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Recurrent idiopathic membranous nephropathy in the renal allograft: successful treatment with the anti-CD20 monoclonal antibody rituximab

Idiopathic membranous glomerulonephritis (IMGN) is one of the most common causes of nephrotic syndrome in adults. Disease progression is associated with the magnitude and duration of proteinuria [Reichert LJ, Koene RA, Wetzels JF. Prognostic factors in idiopathic membranous nephropathy. Am J Kidney...

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Autores principales: Ladino, Marco, Roth, David
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Oxford University Press 2009
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4421397/
https://www.ncbi.nlm.nih.gov/pubmed/25949355
http://dx.doi.org/10.1093/ndtplus/sfp071
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author Ladino, Marco
Roth, David
author_facet Ladino, Marco
Roth, David
author_sort Ladino, Marco
collection PubMed
description Idiopathic membranous glomerulonephritis (IMGN) is one of the most common causes of nephrotic syndrome in adults. Disease progression is associated with the magnitude and duration of proteinuria [Reichert LJ, Koene RA, Wetzels JF. Prognostic factors in idiopathic membranous nephropathy. Am J Kidney Dis 1998; 31: 1–11]. Membranous nephropathy is also one of the glomerular diseases that is well described to recur in the transplanted kidney [Kotanko P, Pusey CD, Levy JB. Recurrent glomerulonephritis following renal transplantation. Transplantation 1997; 63: 1045]. There is no definitive therapy for primary membranous glomerulonephritis or recurrent disease in the graft. Cyclophosphamide plus steroids or cyclosporine [Cattran DC, Greenwood C, Ritchie S et al. Canadian Glomerulonephritis Study Group. A controlled trial of cyclosporine in patients with progressive membranous nephropathy. Kidney Int 1995; 47: 1130–1135] have been the preferred agents for the treatment of MGN involving the native kidneys. More recently, several reports have described the use of the anti-CD20 monoclonal antibody rituximab in patients with IMGN. In the current report, we present a patient with ESRD secondary to IMGN who developed nephrotic range proteinuria 5 months after receiving a kidney transplant from a deceased donor. A biopsy of the allograft demonstrated changes compatible with recurrent membranous glomerulonephritis. The patient was treated with four weekly infusions of rituximab over a 1-month period with a significant decrease in proteinuria and an improvement in renal function.
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spelling pubmed-44213972015-05-06 Recurrent idiopathic membranous nephropathy in the renal allograft: successful treatment with the anti-CD20 monoclonal antibody rituximab Ladino, Marco Roth, David NDT Plus Case Report Idiopathic membranous glomerulonephritis (IMGN) is one of the most common causes of nephrotic syndrome in adults. Disease progression is associated with the magnitude and duration of proteinuria [Reichert LJ, Koene RA, Wetzels JF. Prognostic factors in idiopathic membranous nephropathy. Am J Kidney Dis 1998; 31: 1–11]. Membranous nephropathy is also one of the glomerular diseases that is well described to recur in the transplanted kidney [Kotanko P, Pusey CD, Levy JB. Recurrent glomerulonephritis following renal transplantation. Transplantation 1997; 63: 1045]. There is no definitive therapy for primary membranous glomerulonephritis or recurrent disease in the graft. Cyclophosphamide plus steroids or cyclosporine [Cattran DC, Greenwood C, Ritchie S et al. Canadian Glomerulonephritis Study Group. A controlled trial of cyclosporine in patients with progressive membranous nephropathy. Kidney Int 1995; 47: 1130–1135] have been the preferred agents for the treatment of MGN involving the native kidneys. More recently, several reports have described the use of the anti-CD20 monoclonal antibody rituximab in patients with IMGN. In the current report, we present a patient with ESRD secondary to IMGN who developed nephrotic range proteinuria 5 months after receiving a kidney transplant from a deceased donor. A biopsy of the allograft demonstrated changes compatible with recurrent membranous glomerulonephritis. The patient was treated with four weekly infusions of rituximab over a 1-month period with a significant decrease in proteinuria and an improvement in renal function. Oxford University Press 2009-10 2009-06-17 /pmc/articles/PMC4421397/ /pubmed/25949355 http://dx.doi.org/10.1093/ndtplus/sfp071 Text en © The Author [2009]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org http://creativecommons.org/licenses/by-nc/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com
spellingShingle Case Report
Ladino, Marco
Roth, David
Recurrent idiopathic membranous nephropathy in the renal allograft: successful treatment with the anti-CD20 monoclonal antibody rituximab
title Recurrent idiopathic membranous nephropathy in the renal allograft: successful treatment with the anti-CD20 monoclonal antibody rituximab
title_full Recurrent idiopathic membranous nephropathy in the renal allograft: successful treatment with the anti-CD20 monoclonal antibody rituximab
title_fullStr Recurrent idiopathic membranous nephropathy in the renal allograft: successful treatment with the anti-CD20 monoclonal antibody rituximab
title_full_unstemmed Recurrent idiopathic membranous nephropathy in the renal allograft: successful treatment with the anti-CD20 monoclonal antibody rituximab
title_short Recurrent idiopathic membranous nephropathy in the renal allograft: successful treatment with the anti-CD20 monoclonal antibody rituximab
title_sort recurrent idiopathic membranous nephropathy in the renal allograft: successful treatment with the anti-cd20 monoclonal antibody rituximab
topic Case Report
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4421397/
https://www.ncbi.nlm.nih.gov/pubmed/25949355
http://dx.doi.org/10.1093/ndtplus/sfp071
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