Fibrogenesis in Kidney Transplant: Dysfunction Progress Biomarkers

Bibliographic Details
Main Author: Costa, J S
Publication Date: 2017
Other Authors: Alves, R, Sousa, V, Marinho, C, Romãozinho, C, Santos, L, Macário, F, Pratas, J, Prado E Castro, L, Campos, M, Figueiredo, A
Format: Article
Language: eng
Source: Repositórios Científicos de Acesso Aberto de Portugal (RCAAP)
Download full: http://hdl.handle.net/10400.4/2283
Summary: Fibrogenesis markers, such as alpha-actin (AA), CD163 (macrophages), and E-cadherin, have been studied as chronic kidney allograft injury (CAI) predictors, a major cause of allograft failure. OBJECTIVE: Investigate the value of these markers in predicting CAI and initiation of dialysis. MATERIALS AND METHODS: Retrospective analysis of 26 kidney allograft biopsies (from 22 patients with CAI) during 2 years, evaluating intensity and percentage of marked cells on glomeruli and tubulointerstitial compartment. At the time of the biopsy, patients were 45.5 ± 15.8 years and 4.2 years after transplant, and they had a mean glomerular filtration rate (GFR) of 25.8 ± 9.9 mL/min. From an average of 8.5 glomeruli per biopsy, there was ≤25% sclerosis in 17 cases, 26% to 50% in 5, and >50% in 4. Interstitial fibrosis or tubular atrophy affected ≤25% of cortical area in 14 cases, 26% to 50% in 8, and >50% in 2. Twelve patients started dialysis 5.8 ± 4.7 years after transplant, with an average GFR 20.9 mL/min at the time of the biopsy. RESULTS: There was a higher intensity and percentage of CD163-marked cells in the tubulointerstitial compartment in advanced interstitial fibrosis. We found an association between intensity of AA in the tubulointerstitial compartment and initiation of dialysis (P = .003) and a negative correlation between intensity of E-cadherin loss and GFR (r = -0.56, P = .012). CONCLUSIONS: In our study, intensity of tubulointerstitial AA was shown to be a predictor of initiation of dialysis, and E-cadherin loss intensity was associated to CAI progression. However, prospective and larger studies are needed to evaluate the predictive value of these markers.
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spelling Fibrogenesis in Kidney Transplant: Dysfunction Progress BiomarkersAloenxertosSobrevivência de EnxertoDoenças do RimTransplantação de RimCuidados Pós-operatóriosFibrogenesis markers, such as alpha-actin (AA), CD163 (macrophages), and E-cadherin, have been studied as chronic kidney allograft injury (CAI) predictors, a major cause of allograft failure. OBJECTIVE: Investigate the value of these markers in predicting CAI and initiation of dialysis. MATERIALS AND METHODS: Retrospective analysis of 26 kidney allograft biopsies (from 22 patients with CAI) during 2 years, evaluating intensity and percentage of marked cells on glomeruli and tubulointerstitial compartment. At the time of the biopsy, patients were 45.5 ± 15.8 years and 4.2 years after transplant, and they had a mean glomerular filtration rate (GFR) of 25.8 ± 9.9 mL/min. From an average of 8.5 glomeruli per biopsy, there was ≤25% sclerosis in 17 cases, 26% to 50% in 5, and >50% in 4. Interstitial fibrosis or tubular atrophy affected ≤25% of cortical area in 14 cases, 26% to 50% in 8, and >50% in 2. Twelve patients started dialysis 5.8 ± 4.7 years after transplant, with an average GFR 20.9 mL/min at the time of the biopsy. RESULTS: There was a higher intensity and percentage of CD163-marked cells in the tubulointerstitial compartment in advanced interstitial fibrosis. We found an association between intensity of AA in the tubulointerstitial compartment and initiation of dialysis (P = .003) and a negative correlation between intensity of E-cadherin loss and GFR (r = -0.56, P = .012). CONCLUSIONS: In our study, intensity of tubulointerstitial AA was shown to be a predictor of initiation of dialysis, and E-cadherin loss intensity was associated to CAI progression. However, prospective and larger studies are needed to evaluate the predictive value of these markers.RIHUCCosta, J SAlves, RSousa, VMarinho, CRomãozinho, CSantos, LMacário, FPratas, JPrado E Castro, LCampos, MFigueiredo, A2020-03-30T15:13:32Z2017-052017-05-01T00:00:00Zinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articleapplication/pdfhttp://hdl.handle.net/10400.4/2283eng10.1016/j.transproceed.2017.01.063info:eu-repo/semantics/openAccessreponame:Repositórios Científicos de Acesso Aberto de Portugal (RCAAP)instname:FCCN, serviços digitais da FCT – Fundação para a Ciência e a Tecnologiainstacron:RCAAP2025-01-30T03:20:09Zoai:rihuc.huc.min-saude.pt:10400.4/2283Portal AgregadorONGhttps://www.rcaap.pt/oai/openaireinfo@rcaap.ptopendoar:https://opendoar.ac.uk/repository/71602025-05-28T19:43:14.326951Repositórios Científicos de Acesso Aberto de Portugal (RCAAP) - FCCN, serviços digitais da FCT – Fundação para a Ciência e a Tecnologiafalse
dc.title.none.fl_str_mv Fibrogenesis in Kidney Transplant: Dysfunction Progress Biomarkers
title Fibrogenesis in Kidney Transplant: Dysfunction Progress Biomarkers
spellingShingle Fibrogenesis in Kidney Transplant: Dysfunction Progress Biomarkers
Costa, J S
Aloenxertos
Sobrevivência de Enxerto
Doenças do Rim
Transplantação de Rim
Cuidados Pós-operatórios
title_short Fibrogenesis in Kidney Transplant: Dysfunction Progress Biomarkers
title_full Fibrogenesis in Kidney Transplant: Dysfunction Progress Biomarkers
title_fullStr Fibrogenesis in Kidney Transplant: Dysfunction Progress Biomarkers
title_full_unstemmed Fibrogenesis in Kidney Transplant: Dysfunction Progress Biomarkers
title_sort Fibrogenesis in Kidney Transplant: Dysfunction Progress Biomarkers
author Costa, J S
author_facet Costa, J S
Alves, R
Sousa, V
Marinho, C
Romãozinho, C
Santos, L
Macário, F
Pratas, J
Prado E Castro, L
Campos, M
Figueiredo, A
author_role author
author2 Alves, R
Sousa, V
Marinho, C
Romãozinho, C
Santos, L
Macário, F
Pratas, J
Prado E Castro, L
Campos, M
Figueiredo, A
author2_role author
author
author
author
author
author
author
author
author
author
dc.contributor.none.fl_str_mv RIHUC
dc.contributor.author.fl_str_mv Costa, J S
Alves, R
Sousa, V
Marinho, C
Romãozinho, C
Santos, L
Macário, F
Pratas, J
Prado E Castro, L
Campos, M
Figueiredo, A
dc.subject.por.fl_str_mv Aloenxertos
Sobrevivência de Enxerto
Doenças do Rim
Transplantação de Rim
Cuidados Pós-operatórios
topic Aloenxertos
Sobrevivência de Enxerto
Doenças do Rim
Transplantação de Rim
Cuidados Pós-operatórios
description Fibrogenesis markers, such as alpha-actin (AA), CD163 (macrophages), and E-cadherin, have been studied as chronic kidney allograft injury (CAI) predictors, a major cause of allograft failure. OBJECTIVE: Investigate the value of these markers in predicting CAI and initiation of dialysis. MATERIALS AND METHODS: Retrospective analysis of 26 kidney allograft biopsies (from 22 patients with CAI) during 2 years, evaluating intensity and percentage of marked cells on glomeruli and tubulointerstitial compartment. At the time of the biopsy, patients were 45.5 ± 15.8 years and 4.2 years after transplant, and they had a mean glomerular filtration rate (GFR) of 25.8 ± 9.9 mL/min. From an average of 8.5 glomeruli per biopsy, there was ≤25% sclerosis in 17 cases, 26% to 50% in 5, and >50% in 4. Interstitial fibrosis or tubular atrophy affected ≤25% of cortical area in 14 cases, 26% to 50% in 8, and >50% in 2. Twelve patients started dialysis 5.8 ± 4.7 years after transplant, with an average GFR 20.9 mL/min at the time of the biopsy. RESULTS: There was a higher intensity and percentage of CD163-marked cells in the tubulointerstitial compartment in advanced interstitial fibrosis. We found an association between intensity of AA in the tubulointerstitial compartment and initiation of dialysis (P = .003) and a negative correlation between intensity of E-cadherin loss and GFR (r = -0.56, P = .012). CONCLUSIONS: In our study, intensity of tubulointerstitial AA was shown to be a predictor of initiation of dialysis, and E-cadherin loss intensity was associated to CAI progression. However, prospective and larger studies are needed to evaluate the predictive value of these markers.
publishDate 2017
dc.date.none.fl_str_mv 2017-05
2017-05-01T00:00:00Z
2020-03-30T15:13:32Z
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dc.relation.none.fl_str_mv 10.1016/j.transproceed.2017.01.063
dc.rights.driver.fl_str_mv info:eu-repo/semantics/openAccess
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dc.format.none.fl_str_mv application/pdf
dc.source.none.fl_str_mv reponame:Repositórios Científicos de Acesso Aberto de Portugal (RCAAP)
instname:FCCN, serviços digitais da FCT – Fundação para a Ciência e a Tecnologia
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reponame_str Repositórios Científicos de Acesso Aberto de Portugal (RCAAP)
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