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PHOSPHORUS METABOLISM AND MANAGEMENT IN CHRONIC KIDNEY DISEASE: Renal Osteodystrophy, Phosphate Homeostasis, and Vascular Calcification
Author(s) -
Hruska Keith A.,
Saab Georges,
Mathew Suresh,
Lund Richard
Publication year - 2007
Publication title -
seminars in dialysis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.899
H-Index - 78
eISSN - 1525-139X
pISSN - 0894-0959
DOI - 10.1111/j.1525-139x.2007.00300.x
Subject(s) - hyperphosphatemia , renal osteodystrophy , medicine , kidney disease , secondary hyperparathyroidism , parathyroid hormone , endocrinology , bone remodeling , chronic kidney disease mineral and bone disorder , kidney , vitamin d and neurology , hyperparathyroidism , calcium
New advances in the pathogenesis of renal osteodystrophy (ROD) change the perspective from which many of its features and treatment are viewed. Calcium, phosphate, parathyroid hormone (PTH), and vitamin D have been shown to be important determinants of survival associated with kidney diseases. Now ROD dependent and independent of these factors is linked to survival more than just skeletal frailty. This review focuses on recent discoveries that renal injury impairs skeletal anabolism decreasing the osteoblast compartment of the skeleton and consequent bone formation. This discovery and the discovery that PTH regulates the hematopoietic stem cell niche alters our view of secondary hyperparathyroidism in chronic kidney disease (CKD) from that of a disease to that of a necessary adaptation to renal injury that goes awry. Furthermore, ROD is shown to be an underappreciated factor in the level of the serum phosphorus in CKD. The discovery and the elucidation of the mechanism of hyperphosphatemia as a cardiovascular risk in CKD change the view of ROD. It is now recognized as more than a skeletal disorder, it is an important component of the mortality of CKD that can be treated.