Hyperphosphatemia of chronic kidney disease

Keith A. Hruska; Suresh Mathew; Richard Lund; Ping Qiu; Raymond Pratt

doi:10.1038/ki.2008.130

Hyperphosphatemia of chronic kidney disease

Keith A. Hruska, Suresh Mathew, Richard Lund, Ping Qiu, Raymond Pratt

Research output: Contribution to journal › Short survey › peer-review

353 Scopus citations

Abstract

Observational studies have determined hyperphosphatemia to be a cardiovascular risk factor in chronic kidney disease. Mechanistic studies have elucidated that hyperphosphatemia is a direct stimulus to vascular calcification, which is one cause of morbid cardiovascular events contributing to the excess mortality of chronic kidney disease. This review describes the pathobiology of hyperphosphatemia that develops as a consequence of positive phosphate balance in chronic kidney disease and the mechanisms by which hyperphosphatemia acts on neointimal vascular cells that are stimulated to mineralize in chronic kidney disease. The characterization of hyperphosphatemia of chronic kidney disease as a distinct syndrome in clinical medicine with unique disordered skeletal remodeling, heterotopic mineralization and cardiovascular morbidity is presented.

Original language	English
Pages (from-to)	148-157
Number of pages	10
Journal	Kidney International
Volume	74
Issue number	2
DOIs	https://doi.org/10.1038/ki.2008.130
State	Published - Jul 2008

Keywords

CKD
Osteoblasts
Phosphate
Renal osteodystrophy
Vascular calcification
Vascular smooth muscle cells

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10.1038/ki.2008.130

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title = "Hyperphosphatemia of chronic kidney disease",

abstract = "Observational studies have determined hyperphosphatemia to be a cardiovascular risk factor in chronic kidney disease. Mechanistic studies have elucidated that hyperphosphatemia is a direct stimulus to vascular calcification, which is one cause of morbid cardiovascular events contributing to the excess mortality of chronic kidney disease. This review describes the pathobiology of hyperphosphatemia that develops as a consequence of positive phosphate balance in chronic kidney disease and the mechanisms by which hyperphosphatemia acts on neointimal vascular cells that are stimulated to mineralize in chronic kidney disease. The characterization of hyperphosphatemia of chronic kidney disease as a distinct syndrome in clinical medicine with unique disordered skeletal remodeling, heterotopic mineralization and cardiovascular morbidity is presented.",

keywords = "CKD, Osteoblasts, Phosphate, Renal osteodystrophy, Vascular calcification, Vascular smooth muscle cells",

author = "Hruska, {Keith A.} and Suresh Mathew and Richard Lund and Ping Qiu and Raymond Pratt",

note = "Funding Information: This work and the studies reported here were supported by NIH Grants DK070790 and AR41677, and by grants-in-aid from Genzyme and Shire. KAH received consultation fees from Genzyme and Shire Pharmaceutical. PQ and RP are employees of Shire Pharmaceuticals. SM received consultation fees from Genzyme, and RL received consultation fees from Abbott. ",

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doi = "10.1038/ki.2008.130",

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AU - Hruska, Keith A.

AU - Mathew, Suresh

AU - Lund, Richard

AU - Qiu, Ping

AU - Pratt, Raymond

N1 - Funding Information: This work and the studies reported here were supported by NIH Grants DK070790 and AR41677, and by grants-in-aid from Genzyme and Shire. KAH received consultation fees from Genzyme and Shire Pharmaceutical. PQ and RP are employees of Shire Pharmaceuticals. SM received consultation fees from Genzyme, and RL received consultation fees from Abbott.

PY - 2008/7

Y1 - 2008/7

N2 - Observational studies have determined hyperphosphatemia to be a cardiovascular risk factor in chronic kidney disease. Mechanistic studies have elucidated that hyperphosphatemia is a direct stimulus to vascular calcification, which is one cause of morbid cardiovascular events contributing to the excess mortality of chronic kidney disease. This review describes the pathobiology of hyperphosphatemia that develops as a consequence of positive phosphate balance in chronic kidney disease and the mechanisms by which hyperphosphatemia acts on neointimal vascular cells that are stimulated to mineralize in chronic kidney disease. The characterization of hyperphosphatemia of chronic kidney disease as a distinct syndrome in clinical medicine with unique disordered skeletal remodeling, heterotopic mineralization and cardiovascular morbidity is presented.

AB - Observational studies have determined hyperphosphatemia to be a cardiovascular risk factor in chronic kidney disease. Mechanistic studies have elucidated that hyperphosphatemia is a direct stimulus to vascular calcification, which is one cause of morbid cardiovascular events contributing to the excess mortality of chronic kidney disease. This review describes the pathobiology of hyperphosphatemia that develops as a consequence of positive phosphate balance in chronic kidney disease and the mechanisms by which hyperphosphatemia acts on neointimal vascular cells that are stimulated to mineralize in chronic kidney disease. The characterization of hyperphosphatemia of chronic kidney disease as a distinct syndrome in clinical medicine with unique disordered skeletal remodeling, heterotopic mineralization and cardiovascular morbidity is presented.

KW - CKD

KW - Osteoblasts

KW - Phosphate

KW - Renal osteodystrophy

KW - Vascular calcification

KW - Vascular smooth muscle cells

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DO - 10.1038/ki.2008.130

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VL - 74

SP - 148

EP - 157

JO - Kidney International

JF - Kidney International

IS - 2

ER -

Hyperphosphatemia of chronic kidney disease

Abstract

Keywords

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