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Letter to the Editor |
Department of Nutrition and Health, Research Institute of Child Nutrition, 44225 Dortmund, Germany
Address correspondence to: Dr. Thomas Remer, Forschungsinstitut für Kinderernährung, Research Institute of Child Nutrition, Heinstück 11, 44225 Dortmund, Germany. E-mail: remer{at}fke-do.de.
To the editor:
We read with interest the paper by Frassetto et al. (1) published in a recent issue of the Journal of Clinical Endocrinology and Metabolism. In a controlled, randomized study in 170 postmenopausal women receiving varying doses of potassium bicarbonate, Frassetto et al. observed a significant reduction in urinary calcium excretion in a dose-dependent trend. Reduction was greatest in those subjects with the highest baseline calciuria. A hypercalciuric woman would excrete around 51 mg calcium/d less than at the start of the treatment. These results were interpreted that around 55 g (5%) of bone calcium content could have been potentially saved through potassium treatment over the 36-month intervention period in hypercalciuric subjects. We agree with the authors’ inference that those subjects with the highest calcium excretion would potentially derive the greatest benefit from treatment with potassium bicarbonate regarding risk reduction in the development of calcium urolithiasis and potential bone-anabolic effects. Several studies suggest that alkali therapy inhibits bone resorption (2, 3) and that idiopathic hypercalciuria is associated with postmenopausal osteoporotic bone loss (4).
However, we do not agree that it would be possible to predict the potential bone calcium increase in preselected postmenopausal women (those with the highest baseline calciuria and the most likely urine calcium-lowering effect of potassium bicarbonate treatment). The potential saving of more than 55 g of bone calcium for a 36-month period was assumed by the authors on the basis of earlier short-term studies that did not find changes in intestinal calcium absorption after potassium bicarbonate ingestion (2, 5). Unaltered calcium absorption would in fact imply that a markedly positive calcium balance should be present during periods of reduced renal losses. However, Rafferty et al. (6) have published long-term results in women (mean age, 50.2 yr) showing the same calcium-sparing effects on urinary loss as the studies mentioned above (2, 5), but intestinal calcium absorption dropped in parallel to the fall in renal calcium excretion. Thus, in the long-term, calcium balance appears to be zero (6) and no longer positive, as reported in the short-term studies (2, 5). One could conclude that calcium economy improves due to the potassium-induced reduction in renal calcium excretion in the long term because less calcium needs to be intestinally absorbed for a stable balance, thus leaving a greater amount of calcium in the intestine. This calcium surplus can serve as an increased reserve for further (active) calcium absorption if the metabolic requirement increases. To summarize, the results of Rafferty et al. (6) show that at a given calcium intake, a given sustained decrease in urinary calcium excretion does not allow a long-term prediction of the potential bone calcium increase as suggested by Frassetto et al. (1). It remains exciting to know to what extent hypercalciuric subjects will benefit more from bone anabolic effects of alkali administration and/or a high potassium intake than normocalciuric subjects.
Footnotes
A response to this letter was invited, but the authors of the original article chose not to provide one.
Received April 25, 2005.
References
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