Evolution of Circulating Bone-Related Biomarkers After Kidney Transplantation

Detalhes bibliográficos
Autor(a) principal: Juliana Carvalho Magalhães
Data de Publicação: 2021
Tipo de documento: Dissertação
Idioma: por
Título da fonte: Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos)
Texto Completo: https://hdl.handle.net/10216/134330
Resumo: Aim: Bone disease after kidney transplant (KT) results from multiple factors, including previous bone and mineral metabolism disturbances and effects from transplant-related medications. New biomolecules have been recently associated with the development and progression of the chronic kidney disease-associated bone and mineral disorder (CKD-MBD). These include sclerostin and the soluble receptor activator of nuclear factor-kB ligand (sRANKL). Methods: To better understand the role of new biomarkers in post-transplant bone disease, this study was designed to prospectively evaluate and correlate results from the histomorphometric analysis of bone biopsies after KT with emerging serum biomarkers of the CKD-MBD: sclerostin, Dickkopf-related protein 1 (Dkk-1), sRANKL and osteoprotegerin (OPG). Results: Our data shows a significant increase in plasma levels of bioactive sclerostin after KT accompanied by a significant reduction in plasma levels of Dkk-1, suggesting a promotion of the inhibition of bone formation by osteoblasts through the activation of these inhibitors of the Wnt signaling pathway. In addition, we found a significant increase in plasma levels of free sRANKL after KT accompanied by a significant reduction in plasma levels of its decoy receptor OPG, suggesting an enhanced bone reabsorption by osteoclasts mediated by this mechanism. Conclusions: Taken together, these results suggest that the loss of bone volume observed after KT could be related mainly with the inhibition of bone formation mediated by sclerostin accompanied by an enhanced bone reabsorption mediated by sRANKL.
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spelling Evolution of Circulating Bone-Related Biomarkers After Kidney TransplantationMedicina clínicaClinical medicineAim: Bone disease after kidney transplant (KT) results from multiple factors, including previous bone and mineral metabolism disturbances and effects from transplant-related medications. New biomolecules have been recently associated with the development and progression of the chronic kidney disease-associated bone and mineral disorder (CKD-MBD). These include sclerostin and the soluble receptor activator of nuclear factor-kB ligand (sRANKL). Methods: To better understand the role of new biomarkers in post-transplant bone disease, this study was designed to prospectively evaluate and correlate results from the histomorphometric analysis of bone biopsies after KT with emerging serum biomarkers of the CKD-MBD: sclerostin, Dickkopf-related protein 1 (Dkk-1), sRANKL and osteoprotegerin (OPG). Results: Our data shows a significant increase in plasma levels of bioactive sclerostin after KT accompanied by a significant reduction in plasma levels of Dkk-1, suggesting a promotion of the inhibition of bone formation by osteoblasts through the activation of these inhibitors of the Wnt signaling pathway. In addition, we found a significant increase in plasma levels of free sRANKL after KT accompanied by a significant reduction in plasma levels of its decoy receptor OPG, suggesting an enhanced bone reabsorption by osteoclasts mediated by this mechanism. Conclusions: Taken together, these results suggest that the loss of bone volume observed after KT could be related mainly with the inhibition of bone formation mediated by sclerostin accompanied by an enhanced bone reabsorption mediated by sRANKL.2021-05-282021-05-28T00:00:00Zinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/masterThesisapplication/pdfhttps://hdl.handle.net/10216/134330porJuliana Carvalho Magalhãesinfo:eu-repo/semantics/openAccessreponame:Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos)instname:Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informaçãoinstacron:RCAAP2023-11-29T15:12:50Zoai:repositorio-aberto.up.pt:10216/134330Portal AgregadorONGhttps://www.rcaap.pt/oai/openaireopendoar:71602024-03-20T00:18:08.951895Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) - Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informaçãofalse
dc.title.none.fl_str_mv Evolution of Circulating Bone-Related Biomarkers After Kidney Transplantation
title Evolution of Circulating Bone-Related Biomarkers After Kidney Transplantation
spellingShingle Evolution of Circulating Bone-Related Biomarkers After Kidney Transplantation
Juliana Carvalho Magalhães
Medicina clínica
Clinical medicine
title_short Evolution of Circulating Bone-Related Biomarkers After Kidney Transplantation
title_full Evolution of Circulating Bone-Related Biomarkers After Kidney Transplantation
title_fullStr Evolution of Circulating Bone-Related Biomarkers After Kidney Transplantation
title_full_unstemmed Evolution of Circulating Bone-Related Biomarkers After Kidney Transplantation
title_sort Evolution of Circulating Bone-Related Biomarkers After Kidney Transplantation
author Juliana Carvalho Magalhães
author_facet Juliana Carvalho Magalhães
author_role author
dc.contributor.author.fl_str_mv Juliana Carvalho Magalhães
dc.subject.por.fl_str_mv Medicina clínica
Clinical medicine
topic Medicina clínica
Clinical medicine
description Aim: Bone disease after kidney transplant (KT) results from multiple factors, including previous bone and mineral metabolism disturbances and effects from transplant-related medications. New biomolecules have been recently associated with the development and progression of the chronic kidney disease-associated bone and mineral disorder (CKD-MBD). These include sclerostin and the soluble receptor activator of nuclear factor-kB ligand (sRANKL). Methods: To better understand the role of new biomarkers in post-transplant bone disease, this study was designed to prospectively evaluate and correlate results from the histomorphometric analysis of bone biopsies after KT with emerging serum biomarkers of the CKD-MBD: sclerostin, Dickkopf-related protein 1 (Dkk-1), sRANKL and osteoprotegerin (OPG). Results: Our data shows a significant increase in plasma levels of bioactive sclerostin after KT accompanied by a significant reduction in plasma levels of Dkk-1, suggesting a promotion of the inhibition of bone formation by osteoblasts through the activation of these inhibitors of the Wnt signaling pathway. In addition, we found a significant increase in plasma levels of free sRANKL after KT accompanied by a significant reduction in plasma levels of its decoy receptor OPG, suggesting an enhanced bone reabsorption by osteoclasts mediated by this mechanism. Conclusions: Taken together, these results suggest that the loss of bone volume observed after KT could be related mainly with the inhibition of bone formation mediated by sclerostin accompanied by an enhanced bone reabsorption mediated by sRANKL.
publishDate 2021
dc.date.none.fl_str_mv 2021-05-28
2021-05-28T00:00:00Z
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