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Two Techniques to Create Hypoparathyroid Mice: Parathyroidectomy Using GFP Glands and Diphtheria-Toxin-Mediated Parathyroid Ablation
Published on: March 14, 2017
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Evidence for secondary hyperparathyroidism in idiopathic hypercalciuria
The Journal of Clinical Investigation
|January 1, 1973
Summary
Idiopathic hypercalciuria (IH) may involve secondary hyperparathyroidism due to a primary renal calcium handling defect. Thiazide treatment normalized parathyroid hormone (PTH) levels in patients with IH, suggesting a reversible condition.
Area of Science:
- Nephrology
- Endocrinology
- Calcium Metabolism
Background:
- Idiopathic hypercalciuria (IH) is a condition characterized by high urinary calcium excretion without a known cause.
- The relationship between IH and parathyroid hormone (PTH) levels, particularly secondary hyperparathyroidism, remains incompletely understood.
Purpose of the Study:
- To investigate the role of parathyroid hormone (PTH) in idiopathic hypercalciuria (IH).
- To explore the effects of thiazide and furosemide on PTH levels in patients with IH and healthy subjects.
Main Methods:
- Measured circulating immunoreactive parathyroid hormone (PTH) in 40 patients with IH before and during thiazide treatment.
- Administered furosemide to four normal subjects to induce hypercalciuria and measured PTH levels.
Main Results:
- 26 patients with IH had elevated PTH levels; PTH normalized with thiazide treatment.
- Furosemide-induced hypercalciuria in normal subjects elevated PTH levels similarly to those seen in IH patients.
- Thiazide did not increase serum calcium, and alimentary calcium hyperabsorption was ruled out as a cause for high PTH in IH.
Conclusions:
- IH with elevated PTH is likely secondary hyperparathyroidism, not primary hyperparathyroidism or alimentary hyperabsorption.
- A primary renal defect in calcium handling is a plausible cause for IH and associated secondary hyperparathyroidism.
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