1995New England Journal of MedicineRequires access

Renal Osteodystrophy

Keith A. Hruska, Steven L. Teitelbaum

Open publisher page 404 citations

Abstract

Renal osteodystrophy, the term used to describe the skeletal complications of end-stage renal disease, is a multifactorial disorder of bone remodeling. The actions of some of the factors involved are well defined, and successful strategies have been designed to prevent them. For example, the identification of secondary hyperparathyroidism and 1α,25-dihydroxycholecalciferol (1α,25-dihydroxyvitamin D3) deficiency as major contributors to renal osteodystrophy has led to the development of treatment regimens that can maintain normal serum calcium and phosphate concentrations, reduce parathyroid hormone secretion, and correct a deficiency of 1α,25-dihydroxycholecalciferol. These improvements in treatment have resulted in decreases in the frequency and . . .

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Renal osteodystrophy, the term used to describe the skeletal complications of end-stage renal disease, is a multifactorial disorder of bone remodeling. The actions of some of the factors involved are well defined, and successful strategies have been designed to prevent them. For example, the identification of secondary hyperparathyroidism and 1α,25-dihydroxycholecalciferol (1α,25-dihydroxyvitamin D3) deficiency as major contributors to renal osteodystrophy has led to the development of treatment regimens that can maintain normal serum calcium and phosphate concentrations, reduce parathyroid hormone secretion, and correct a deficiency of 1α,25-dihydroxycholecalciferol. These improvements in treatment have resulted in decreases in the frequency and . . .

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Available abstract

Renal osteodystrophy, the term used to describe the skeletal complications of end-stage renal disease, is a multifactorial disorder of bone remodeling. The actions of some of the factors involved are well defined, and successful strategies have been designed to prevent them. For example, the identification of secondary hyperparathyroidism and 1α,25-dihydroxycholecalciferol (1α,25-dihydroxyvitamin D3) deficiency as major contributors to renal osteodystrophy has led to the development of treatment regimens that can maintain normal serum calcium and phosphate concentrations, reduce parathyroid hormone secretion, and correct a deficiency of 1α,25-dihydroxycholecalciferol. These improvements in treatment have resulted in decreases in the frequency and . . .

Key concepts: Renal osteodystrophy, Secondary hyperparathyroidism, Parathyroid hormone, Medicine, Osteodystrophy, Chronic kidney disease-mineral and bone disorder, Endocrinology, Internal medicine

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