title: Cell biology of renal osteodystrophy.
abstract: Renal osteodystrophy, a well-recognized complication of chronic renal failure, encompasses a spectrum of skeletal disorders ranging from high-turnover lesions of secondary hyperparathyroidism, the most common histologic lesion in pediatric patients with end-stage renal disease, to low-turnover lesions of adynamic renal osteodystrophy, which has become a common skeletal lesion in adults with chronic renal failure. Several advances have been made in the understanding of the pathogenesis of secondary hyperparathyroidism, particularly the critical roles of calcium, phosphorus, and vitamin D in promoting excess parathyroid hormone (PTH) synthesis and secretion, and parathyroid gland hyperplasia in renal failure. These insights will guide the development of more effective strategies for the prevention and management of renal bone disease.
authors.affiliation: Department of Pediatrics, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA.
authors.forename: Beatriz D
authors.initials: BD
authors.lastname: Kuizon
authors.forename: Isidro B
authors.initials: IB
authors.lastname: Salusky
mesh_terms: D000818:Animals; D001847:Bone Diseases / Q000209:etiology / Q000473:pathology; D012080:Chronic Kidney Disease-Mineral and Bone Disorder / Q000473:pathology* / Q000503:physiopathology; D006132:Growth Plate / Q000473:pathology; D006801:Humans; D010280:Parathyroid Glands / Q000473:pathology / Q000503:physiopathology; D051437:Renal Insufficiency / Q000473:pathology / Q000503:physiopathology