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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Is there an optimal parathyroid hormone level in end-stage renal failure: the lower the better?

Skeletal resistance to parathyroid hormone is well defined in patients with chronic renal failure. In recent years, with the increased frequency of development of adynamic bone disease, it has been recognized that secondary hyperparathyroidism must exist as a 'trade off' mechanism to maintain skeletal bone remodeling in this patient population. An optimal level of intact parathyroid hormone to maintain the normal skeletal bone turnover is believed to be between 2.0 and 2.5 times the upper limit of normal parathyroid hormone. It has very recently been argued that the optimal parathyroid hormone level for maintenance of skeletal bone remodeling may be insufficient to prevent the extraskeletal complications of coronary artery calcifications, calcific valvular heart disease, and cardiac death. To provide optimal health care for these patients several new treatments have been developed, including use of new vitamin D analogs, calcimimetic agents, and noncalcium-based phosphorus binders. It is anticipated that with lower suppression of parathyroid hormone by these vitamin D analogs, intermittent suppression of parathyroid hormone with calcimimetic agents, and the use of noncalcium phosphorus binders (Renageltrade) by regulating serum calcium, the resultant phosphorus concentrations will provide an optimal parathyroid hormone activity to maintain skeletal bone remodeling, while preventing extraskeletal complications.[1]


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