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.contributor.authorBover, Jordi
dc.contributor.authorUreña-Torres, Pablo
dc.contributor.authorLloret, María Jesús
dc.contributor.authorRuiz-García, C.
dc.contributor.authorDaSilva, I.
dc.contributor.authorDiaz-Encarnacion, MM.
dc.contributor.authorMercado, C.
dc.contributor.authorMateu, S.
dc.contributor.authorFernández i Giráldez, Elvira
dc.contributor.authorBallarín, José
dc.date.accessioned2018-04-30T08:27:29Z
dc.date.available2018-04-30T08:27:29Z
dc.date.issued2016-06-17
dc.date.updated2018-04-30T08:27:29Z
dc.description.abstractNTRODUCTION: 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.sponsorshipDr 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.mimetypeapplication/pdf
dc.identifier.doihttps://doi.org/10.1080/14656566.2016.1182155
dc.identifier.idgrec025666
dc.identifier.issn1465-6566
dc.identifier.urihttp://hdl.handle.net/10459.1/63216
dc.language.isoeng
dc.publisherTaylor & Francis
dc.relation.isformatofVersió postprint del document publicat a: https://doi.org/10.1080/14656566.2016.1182155
dc.relation.ispartofExpert Opinion On Pharmacotherapy, 2016, vol. 17, num. 9, p. 1247-1258
dc.rights(c) Taylor & Francis, 2016
dc.rights.accessRightsinfo:eu-repo/semantics/openAccess
dc.subjectChronic kidney disease
dc.subjectCKD-MBD
dc.subjectPhosphate
dc.titleIntegral 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.alternativeIntegral pharmacological management of CKD-MBD I
dc.typeinfo:eu-repo/semantics/article
dc.type.versioninfo:eu-repo/semantics/acceptedVersion
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