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Integral pharmacological management of bone mineral disorders in chronic kidney disease (part I): from treatment of phosphate imbalance to control of PTH and prevention of progression of cardiovascular calcification

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dc.creator Bover, Jordi
dc.creator Ureña-Torres, Pablo
dc.creator Lloret, María Jesús
dc.creator Ruiz-García, C.
dc.creator DaSilva, I.
dc.creator Diaz-Encarnacion, MM.
dc.creator Mercado, C.
dc.creator Mateu, S.
dc.creator Fernández i Giráldez, Elvira
dc.creator Ballarín, José
dc.date 2016-06-17
dc.date.accessioned 2025-11-03T12:17:38Z
dc.date.available 2025-11-03T12:17:38Z
dc.identifier https://doi.org/10.1080/14656566.2016.1182155
dc.identifier 1465-6566
dc.identifier http://hdl.handle.net/10459.1/63216
dc.identifier.uri http://fima-docencia.ub.edu:8080/xmlui/handle/123456789/24558
dc.description NTRODUCTION: Chronic kidney disease-mineral and bone disorders (CKD-MBD), involving a triad of laboratory and bone abnormalities, and tissue calcifications, are associated with dismal hard-outcomes. AREAS COVERED: In two comprehensive articles, we review contemporary and future pharmacological options for treatment of phosphate (P) imbalance (this part 1) and hyperparathyroidism (part 2), taking into account CKD-accelerated atheromatosis/atherosclerosis and/or cardiovascular calcification (CVC) processes. EXPERT OPINION: Improvements in CKD-MBD require an integral approach, addressing all three components of the CKD-MBD triad. Individualization of treatment with P-binders and combinations of anti-parathyroid agents may improve biochemical control with lower incidence of undesirable effects. Isolated biochemical parameters do not accurately reflect calcium or P load or bone activity and do not stratify high cardiovascular risk patients with CKD. Initial guidance is provided on reasonable therapeutic strategies which consider the presence of CVC. This part reflects that although there is not an absolute evidence, many studies point to the need to improve P imbalance while trying to, at least, avoid progression of CVC by restriction of Ca-based P-binders if economically feasible. The availability of new drugs (i.e. inhibitors of intestinal transporters), and studies including early CKD should ultimately lead to clearer and more cost/effective clinical targets for CKD-MBD.
dc.description Dr Jordi Bover belongs to the Spanish National Network of Kidney Research RedinRen (RD06/0016/0001 and RD12/0021/0033) and the Spanish National Biobank network RD09/0076/00064. Dr Jordi Bover also belongs to the Catalan Nephrology Research Group AGAUR 2009 SGR-1116. Dr Jordi Bover and Dr. M.M. Diaz-Encarnacion collaborate with the Spanish “Fundación Iñigo Alvarez de Toledo” (FRIAT).
dc.format application/pdf
dc.language eng
dc.publisher Taylor & Francis
dc.relation Versió postprint del document publicat a: https://doi.org/10.1080/14656566.2016.1182155
dc.relation Expert Opinion On Pharmacotherapy, 2016, vol. 17, num. 9, p. 1247-1258
dc.rights (c) Taylor & Francis, 2016
dc.rights info:eu-repo/semantics/openAccess
dc.subject Chronic kidney disease
dc.subject CKD-MBD
dc.subject Phosphate
dc.title Integral pharmacological management of bone mineral disorders in chronic kidney disease (part I): from treatment of phosphate imbalance to control of PTH and prevention of progression of cardiovascular calcification
dc.title Integral pharmacological management of CKD-MBD I
dc.type info:eu-repo/semantics/article
dc.type info:eu-repo/semantics/acceptedVersion


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