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Title
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Sclerostin in chronic kidney diseasemineral bone disorder : think first before you block it!
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Author
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Abstract
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| Canonical Wnt signalling activity is a major player in physiological and adaptive bone metabolism. Wnt signalling is regulated by soluble inhibitors, with sclerostin being the most widely studied. Sclerostins main origin is the osteocyte and its major function is blockade of osteoblast differentiation and function. Therefore, sclerostin is a potent inhibitor of bone formation and mineralization. Consequently, blocking sclerostin via human monoclonal antibodies (such as romosozumab) represents a promising perspective for the treatment of (postmenopausal) osteoporosis. However, sclerostins physiology and the effects of sclerostin monoclonal antibody treatment are not limited to the skeleton. Specifically, the potential roles of sclerostin in chronic kidney disease (CKD) and associated pathologies covered by the term chronic kidney disease and mineral bone disorder (CKD-MBD), which also includes accelerated cardiovascular calcification, warrant specific attention. CKD-MBD is a complex disease condition in which sclerostin antibodies may interfere at different levels and influence the multiform interplay of hyperparathyroidism, renal osteodystrophy and vascular calcification, but the clinical sequelae remain obscure. The present review summarizes the potential effects of sclerostin blockade in CKD-MBD. We will address and summarize the urgent research targets that are being identified and that need to be addressed before a valid riskbenefit ratio can be established in the clinical setting of CKD. |
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Language
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English
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Source (journal)
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Nephrology, dialysis, transplantation. - Berlin
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Publication
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Oxford
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Oxford univ press
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2019
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ISSN
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0931-0509
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DOI
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10.1093/NDT/GFY129
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Volume/pages
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34
:3
(2019)
, p. 408-414
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ISI
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000461162000008
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Pubmed ID
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29846712
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Full text (Publisher's DOI)
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Full text (open access)
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