The role of dietary sodium on renal excretion and intestinal absorption of calcium and on vitamin D metabolism

N. A. Breslau, J. L. McGuire, J. E. Zerwekh, C. Y C Pak

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Abstract

Earlier studies have shown that an oral sodium (Na) load may induce hypercalciuria in previously normocalciuric subjects and may also increase intestinal calcium (Ca) absorption. To probe the cause of the increased intestinal Ca absorption, we simultaneously measured parathyroid function, serum 1,25-hydroxyvitamin D [1,25-(OH)2D], and fractional intestinal 47Ca absorption before and after a salt load. Eleven normal subjects and two patients with postsurgical hypoparathyroidism were placed on a 10 meq Na, 400 mg Ca per day diet for 10 days, followed by another 10-day period in which the same diet was supplemented by 240 meq Na daily. Measurements were performed on the final 3 days of each phase. In the normal subjects, urinary Na excretion increased from 7 ± 2 to 226 ± 8 meq/day (mean ± SEM), urinary Ca rose from 110 ± 14 to 167 ± 16 mg/day, serum parathyroid hormone (PTH) increased from 20 ± 1 to 22 ± 1 μleq/ml, serum 1,25-(OH)2D rose from 38 ± 4 to 51 ± 7 pg/ml, and fractional intestinal 47Ca absorption increased from 0.39 ± 0.03 to 0.49 ± 0.03 (P < 0.05 for all changes). Serum Ca corrected for total protein did not change (9.9 ± 0.1 to 9.8 ± 0.1 mg/dl). The patients with hypoparathyroidism who were maintained on vitamin D therapy also showed increases in urinary Na (20 ± 12 to 245 ± 11 meq/day) and urinary Ca (271 ± 48 to 305 ± 43; P < 0.05). However, there were no increases in serum PTH (13 ± 1 to 11 ± 1 μleq/ml), serum 1,25-(OH)2D (44 ± 1 to 40 ± 6 pg/ml), or intestinal Ca absorption (0.41 ± 0.03 to 0.42 ± 0.05). Corrected serum Ca decreased from 9.4 ± 0.2 to 8.6 ± 0.2 mg/dl. We conclude that in normal subjects, Na-induced renal hypercalciuria is accompanied by increased 1,25-(OH)2D synthesis and enhanced intestinal Ca absorption. Since this adaptive mechanism did not occur in two patients with hypoparathyroidism, mediation by PTH is suggested.

Original languageEnglish (US)
Pages (from-to)369-373
Number of pages5
JournalJournal of Clinical Endocrinology and Metabolism
Volume55
Issue number2
StatePublished - 1982

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Dietary Sodium
Intestinal Absorption
Metabolism
Vitamin D
Sodium
Calcium
Hypoparathyroidism
Serum
Parathyroid Hormone
Hypercalciuria
Nutrition
Diet
Renal Reabsorption
Renal Elimination
Salts
Kidney
Scanning electron microscopy

ASJC Scopus subject areas

  • Biochemistry
  • Endocrinology, Diabetes and Metabolism

Cite this

The role of dietary sodium on renal excretion and intestinal absorption of calcium and on vitamin D metabolism. / Breslau, N. A.; McGuire, J. L.; Zerwekh, J. E.; Pak, C. Y C.

In: Journal of Clinical Endocrinology and Metabolism, Vol. 55, No. 2, 1982, p. 369-373.

Research output: Contribution to journalArticle

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abstract = "Earlier studies have shown that an oral sodium (Na) load may induce hypercalciuria in previously normocalciuric subjects and may also increase intestinal calcium (Ca) absorption. To probe the cause of the increased intestinal Ca absorption, we simultaneously measured parathyroid function, serum 1,25-hydroxyvitamin D [1,25-(OH)2D], and fractional intestinal 47Ca absorption before and after a salt load. Eleven normal subjects and two patients with postsurgical hypoparathyroidism were placed on a 10 meq Na, 400 mg Ca per day diet for 10 days, followed by another 10-day period in which the same diet was supplemented by 240 meq Na daily. Measurements were performed on the final 3 days of each phase. In the normal subjects, urinary Na excretion increased from 7 ± 2 to 226 ± 8 meq/day (mean ± SEM), urinary Ca rose from 110 ± 14 to 167 ± 16 mg/day, serum parathyroid hormone (PTH) increased from 20 ± 1 to 22 ± 1 μleq/ml, serum 1,25-(OH)2D rose from 38 ± 4 to 51 ± 7 pg/ml, and fractional intestinal 47Ca absorption increased from 0.39 ± 0.03 to 0.49 ± 0.03 (P < 0.05 for all changes). Serum Ca corrected for total protein did not change (9.9 ± 0.1 to 9.8 ± 0.1 mg/dl). The patients with hypoparathyroidism who were maintained on vitamin D therapy also showed increases in urinary Na (20 ± 12 to 245 ± 11 meq/day) and urinary Ca (271 ± 48 to 305 ± 43; P < 0.05). However, there were no increases in serum PTH (13 ± 1 to 11 ± 1 μleq/ml), serum 1,25-(OH)2D (44 ± 1 to 40 ± 6 pg/ml), or intestinal Ca absorption (0.41 ± 0.03 to 0.42 ± 0.05). Corrected serum Ca decreased from 9.4 ± 0.2 to 8.6 ± 0.2 mg/dl. We conclude that in normal subjects, Na-induced renal hypercalciuria is accompanied by increased 1,25-(OH)2D synthesis and enhanced intestinal Ca absorption. Since this adaptive mechanism did not occur in two patients with hypoparathyroidism, mediation by PTH is suggested.",
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N2 - Earlier studies have shown that an oral sodium (Na) load may induce hypercalciuria in previously normocalciuric subjects and may also increase intestinal calcium (Ca) absorption. To probe the cause of the increased intestinal Ca absorption, we simultaneously measured parathyroid function, serum 1,25-hydroxyvitamin D [1,25-(OH)2D], and fractional intestinal 47Ca absorption before and after a salt load. Eleven normal subjects and two patients with postsurgical hypoparathyroidism were placed on a 10 meq Na, 400 mg Ca per day diet for 10 days, followed by another 10-day period in which the same diet was supplemented by 240 meq Na daily. Measurements were performed on the final 3 days of each phase. In the normal subjects, urinary Na excretion increased from 7 ± 2 to 226 ± 8 meq/day (mean ± SEM), urinary Ca rose from 110 ± 14 to 167 ± 16 mg/day, serum parathyroid hormone (PTH) increased from 20 ± 1 to 22 ± 1 μleq/ml, serum 1,25-(OH)2D rose from 38 ± 4 to 51 ± 7 pg/ml, and fractional intestinal 47Ca absorption increased from 0.39 ± 0.03 to 0.49 ± 0.03 (P < 0.05 for all changes). Serum Ca corrected for total protein did not change (9.9 ± 0.1 to 9.8 ± 0.1 mg/dl). The patients with hypoparathyroidism who were maintained on vitamin D therapy also showed increases in urinary Na (20 ± 12 to 245 ± 11 meq/day) and urinary Ca (271 ± 48 to 305 ± 43; P < 0.05). However, there were no increases in serum PTH (13 ± 1 to 11 ± 1 μleq/ml), serum 1,25-(OH)2D (44 ± 1 to 40 ± 6 pg/ml), or intestinal Ca absorption (0.41 ± 0.03 to 0.42 ± 0.05). Corrected serum Ca decreased from 9.4 ± 0.2 to 8.6 ± 0.2 mg/dl. We conclude that in normal subjects, Na-induced renal hypercalciuria is accompanied by increased 1,25-(OH)2D synthesis and enhanced intestinal Ca absorption. Since this adaptive mechanism did not occur in two patients with hypoparathyroidism, mediation by PTH is suggested.

AB - Earlier studies have shown that an oral sodium (Na) load may induce hypercalciuria in previously normocalciuric subjects and may also increase intestinal calcium (Ca) absorption. To probe the cause of the increased intestinal Ca absorption, we simultaneously measured parathyroid function, serum 1,25-hydroxyvitamin D [1,25-(OH)2D], and fractional intestinal 47Ca absorption before and after a salt load. Eleven normal subjects and two patients with postsurgical hypoparathyroidism were placed on a 10 meq Na, 400 mg Ca per day diet for 10 days, followed by another 10-day period in which the same diet was supplemented by 240 meq Na daily. Measurements were performed on the final 3 days of each phase. In the normal subjects, urinary Na excretion increased from 7 ± 2 to 226 ± 8 meq/day (mean ± SEM), urinary Ca rose from 110 ± 14 to 167 ± 16 mg/day, serum parathyroid hormone (PTH) increased from 20 ± 1 to 22 ± 1 μleq/ml, serum 1,25-(OH)2D rose from 38 ± 4 to 51 ± 7 pg/ml, and fractional intestinal 47Ca absorption increased from 0.39 ± 0.03 to 0.49 ± 0.03 (P < 0.05 for all changes). Serum Ca corrected for total protein did not change (9.9 ± 0.1 to 9.8 ± 0.1 mg/dl). The patients with hypoparathyroidism who were maintained on vitamin D therapy also showed increases in urinary Na (20 ± 12 to 245 ± 11 meq/day) and urinary Ca (271 ± 48 to 305 ± 43; P < 0.05). However, there were no increases in serum PTH (13 ± 1 to 11 ± 1 μleq/ml), serum 1,25-(OH)2D (44 ± 1 to 40 ± 6 pg/ml), or intestinal Ca absorption (0.41 ± 0.03 to 0.42 ± 0.05). Corrected serum Ca decreased from 9.4 ± 0.2 to 8.6 ± 0.2 mg/dl. We conclude that in normal subjects, Na-induced renal hypercalciuria is accompanied by increased 1,25-(OH)2D synthesis and enhanced intestinal Ca absorption. Since this adaptive mechanism did not occur in two patients with hypoparathyroidism, mediation by PTH is suggested.

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