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Renal osteodystrophy or renal bone disease is one of the most common and potentially debilitating complications affecting patients with chronic renal insufficiency both before and after the initiation of maintenance dialysis. The term is used to describe the wide spectrum of skeletal abnormalities encountered in the setting of impaired renal function, which range from states of high to low bone turnover such as osteitis fibrosa cystica and adynamic bone disease, respectively.1,2Osteitis fibrosa results from high circulating levels of parathyroid hormone (PTH), which may occur in patients with only mild reductions in renal function. The principal factors involved in the pathogenesis of the secondary hyperparathyroidism of chronic renal failure include retention of serum phosphorus because of reduced renal function, altered production of 1,25 (OH)2 vitamin D3 (calcitriol) by the kidney, abnormal parathyroid growth and function, and resistance to the calcemic effect of PTH. Bone histology in osteitis fibrosa is characterized by increased osteoclast number and increased bone resorption, as well as increased osteoblast number and bone formation. In contrast, adynamic bone disease is a low bone turnover state, which is being increasingly recognized in patients on long-term dialysis, and is now a major category of abnormal bone histology in patients with renal disease. The pathogenesis of this entity is not well understood. However, it is possible that it represents oversuppression of bone turnover as a consequence of the increased use of calcitriol and calcium salts.1-3Our understanding of the pathogenesis of renal osteodystrophy has provided the basis for the management of patients with this disorder. Thus, the prevention and treatment of hyperparathyroidism centers around the control of serum phosphorus and the administration of vitamin D compounds. The former is accomplished by dietary phosphorus restriction and the administration of intestinal phosphate binders, and the latter involves the …
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