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Abnormalities of calcium metabolism in essential hypertension
Insights
Essential hypertension patients show increased renal calcium loss and higher parathyroid hormone levels, suggesting a primary kidney calcium leak. This may lead to compensatory parathyroid gland overactivity.
Area of Science:
- Nephrology
- Endocrinology
- Hypertension Research
Background:
- Essential hypertension is common, but its underlying mechanisms, particularly calcium metabolism, are not fully understood.
- Previous studies suggest altered renal calcium handling in hypertensive individuals.
Purpose of the Study:
- To investigate renal calcium handling in patients with essential hypertension and normal renal function.
- To evaluate the relationship between calcium excretion, parathyroid hormone, and urinary cAMP levels in hypertension.
Main Methods:
- Compared 55 hypertensive patients with 55 age- and sex-matched normotensive controls.
- Measured creatinine clearance, serum calcium (total and ionized), plasma parathyroid hormone, and 24-hour urinary excretion of calcium, sodium, and cAMP.
- Performed intravenous calcium infusion tests in a subgroup to assess calcium excretion capacity.
Main Results:
- Hypertensive patients exhibited significantly higher 24-hour and fasting urinary calcium excretion rates.
- Plasma parathyroid hormone and urinary cAMP levels were elevated in the hypertensive group.
- Hypertensive patients excreted more calcium during intravenous calcium infusion across all serum calcium concentrations.
Conclusions:
- The findings support the hypothesis of a primary renal calcium leak in essential hypertension.
- Increased urinary calcium excretion may trigger compensatory parathyroid overactivity in hypertensive individuals.
Abstract:
Calcium metabolism has been investigated in patients with essential hypertension and normal renal function to evaluate the renal calcium handling and the reported increase in renal calcium loss. In 55 hypertensive and 55 sex- and age-matched healthy normotensive subjects creatinine clearance, serum total and ionized calcium, plasma parathyroid hormone and 24 h urinary excretion of calcium, sodium and cAMP were measured. In a subgroup of 20 hypertensive patients and 20 controls the fasting calcium excretion rate was also measured. Both 24 h and fasting calcium excretion rates were higher in the hypertensive group; so also were plasma parathyroid hormone and urinary cAMP. Serum total and ionized calcium levels were not different in the two groups. After intravenous calcium infusion (15 mg 3 h-1 kg-1) in seven hypertensive patients and controls, the hypertensive patients excreted more calcium at all serum calcium concentrations. These results support the hypothesis of primary renal calcium leak in essential hypertension. Enhanced urinary calcium excretion rate may cause compensatory parathyroid overactivity.