2.50
Hdl Handle:
http://hdl.handle.net/2336/30913
Title:
Hyperphosphatemia in end-stage renal disease
Authors:
Indridason, Olafur S; Quarles, L Darryl
Citation:
Adv Ren Replace Ther. 2002, 9(3):184-92
Issue Date:
1-Jul-2002
Abstract:
Hyperphosphatemia occurs universally in end-stage renal disease (ESRD) unless efforts are made to prevent positive phosphate balance. Positive phosphate balance results from the loss of renal elimination of phosphate and continued obligatory intestinal absorption of dietary phosphate. Increased efflux of phosphate from bone because of excess parathyroid hormone-mediated bone resorption can also contribute to increased serum phosphate concentrations in the setting of severe hyperparathyroidism. It is important to treat hyperphosphatemia because it contributes to the pathogenesis of hyperparathyroidism, vascular calcifications, and increased cardiovascular mortality in ESRD patients. Attaining a neutral phosphate balance, which is the key to the management of hyperphosphatemia in ESRD, is a challenge. Control of phosphorus depends on its removal during dialysis and the limitation of gastrointestinal absorption by dietary phosphate restriction and chelation of phosphate. Knowledge of the quantitative aspects of phosphate balance is useful in optimizing our use of phosphate binders, dialysis frequency, and vitamin D sterols. The development of new phosphate binders and efforts to find new ways to inhibit gastrointestinal absorption of phosphate will lead to improvements in the control of serum phosphate levels in ESRD.

Full metadata record

DC FieldValue Language
dc.contributor.authorIndridason, Olafur S-
dc.contributor.authorQuarles, L Darryl-
dc.date.accessioned2008-07-03T14:02:02Z-
dc.date.available2008-07-03T14:02:02Z-
dc.date.issued2002-07-01-
dc.date.submitted2008-07-03-
dc.identifier.citationAdv Ren Replace Ther. 2002, 9(3):184-92en
dc.identifier.issn1073-4449-
dc.identifier.pmid12203200-
dc.identifier.urihttp://hdl.handle.net/2336/30913-
dc.description.abstractHyperphosphatemia occurs universally in end-stage renal disease (ESRD) unless efforts are made to prevent positive phosphate balance. Positive phosphate balance results from the loss of renal elimination of phosphate and continued obligatory intestinal absorption of dietary phosphate. Increased efflux of phosphate from bone because of excess parathyroid hormone-mediated bone resorption can also contribute to increased serum phosphate concentrations in the setting of severe hyperparathyroidism. It is important to treat hyperphosphatemia because it contributes to the pathogenesis of hyperparathyroidism, vascular calcifications, and increased cardiovascular mortality in ESRD patients. Attaining a neutral phosphate balance, which is the key to the management of hyperphosphatemia in ESRD, is a challenge. Control of phosphorus depends on its removal during dialysis and the limitation of gastrointestinal absorption by dietary phosphate restriction and chelation of phosphate. Knowledge of the quantitative aspects of phosphate balance is useful in optimizing our use of phosphate binders, dialysis frequency, and vitamin D sterols. The development of new phosphate binders and efforts to find new ways to inhibit gastrointestinal absorption of phosphate will lead to improvements in the control of serum phosphate levels in ESRD.en
dc.language.isoenen
dc.publisherW.B. Saunders Co.en
dc.subject.meshHumansen
dc.subject.meshHyperparathyroidism, Secondaryen
dc.subject.meshKidney Failure, Chronicen
dc.subject.meshPhosphatesen
dc.subject.meshRenal Dialysisen
dc.titleHyperphosphatemia in end-stage renal diseaseen
dc.typeArticleen
dc.contributor.departmentDepartment of Medicine, Division of Nephrology, University Hospital, Reykjavik, Iceland.en
dc.identifier.journalAdvances in renal replacement therapyen
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