Renal osteodystrophy, phosphate homeostasis, and vascular calcification.

Abstract:

: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.

journal_name

Semin Dial

journal_title

Seminars in dialysis

authors

Hruska KA,Saab G,Mathew S,Lund R

doi

10.1111/j.1525-139X.2007.00300.x

subject

Has Abstract

pub_date

2007-07-01 00:00:00

pages

309-15

issue

4

eissn

0894-0959

issn

1525-139X

pii

SDI300

journal_volume

20

pub_type

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