changes in architecture of histopathology can happen due to: (1) exposure to the immunosuppression specifically the calcineurin inhibitors (CNI); (2) in vascular and tubulointerstitial alterations as a result of antibody mediated or cell-mediated immunological onslaught; (3) post-transplant viral infections; (4) ischemia-reperfusion injury; and (5) hyperfiltration injury. The pathogenesis of the de novo glomerular diseases differs with each type. Stimulation of B-cell clones with subsequent production of the monoclonal IgG, particularly IgG3 subtype that has higher affinity to the negatively charged glomerular tissue, is suggested to be included in PGNMID pathogenesis. De novo membranous nephropathy can be seen after exposure to the cryptogenic podocyte antigens. The role of the toxic effects of CNI including tissue fibrosis and the hemodynamic alterations may be involved in the de novo FSGS pathophysiology. The well-known deleterious effects of HCV infection and its relation to MPGN disease are frequently reported. The new concepts have emerged that demonstrate the role of dysregulation of alternative complement pathway in evolution of MPGN that led to classifying into two subgroups, immune complex mediated MPGN and complement-mediated MPGN. The latter comprises of the dense deposit disease and the C3 GN disease. De novo C3 disease is rather rare. Prognosis of de novo diseases varies with each type and their management continues to be empirical to a large extent. Baishideng Publishing Group Inc 2017-12-24 2017-12-24 /pmc/articles/PMC5743866/ /pubmed/29312858 http://dx.doi.org/10.5500/wjt.v7.i6.285 Text en ©The Author(s) 2017. Published by Baishideng Publishing Group Inc. All rights reserved. http://creativecommons.org/licenses/by-nc/4.0/ Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/ |
spellingShingle | Review Abbas, Fedaey El Kossi, Mohsen Jin, Jon Kim Sharma, Ajay Halawa, Ahmed De novo glomerular diseases after renal transplantation: How is it different from recurrent glomerular diseases? |
title | De novo glomerular diseases after renal transplantation: How is it different from recurrent glomerular diseases? |
title_full | De novo glomerular diseases after renal transplantation: How is it different from recurrent glomerular diseases? |
title_fullStr | De novo glomerular diseases after renal transplantation: How is it different from recurrent glomerular diseases? |
title_full_unstemmed | De novo glomerular diseases after renal transplantation: How is it different from recurrent glomerular diseases? |
title_short | De novo glomerular diseases after renal transplantation: How is it different from recurrent glomerular diseases? |
title_sort | de novo glomerular diseases after renal transplantation: how is it different from recurrent glomerular diseases? |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5743866/ https://www.ncbi.nlm.nih.gov/pubmed/29312858 http://dx.doi.org/10.5500/wjt.v7.i6.285 |
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