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Journal ArticleDOI

Arrest of Hyperparathyroid Bone Disease with Dihydrotachysterol in Patients Undergoing Chronic Hemodialysis

Kaye M, +3 more
- 01 Aug 1970 - 
- Vol. 73, Iss: 2, pp 225-233
TLDR
There was marked improvement in patients with active bone disease who were on a chronic dialysis program who were treated with dihydrotachysterol, 0.25 to 0.375 mg/day, probably due in part to the drug’s ability to relax the immune system.
Abstract
Six patients with active bone disease who were on a chronic dialysis program were treated with dihydrotachysterol, 0.25 to 0.375 mg/day. There was marked improvement, probably due in part ...

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Citations
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Renal osteodystrophy

汪关煜
Journal ArticleDOI

The kidney as an endocrine organ for the production of 1,25-dihydroxyvitamin D 3 , a calcium-mobilizing hormone.

TL;DR: A large number of studies have shown that high levels of vitamin D in the blood stream is beneficial for the physical and mental well-being of mice and young people.
Journal ArticleDOI

Vitamin D in solution: conformations of vitamin D3, 1alpha,25-dihydroxyvitamin D3, and dihydrotachysterol3.

TL;DR: In this article, the A and seco B rings of vitamin D(3), 1(alpha), 25-dihydroxyvitamin D (3), and dihydrotachysterol(3) have been established by high resolution, 300-megahertz proton magnetic resonance spectroscopy.
References
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Journal ArticleDOI

Modifications of a specific assay for hydroxyproline in urine

TL;DR: Several modifications of a specific chemical assay for hydroxyproline in urine are presented which make the procedure more rapid without reducing its specificity or accuracy.
Journal ArticleDOI

Caclium, phosphorus, and bone in renal disease and transplantation.

TL;DR: In patients receiving long-term hemodialysis, if hyperphosphatemia and hypocalcemia persist, PTH levels may remain high and osteitis fibrosa may progress, and severe hypercalcemia must be guarded against.
Journal ArticleDOI

The metabolic fate of vitamin D3-3H in chronic renal failure

TL;DR: The experiments support the conclusion that the resistance to therapeutic doses of vitamin D often seen in patients with chronic renal failure and renal osteodystrophy results from an acquired defect in the metabolism and excretion of Vitamin D.
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