The kidney and essential hypertension: a link to osteoporosis?

Abnormalities of calcium metabolism independent of changes in intracellular calcium have been described in patients with essential hypertension. These include increased urinary calcium excretion for a given salt intake, a raised parathyroid hormone level, an increase in urinary cyclic AMP, a tendency for a low serum ionized calcium level, a raised 1,25-dihydroxyvitamin D level and an increased intestinal calcium reabsorption. These changes have been seen as a consequence of a primary renal calcium leak.

We propose that these changes are secondary to a genetic defect in the ability of the kidney to excrete sodium. On the high salt intake in most Western countries (i.e. approximately 170 mmol/day sodium) compensatory mechanisms occur to try to overcome this defect. These compensatory mechanisms are responsible for the rise in blood pressure, but also cause an increase in central blood volume which is the direct cause of the increase in urinary calcium excretion. This causes a slightly negative calcium balance, and the other abnormalities of calcium metabolism can then be seen as a compensatory response to try to restore calcium balance to normal.

This hypothesis explains the increase in kidney stones in essential hypertension and predicts that hypertensives, in the long term, will be more likely to develop bone demineralization (osteoporosis), as has been demonstrated in some animal models of hypertension. Increases in salt intake will not only cause a further rise in blood pressure, but will also increase urinary calcium excretion and aggravate the other abnormalities. A moderate reduction in salt intake from 170 to 70 mmol/day will lower the blood pressure and will tend to correct the abnormalities of calcium metabolism. It should simultaneously reduce the incidence of renal stones and the long-term risk of bone demineralization.