Secondary hyperparathyroidism in chronic renal failure.
The metabolic bone disease associated with chronic renal failure has been described collectively by the terms "renal osteodystrophy" or "renal-glomerular-osteodystrophy" and consists of osteomalacia, osteitis fibrosa, and osteosclerosis. The skeletal abnormalities may occur either alone or in combination with one another. An increased concentration of circulating immunoreactive-parathyroid hormone (i-PTH) is a recognized feature of patients with chronic renal failure, and the values are usually much higher than those found in patients with primary hyperparathyroidism associated with a parathyroid adenoma. It must, however, be recognized that the high circulatory concentrations of parathyroid hormone found in patients with chronic renal failure are of immunoassayable material which may or may not be of biological significance in respect of activity. A disturbance in the homeostatic control mechanism governing parathyroid hormone, the secretion rate, its metabolism, and target organ resistance to its action are of major importance in the pathogenesis of some  aspects of the metabolic bone disease in patients with chronic renal failure. The pathogenesis of the secondary hyperparathyroidism of chronic renal failure, however, also involves disturbances in cholecalciferol metabolism, phosphate retention, and the uremic state per se.
D002118:Calcium / Q000378:metabolism; D002762:Cholecalciferol / Q000378:metabolism; D012080:Chronic Kidney Disease-Mineral and Bone Disorder / Q000209:etiology; D006706:Homeostasis; D006801:Humans; D006962:Hyperparathyroidism, Secondary / Q000209:etiology* / Q000378:metabolism; D007676:Kidney Failure, Chronic / Q000150:complications* / Q000378:metabolism; D010281:Parathyroid Hormone / Q000378:metabolism; D010710:Phosphates / Q000378:metabolism
D010281:Parathyroid Hormone; D010710:Phosphates; D002762:Cholecalciferol; D002118:Calcium