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The kidneys play a crucial role in the regulation of mineral metabolism by serving both excretory and endocrine functions. Each of these components becomes compromised as renal function declines. In the broadest sense, the term renal osteodystrophy encompasses all of the disorders of bone and mineral metabolism that are associated with chronic kidney disease (CKD). Often, however, the term is used more narrowly to describe the various skeletal disorders and their histologic manifestations among patients with renal dysfunction.

Disturbances in calcium, phosphorus, and vitamin D metabolism, alterations in the regulation of parathyroid hormone (PTH) synthesis and secretion, and factors that lead to the development of parathyroid gland hyperplasia are key components in the pathogenesis of renal bone disease. Additional pathogenic factors include systemic acidosis, aluminum retention, and the accumulation of β2-microglobulin (β2M) in bone and joints. The skeletal manifestations of renal bone disease in individual patients are determined ultimately by the interplay among one or more of these causative factors.

  • Disorder of bone and mineral metabolism associated with chronic renal disease.
  • Skeletal disorders associated with renal dysfunction.
  • Disturbances in calcium, phosphorus, and vitamin D metabolism.
  • Parathyroid gland hyperplasia.
  • Systemic acidosis, aluminum retention, accumulation of β2M in bone and joints.

The renal bone diseases represent a spectrum of skeletal disorders ranging from high-turnover lesions arising predominantly from excess PTH secretion to low-turnover lesions of diverse etiology that are typically associated with normal or reduced plasma PTH levels (Figure 20–1). Transitions among histologic subtypes are determined by one or more dominant pathogenic factors. Such changes can be documented by bone biopsy and quantitative bone histology, which represent the definitive method for the diagnosis of renal osteodystrophy. Because plasma PTH levels are a major determinant of bone formation and turnover among patients with CKD, alterations in parathyroid gland function play a key role in the pathogenesis and evolution of renal osteodystrophy. Other factors, however, including diabetes, age-related bone loss, postmenopausal osteoporosis, gender, and race have been recognized increasingly as potentially important additional modifiers of skeletal metabolism and bone turnover among patients undergoing dialysis regularly. Such considerations are particularly relevant given the evolving demographics of the dialysis population in the United States, which is composed increasingly of persons older than 65 years of age and those with diabetes.

Figure 20–1.

Spectrum of the renal bone diseases. PTH, parathyroid hormone.

High-Turnover Renal Bone Disease

Secondary Hyperparathyroidism

Several factors contribute to sustained increases in plasma PTH levels and, ultimately, to the development of high-turnover skeletal lesions in patients with chronic renal failure. Among these are hypocalcemia, impaired renal calcitriol, or 1,25-dihydroxyvitamin D, production, skeletal resistance to the calcemic actions of PTH, alterations in the regulation of prepro-PTH gene transcription, reductions in vitamin D receptor (VDR) and calcium-sensing receptor (CaSR) expression ...

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