The bone-vascular axis in chronic kidney disease.
OBJECTIVE
This review highlights the most recent publications addressing the relationship between bone and vascular calcification in patients with chronic and end-stage kidney disease.


RESULTS
The relatively new term 'chronic kidney disease-mineral bone disorder' reflects the growing reach of chronic kidney disease research into the realm of systems physiology, involving a triad of renal, skeletal, and vascular tissues. Recent studies address underlying mechanisms of the bone and vascular complications of chronic kidney disease and point to a variety of biochemical factors, including phosphatonins (fibroblast growth factor-23, matrix extracellular phosphoglycoprotein), bone morphogenetic protein 7, osteoprotegerin, matrix GLA protein, ectonucleotide pyrophosphatase/phosphodiesterase 1, alkaline phosphatase, and lipid oxidation products. Studies also demonstrate that agents used for treatment of one component of the triad often act on the other components of the triad - beneficially or adversely. These findings emphasize the importance of avoiding the subspecialty, single organ viewpoint when treating individual components of chronic kidney disease-mineral bone disorder.


CONCLUSIONS
The consistent synchrony among chronic kidney disease, aortic calcification, and bone loss offers clues to underlying mechanisms for the systemic abnormalities.
Department of Medicine, University of California, Los Angeles, California 90095-1679, USA. Ldemer@mednet.ucla.edu
Linda
L
Demer
Yin
Y
Tintut
D000818:Animals; D001808:Blood Vessels / Q000187:drug effects / Q000473:pathology*; D001842:Bone and Bones / Q000187:drug effects / Q000473:pathology*; D004195:Disease Models, Animal; D006801:Humans; D007676:Kidney Failure, Chronic / Q000188:drug therapy / Q000473:pathology*