Urinary calcium excretion in essential hypertension

Eric W. Young, Cynthia D. Morris, David A. McCarron

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Abstract

Patients with essential hypertension have been reported to have higher levels of urinary calcium excretion (UCaV) than normotensive persons. We tested the hypothesis that the calciuria of hypertension is due to dietary factors and evaluated several alternate mechanisms. UCaV was studied in 15 patients with essential hypertension compared with 16 age- and gender-matched normotensive control subjects. For subjects taking self-selected, free-living diets, the difference in UCaV between normotensive (130 ± 14 mg/day) and hypertensive subjects (201 ± 37 mg/day) was not significant (p = 0.1). However, in a controlled diet with moderately restricted sodium intake (88 mEq), urinary calcium excretion was significantly higher (p = 0.02) in the hypertensive than in the normotensive group receiving 400 mg calcium (204 ± 25 vs 132 ± 13 mg/day) and 1400 mg calcium (272 ± 31 vs 187 ± 25 mg/day). Twenty-four-hour U CaV was directly and significantly correlated with blood pressure (r = 0.63 for standing systolic blood pressure; p < 0.001). A 1000 mg oral calcium load caused similar changes In UCaV (0.12 ± 0.11 vs 0.12 ± 0.07 mg per 100 ml glomerular filtration) and serum ionized calcium level (0.06 ± 0.08 vs 0.06 ± 0.02 mmol/L) in normotensive and hypertensive subjects, respectively, suggesting that there was no difference in intestinal calcium absorption between the groups. Fasting UCaV did not differ between the hypertensive (8.9 ± 4.5 mg per 2 hours) and normotensive groups (10.9 ± 11.5 mg per 2 hours). Serum ionized calcium level was significantly lower (p < 0.02) in hypertensive (1.23 ± 0.01 mmol/L) compared with normotensive subjects (1.27 ± 0.02 mmol/L). Despite evidence of impaired calcium metabolism, there were no significant differences in serum levels of intact parathyroid hormone (3.0 ± 0.3 vs 3.0 ± 0.2 pmol/L) or 1,25-dehydroxy vitamin D (1,25(OH)2D) (34.5 ± 7.0 vs 35.1 ± 7.8 pg/ml) between the hypertensive and normotensive groups. Our findings were similar at both levels of calcium intake. We conclude that relative hypercalciuria is a feature of essential hypertension that cannot be explained by primary intestinal hyperabsorption of calcium or by increased serum 1,25(OH)2D concentration. Relationships among calcium absorption, calcium excretion, serum ionized calcium, parathyroid hormone, and 1,25(OH)2D appear to be altered in essential hypertension.

Original languageEnglish (US)
Pages (from-to)624-632
Number of pages9
JournalThe Journal of Laboratory and Clinical Medicine
Volume120
Issue number4
StatePublished - Oct 1992

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ASJC Scopus subject areas

  • Pathology and Forensic Medicine

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