Could Bone Biomarkers Predict Bone Turnover after Kidney Transplantation?-A Proof-of-Concept Study

• Tipo: Artigo em Revista Científica Internacional
• Data: 2022

Autores

Magalhaes, J (Autor) Outra; Quelhas Santos, J (Autor) FMUP; Pereira, L (Autor) Outra; Ricardo Neto (Autor) FMUP; Castro Ferreira, I (Autor) Outra; Martins, S (Autor) Outra; João Frazão (Autor) FMUP; Carvalho, C (Autor) Outra

Revista

Título: Journal of Clinical Medicine

Vol. 11

Página Final: 457

ISSN: 2077-0383

Editora: MDPI

Indexação

ISI Web of Knowledge - 3 Citações

Scopus - 4 Citações

Outras Informações

ID Authenticus: P-00V-ZC6

DOI: 10.3390/jcm11020457

Abstract (EN): Aim: Bone disease after kidney transplant (KT) results from multiple factors, including previous bone and mineral metabolism disturbances and effects of 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 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 osteo-protegerin (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 resorption by osteoclasts mediated by this mechanism. Conclusions: Taken together, these results suggest that the loss of bone volume observed after KT could be explain mainly by the inhibition of bone formation mediated by sclerostin accompanied by an enhanced bone resorption mediated by sRANKL.

Idioma: Inglês

Tipo (Avaliação Docente): Científica

Nº de páginas: 14