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Article: Calcium balance and negative impact of calcium load in peritoneal dialysis patients

TitleCalcium balance and negative impact of calcium load in peritoneal dialysis patients
Authors
KeywordsCalcium balance
Issue Date2014
Citation
Peritoneal Dialysis International, 2014, v. 34, n. 4, p. 345-352 How to Cite?
Abstract© 2014 International Society for Peritoneal DialysisLike hemodialysis patients, peritoneal dialysis (PD) patients are facing an excessively increased burden of vascular and valvular calcification. According to some surveys, more than 80% of prevalent PD patients are complicated with vascular calcification, and more than one third have heart valve calcification. Dysregulated phosphate metabolism is well recognized to play an important rolein inducing vascular calcification, but increasing evidence is suggesting that dysregulated calcium metabolism also promotes vascular calcification and might in fact be more potent than phosphate in inducing that calcification. Growing evidence from randomized controlled trials shows more progression of vascular calcification and higher mortality among chronic kidney disease (CKD) patients receiving calcium-based phosphate binders than among those receiving non-calcium-containing phosphate binders. Those results raise important safety concern about the use of high-dose calcium-based phosphate binders in the CKD population, including both non-dialysis and dialysis patients (especially anuric dialysis patients), who have markedly reduced urinary calcium excretion. To prevent calcium overload, this review recommends restricting the dose of calcium-based phosphate binders in CKD patients, especially those who are elderly, who have increased cardiovascular risk, who already have baseline vascular or valvular calcification, or who have low intact parathyroid hormone and adynamic bone disease.
Persistent Identifierhttp://hdl.handle.net/10722/228481
ISSN
2015 Impact Factor: 1.298
2015 SCImago Journal Rankings: 0.683

 

DC FieldValueLanguage
dc.contributor.authorWang, Angela Yee Moon-
dc.date.accessioned2016-08-13T08:02:31Z-
dc.date.available2016-08-13T08:02:31Z-
dc.date.issued2014-
dc.identifier.citationPeritoneal Dialysis International, 2014, v. 34, n. 4, p. 345-352-
dc.identifier.issn0896-8608-
dc.identifier.urihttp://hdl.handle.net/10722/228481-
dc.description.abstract© 2014 International Society for Peritoneal DialysisLike hemodialysis patients, peritoneal dialysis (PD) patients are facing an excessively increased burden of vascular and valvular calcification. According to some surveys, more than 80% of prevalent PD patients are complicated with vascular calcification, and more than one third have heart valve calcification. Dysregulated phosphate metabolism is well recognized to play an important rolein inducing vascular calcification, but increasing evidence is suggesting that dysregulated calcium metabolism also promotes vascular calcification and might in fact be more potent than phosphate in inducing that calcification. Growing evidence from randomized controlled trials shows more progression of vascular calcification and higher mortality among chronic kidney disease (CKD) patients receiving calcium-based phosphate binders than among those receiving non-calcium-containing phosphate binders. Those results raise important safety concern about the use of high-dose calcium-based phosphate binders in the CKD population, including both non-dialysis and dialysis patients (especially anuric dialysis patients), who have markedly reduced urinary calcium excretion. To prevent calcium overload, this review recommends restricting the dose of calcium-based phosphate binders in CKD patients, especially those who are elderly, who have increased cardiovascular risk, who already have baseline vascular or valvular calcification, or who have low intact parathyroid hormone and adynamic bone disease.-
dc.languageeng-
dc.relation.ispartofPeritoneal Dialysis International-
dc.subjectCalcium balance-
dc.titleCalcium balance and negative impact of calcium load in peritoneal dialysis patients-
dc.typeArticle-
dc.description.natureLink_to_subscribed_fulltext-
dc.identifier.doi10.3747/pdi.2013.00177-
dc.identifier.pmid24497596-
dc.identifier.scopuseid_2-s2.0-84925883334-
dc.identifier.volume34-
dc.identifier.issue4-
dc.identifier.spage345-
dc.identifier.epage352-
dc.identifier.eissn1718-4304-

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