Complement System and C4d expression in cases of Membranous nephropathy

Abstract Introduction: Membranous nephropathy (MN) is one of the major causes of nephrotic syndrome. The complement system plays a key role in the pathophysiology of MN. Objectives: To identify the complement pathway possibly activated in MN cases and correlate the presence of C4d with more severe clinical and histological markers. Methods: Sixty nine cases from renal biopsy with membranous nephropathy were investigated. The presence of C1q was analyzed by direct immunofluorescence; and expression of C4d by immunohistochemistry. Clinical and epidemiological data were obtained upon biopsy request. Results: The presence of focal segmental glomerulosclerosis, global glomerulosclerosis, vascular lesions and tubulointerstitial fibrosis were collected by anatomopathological report. C4d(+) was found in 58 (84%), and C1q(+) was found in 12 (17%) of the cases. Twelve patients had C4d(+)/C1q(+), 46 had C4d(+)/C1q(-), and 11 patients had C4d(-)/C1q(-), probably indicating the activation of the classical, lectin and alternative pathways, respectively. Conclusion: C4d was associated with increased interstitial fibrosis, but not with clinical markers of poor prognosis. Through the deposition of C4d and C1q we demonstrated that all complement pathways may be involved in MN, highlighting the lectin pathway. The presence of C4d has been associated with severe tubulointerstitial lesions, but not with clinical markers, or can be taken as a universal marker of all cases of MN.

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Main Authors: Custódio,Fabiano Bichuette, Silva,Crislaine Aparecida da, Helmo,Fernanda Rodrigues, Machado,Juliana Reis, Reis,Marlene Antônia dos
Format: Digital revista
Language:English
Published: Sociedade Brasileira de Nefrologia 2017
Online Access:http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0101-28002017000400370
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spelling oai:scielo:S0101-280020170004003702018-01-04Complement System and C4d expression in cases of Membranous nephropathyCustódio,Fabiano BichuetteSilva,Crislaine Aparecida daHelmo,Fernanda RodriguesMachado,Juliana ReisReis,Marlene Antônia dos complement activating enzimes complement system proteins glomerulonephritis, membranous Abstract Introduction: Membranous nephropathy (MN) is one of the major causes of nephrotic syndrome. The complement system plays a key role in the pathophysiology of MN. Objectives: To identify the complement pathway possibly activated in MN cases and correlate the presence of C4d with more severe clinical and histological markers. Methods: Sixty nine cases from renal biopsy with membranous nephropathy were investigated. The presence of C1q was analyzed by direct immunofluorescence; and expression of C4d by immunohistochemistry. Clinical and epidemiological data were obtained upon biopsy request. Results: The presence of focal segmental glomerulosclerosis, global glomerulosclerosis, vascular lesions and tubulointerstitial fibrosis were collected by anatomopathological report. C4d(+) was found in 58 (84%), and C1q(+) was found in 12 (17%) of the cases. Twelve patients had C4d(+)/C1q(+), 46 had C4d(+)/C1q(-), and 11 patients had C4d(-)/C1q(-), probably indicating the activation of the classical, lectin and alternative pathways, respectively. Conclusion: C4d was associated with increased interstitial fibrosis, but not with clinical markers of poor prognosis. Through the deposition of C4d and C1q we demonstrated that all complement pathways may be involved in MN, highlighting the lectin pathway. The presence of C4d has been associated with severe tubulointerstitial lesions, but not with clinical markers, or can be taken as a universal marker of all cases of MN.info:eu-repo/semantics/openAccessSociedade Brasileira de NefrologiaBrazilian Journal of Nephrology v.39 n.4 20172017-12-01info:eu-repo/semantics/articletext/htmlhttp://old.scielo.br/scielo.php?script=sci_arttext&pid=S0101-28002017000400370en10.5935/0101-2800.20170068
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libraryname SciELO
language English
format Digital
author Custódio,Fabiano Bichuette
Silva,Crislaine Aparecida da
Helmo,Fernanda Rodrigues
Machado,Juliana Reis
Reis,Marlene Antônia dos
spellingShingle Custódio,Fabiano Bichuette
Silva,Crislaine Aparecida da
Helmo,Fernanda Rodrigues
Machado,Juliana Reis
Reis,Marlene Antônia dos
Complement System and C4d expression in cases of Membranous nephropathy
author_facet Custódio,Fabiano Bichuette
Silva,Crislaine Aparecida da
Helmo,Fernanda Rodrigues
Machado,Juliana Reis
Reis,Marlene Antônia dos
author_sort Custódio,Fabiano Bichuette
title Complement System and C4d expression in cases of Membranous nephropathy
title_short Complement System and C4d expression in cases of Membranous nephropathy
title_full Complement System and C4d expression in cases of Membranous nephropathy
title_fullStr Complement System and C4d expression in cases of Membranous nephropathy
title_full_unstemmed Complement System and C4d expression in cases of Membranous nephropathy
title_sort complement system and c4d expression in cases of membranous nephropathy
description Abstract Introduction: Membranous nephropathy (MN) is one of the major causes of nephrotic syndrome. The complement system plays a key role in the pathophysiology of MN. Objectives: To identify the complement pathway possibly activated in MN cases and correlate the presence of C4d with more severe clinical and histological markers. Methods: Sixty nine cases from renal biopsy with membranous nephropathy were investigated. The presence of C1q was analyzed by direct immunofluorescence; and expression of C4d by immunohistochemistry. Clinical and epidemiological data were obtained upon biopsy request. Results: The presence of focal segmental glomerulosclerosis, global glomerulosclerosis, vascular lesions and tubulointerstitial fibrosis were collected by anatomopathological report. C4d(+) was found in 58 (84%), and C1q(+) was found in 12 (17%) of the cases. Twelve patients had C4d(+)/C1q(+), 46 had C4d(+)/C1q(-), and 11 patients had C4d(-)/C1q(-), probably indicating the activation of the classical, lectin and alternative pathways, respectively. Conclusion: C4d was associated with increased interstitial fibrosis, but not with clinical markers of poor prognosis. Through the deposition of C4d and C1q we demonstrated that all complement pathways may be involved in MN, highlighting the lectin pathway. The presence of C4d has been associated with severe tubulointerstitial lesions, but not with clinical markers, or can be taken as a universal marker of all cases of MN.
publisher Sociedade Brasileira de Nefrologia
publishDate 2017
url http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0101-28002017000400370
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