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Division of Nephrology and Hypertension and Department of Medicine, Hadassah Medical Organization, Hebrew University, Ein-Karem, Jerusalem, Israel
Correspondence to: A. Gal-Moscovici, Division of Nephrology and Hypertension, Hadassah Medical Organization, POB 12000, Jerusalem 91120 Israel. galanca{at}hadassah.org.il
Bone disease is one of the most challenging complications in patients
with chronic kidney disease. Today, it is considered to be part of a complex
systemic disorder manifested by disturbances of mineral metabolism and
vascular calcifications called chronic kidney disease – mineral bone
disorder (CKD-MBD).
The term renal osteodystrophy is reserved to define the specific bone
lesion in CKD-MBD, whose spectrum ranges from high turnover to low turnover
disease. Phosphate retention, decreased serum calcium, and 1,25-dihydroxy
vitamin D synthesis are involved in the pathogenesis of high bone turnover.
However, the various therapeutic approaches (calcium supplements, phosphate
binders, and vitamin D metabolites, among others), the renal replacement
modality (hemodialysis or continuous ambulatory peritoneal dialysis), and the
types of patients to whom dialysis is offered (more patients who are diabetic
or older, or both) may influence the evolution of the bone disorder. As a
result, recent studies have reported a greater prevalence of adynamic forms of
renal osteodystrophy, especially in diabetic and peritoneal dialysis
patients.
The present article reviews, for patients treated with peritoneal
dialysis, the pathophysiologic mechanisms involved in the evolution and
perpetuation of this bone disease and the therapeutic modalities for treating
and preventing adynamic bone.
KEY WORDS: Adynamic bone; diabetes; AGEs; histomorphometry.
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