
| 10.1007/BF03350753
http://scihub22266oqcxt.onion/10.1007/BF03350753
 2592738!�!2592738
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J+Endocrinol+Invest 1989 ; 12 (8): 531-5 Nephropedia Template TP
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Direct tubular effect on calcium retention by hydrochlorothiazide #MMPMID2592738Krause U; Zielke A; Schmidt-Gayk H; Ehrenthal W; Beyer JJ Endocrinol Invest 1989[Sep]; 12 (8): 531-5 PMID2592738show ga
Previous studies with hydrochlorothiazide revealed a calcium retaining effect of this substance. The mechanism by what this is done is still matter of controverse discussion. Effects of hydrochlorothiazide on vitamin D metabolism have been reported as well as those on parathyroid function. To further clarify the calcium retaining potency of hydrochlorothiazide (HCTZ) we treated 10 healthy young volunteers for four weeks with 2 x 50 mg HCTZ. In all volunteers we observed a marked decrease in urinary calcium excretion as well as in calcium clearance. Furthermore, we found a slight rise in ionized serum calcium (6.7%) and in intact PTH, as well as a 36% drop in 1,25-(OH)2-D3-levels. These effects were reversible after discontinuation of the treatment. No change was observed in urinary cAMP, phosphate excretion, serum anorganic phosphate levels, serum calcitonin and magnesium levels. Data presented here suggest that treatment with HCTZ causes a persistent reduction in calcium excretion through direct tubular effects, inhibits hydroxylation of vitamin D, and does not affect parathyroid function.|Adult[MESH]|Alkaline Phosphatase/blood[MESH]|Calcium/blood/*metabolism/urine[MESH]|Creatinine/blood[MESH]|Humans[MESH]|Hydrochlorothiazide/*pharmacology[MESH]|Kidney Tubules/drug effects/*physiology[MESH]|Magnesium/blood[MESH]|Parathyroid Hormone/metabolism[MESH]|Phosphates/blood[MESH]
  
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