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Urinary calcium excretion in essential hypertension
E W Young1, C D Morris, D A McCarron
1Division of Nephrology, Oregon Health Sciences University, Portland 97201.
Insights
Essential hypertension is linked to higher urinary calcium excretion (UCaV), particularly under controlled sodium intake. This calciuria correlates with blood pressure but doesn't stem from altered intestinal calcium absorption.
Area of Science:
- Nephrology
- Cardiovascular Medicine
- Nutritional Science
Background:
- Essential hypertension is associated with elevated urinary calcium excretion (UCaV).
- The underlying causes of increased UCaV in hypertension are not fully understood.
- Dietary factors are hypothesized to contribute to calciuria in hypertensive individuals.
Purpose of the Study:
- To investigate the relationship between essential hypertension and urinary calcium excretion.
- To test the hypothesis that dietary factors influence calciuria in hypertension.
- To evaluate alternative mechanisms for increased UCaV in hypertensive patients.
Main Methods:
- Compared UCaV in 15 hypertensive patients and 16 normotensive controls.
- Assessed UCaV under free-living and controlled sodium intake diets (88 mEq).
- Administered oral calcium loads and measured serum ionized calcium and UCaV.
Main Results:
- No significant difference in UCaV between groups on self-selected diets (p=0.1).
- Significantly higher UCaV in hypertensive subjects on controlled diets with 400 mg and 1400 mg calcium (p=0.02).
- UCaV directly correlated with systolic blood pressure (r=0.63, p<0.001).
- No difference in intestinal calcium absorption or fasting UCaV between groups.
Conclusions:
- Hypertension is associated with increased urinary calcium excretion, especially under restricted sodium intake.
- Dietary calcium intake significantly impacts UCaV in hypertensive individuals.
- The calciuria of hypertension is not explained by impaired intestinal calcium absorption.
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 UCaV 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).(ABSTRACT TRUNCATED AT 250 WORDS)