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Letters to the Editor |
Research Institute of Child Nutrition D-44225 Dortmund, Germany
Address correspondence to: Thomas Remer, Ph.D., Research Institute of Child Nutrition, D-44225 Dortmund, Germany. E-mail: remer{at}fke-do.de
To the editor:
In the June 2001 issue of JCEM Coruzzi et al. (1) reported an increased systolic blood pressure and an elevated urinary calcium excretion in patients with essential hypertension after a 10-d period with low potassium intake.
It is now well established that reducing the alkali load (or increasing the acid load) in the diet can substantially increase urinary calcium excretion (2, 3, 4, 5, 6, 7). If, for example, 20 mmol (3.0 g/d) of the acidifying amino acid L-methionine is added to a diet (under controlled experimental conditions) a marked increase in urinary calcium excretion (averaging 36 mg/d) occurs in response to the rise in renal net acid excretion (of about 40 mEq/d) in healthy adult volunteers (3). Despite this known impact of changes in the acid base status on calcium metabolism, Coruzzi et al. (1) did not provide any information as to which kind of potassium salt was used in their study during the period of normal potassium intake.
Did the authors administer an alkalizing potassium salt (e.g. potassium bicarbonate or tripotassium citrate) or did they use potassium chloride instead? Potassium chloride has a small acidifying effect due to the lower intestinal net absorption of the potassium cation as compared with the chloride anion (7, 8).
The marked positive impact of oral administration of alkalizing
potassium bicarbonate on the calcium and phosphorus balance (
), bone
resorption (
), and bone formation (
) has been demonstrated
especially by Sebastian et al. (4) in
postmenopausal women. Similar effects on calcium metabolism in women
have been observed after administration of alkalizing sodium (instead
of potassium) bicarbonate (2). Thus, it is possible that
the changes in urinary calcium excretion observed by Coruzzi et
al. (1) may not be primarily due to the cation
potassium per se, but could also have been caused by the
alkalizing effect of the corresponding anion.
In principle, endocrine, metabolic and/or clinical effects resulting from an altered mineral intake are not necessarily due to the mineral cation itself but may result from an altered acid base status, too. Therefore, for similar studies it seems necessary to take potential renal acid loads (5, 8, 9) of both mineral salts and foods into account and to control parameters of acid base metabolism.
Received August 23, 2001.
References
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