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Complement related kidney diseases: Recurrence after transplantation
The recurrence of renal disease after renal transplantation is becoming one of the main causes of graft loss after kidney transplantation. This principally concerns some of the original diseases as the atypical hemolytic uremic syndrome (HUS), the membranoproliferative glomerulonephritis (MPGN), in...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Baishideng Publishing Group Inc
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5175220/ https://www.ncbi.nlm.nih.gov/pubmed/28058212 http://dx.doi.org/10.5500/wjt.v6.i4.632 |
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author | Salvadori, Maurizio Bertoni, Elisabetta |
author_facet | Salvadori, Maurizio Bertoni, Elisabetta |
author_sort | Salvadori, Maurizio |
collection | PubMed |
description | The recurrence of renal disease after renal transplantation is becoming one of the main causes of graft loss after kidney transplantation. This principally concerns some of the original diseases as the atypical hemolytic uremic syndrome (HUS), the membranoproliferative glomerulonephritis (MPGN), in particular the MPGN now called C3 glomerulopathy. Both this groups of renal diseases are characterized by congenital (genetic) or acquired (auto-antibodies) modifications of the alternative pathway of complement. These abnormalities often remain after transplantation because they are constitutional and poorly influenced by the immunosuppression. This fact justifies the high recurrence rate of these diseases. Early diagnosis of recurrence is essential for an optimal therapeutically approach, whenever possible. Patients affected by end stage renal disease due to C3 glomerulopathies or to atypical HUS, may be transplanted with extreme caution. Living donor donation from relatives is not recommended because members of the same family may be affected by the same gene mutation. Different therapeutically approaches have been attempted either for recurrence prevention and treatment. The most promising approach is represented by complement inhibitors. Eculizumab, a monoclonal antibody against C5 convertase is the most promising drug, even if to date is not known how long the therapy should be continued and which are the best dosing. These facts face the high costs of the treatment. Eculizumab resistant patients have been described. They could benefit by a C3 convertase inhibitor, but this class of drugs is by now the object of randomized controlled trials. |
format | Online Article Text |
id | pubmed-5175220 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Baishideng Publishing Group Inc |
record_format | MEDLINE/PubMed |
spelling | pubmed-51752202017-01-06 Complement related kidney diseases: Recurrence after transplantation Salvadori, Maurizio Bertoni, Elisabetta World J Transplant Review The recurrence of renal disease after renal transplantation is becoming one of the main causes of graft loss after kidney transplantation. This principally concerns some of the original diseases as the atypical hemolytic uremic syndrome (HUS), the membranoproliferative glomerulonephritis (MPGN), in particular the MPGN now called C3 glomerulopathy. Both this groups of renal diseases are characterized by congenital (genetic) or acquired (auto-antibodies) modifications of the alternative pathway of complement. These abnormalities often remain after transplantation because they are constitutional and poorly influenced by the immunosuppression. This fact justifies the high recurrence rate of these diseases. Early diagnosis of recurrence is essential for an optimal therapeutically approach, whenever possible. Patients affected by end stage renal disease due to C3 glomerulopathies or to atypical HUS, may be transplanted with extreme caution. Living donor donation from relatives is not recommended because members of the same family may be affected by the same gene mutation. Different therapeutically approaches have been attempted either for recurrence prevention and treatment. The most promising approach is represented by complement inhibitors. Eculizumab, a monoclonal antibody against C5 convertase is the most promising drug, even if to date is not known how long the therapy should be continued and which are the best dosing. These facts face the high costs of the treatment. Eculizumab resistant patients have been described. They could benefit by a C3 convertase inhibitor, but this class of drugs is by now the object of randomized controlled trials. Baishideng Publishing Group Inc 2016-12-24 2016-12-24 /pmc/articles/PMC5175220/ /pubmed/28058212 http://dx.doi.org/10.5500/wjt.v6.i4.632 Text en ©The Author(s) 2016. Published by Baishideng Publishing Group Inc. All rights reserved. http://creativecommons.org/licenses/by-nc/4.0/ 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. |
spellingShingle | Review Salvadori, Maurizio Bertoni, Elisabetta Complement related kidney diseases: Recurrence after transplantation |
title | Complement related kidney diseases: Recurrence after transplantation |
title_full | Complement related kidney diseases: Recurrence after transplantation |
title_fullStr | Complement related kidney diseases: Recurrence after transplantation |
title_full_unstemmed | Complement related kidney diseases: Recurrence after transplantation |
title_short | Complement related kidney diseases: Recurrence after transplantation |
title_sort | complement related kidney diseases: recurrence after transplantation |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5175220/ https://www.ncbi.nlm.nih.gov/pubmed/28058212 http://dx.doi.org/10.5500/wjt.v6.i4.632 |
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