Renal osteodystrophy and vitamin D derivatives: cellular mechanisms of hyperparathyroidism in uremia.
In the early phase of chronic renal failure, physiological concentrations of 1,25(OH)2D in circulation may become insufficient to regulate parathyroid cell function normally. As a result, the set-point of PTH secretion to plasma Ca ion concentration shifts to the right, PTH synthesis becomes enhanced at transcriptional level, and parathyroid cells begin to proliferate. This resistance of the parathyroid cells to the physiological concentration of 1,25(OH)2D may be in part due to the reduction of 1,25(OH)2D receptor density in parathyroid cells. However, the mechanism by which the number of 1,25(OH)2D receptors decreases in parathyroid cells in early renal failure remains to be elucidated.
Fukagawa
M
M
First Department of Internal Medicine, University of Tokyo Faculty of Medicine, Japan.
Kurokawa
K
K
D002117:Calcitriol / Q000008:administration & dosage; D002455:Cell Division / Q000502:physiology; D012080:Chronic Kidney Disease-Mineral and Bone Disorder / Q000188:drug therapy* / Q000209:etiology; D006801:Humans; D006962:Hyperparathyroidism, Secondary / Q000188:drug therapy* / Q000209:etiology; D007676:Kidney Failure, Chronic / Q000150:complications / Q000378:metabolism / Q000628:therapy*; D010280:Parathyroid Glands / Q000166:cytology; D010281:Parathyroid Hormone / Q000096:biosynthesis / Q000378:metabolism; D018167:Receptors, Calcitriol; D011987:Receptors, Steroid / Q000378:metabolism; D006435:Renal Dialysis / Q000009:adverse effects*; D014511:Uremia / Q000209:etiology / Q000628:therapy*
D010281:Parathyroid Hormone; D018167:Receptors, Calcitriol; D011987:Receptors, Steroid; D002117:Calcitriol