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- W3023978302 abstract "Publisher SummaryThis chapter discusses renal osteodystrophy. When the life of a patient with advanced renal failure is prolonged, either through conservative therapy or renal replacement with dialysis, renal osteodystrophy may arise as a formidable consequence. The increased secretion of parathyroid hormone, which occurs in renal insufficiency, is a major factor leading to altered skeletal structure and may even contribute to other uremic symptoms. The pathogenesis of osteomalacia or the defective mineralization seen in patients with advanced renal failure is less certain than are the factors leading to secondary hyperparathyroidism and osteitis fibrosa; osteomalacia arises because of the altered vitamin D metabolism. Alternations in collagen synthesis or in crystal maturation may also contribute to osteomalacia or be an integral component of this skeletal abnormality. Other factors in patients with advanced renal failure lead to alterations in skeletal mineralization. These include magnesium accumulation, chronic acidosis, an increase in skeletal pyrophosphate, regular treatment with heparin, and reduced bone bicarbonate. Another factor that has been implicated as a possible contributor to the development of pure osteomalacia and the low rate of bone turnover is the presence of low levels of parathyroid hormone (PTH). In addition, the lack of hypophosphatemia could be a factor that prevents the development of osteomalacia in many uremic patients. The use of precise and careful radiographic techniques can improve substantially the sensitivity and precision of the X-ray examination in both detecting and identifying metabolic bone disease." @default.
- W3023978302 created "2020-05-13" @default.
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- W3023978302 date "1982-01-01" @default.
- W3023978302 modified "2023-09-25" @default.
- W3023978302 title "Renal osteodystrophy" @default.
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- W3023978302 doi "https://doi.org/10.1016/b978-0-407-02273-7.50012-9" @default.
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