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  • Treatment of primary hypercalciuria: Potassium citrate

Citrate supplementation, as alkaline potassium salt, was for­merly introduced in the treatment of distal renal tubular acido- sis and subsequently extended to idiopathic hypocitraturic calcium nephrolithiasis. Regardless of the accompanying cation (sodium, potassium, magnesium) citrate salts exhibit di­rect effects on calcium excretion, acting by two distinct mecha­nisms: first, citrate anion is a strong ligand of calcium, and this will result in a decrease in free ionised calcium concentration; second, alkalinisation is expected to reduce bone resorp­tion, thereby decreasing total calcium excretion. The principal effect of citrate on calcium excretion is due to its ability to bind calcium, so that the calcium-citrate soluble com­plex accounts for by about 10 to 40% of total urinary calcium (Figure 1). Therefore, an increase in urinary citrate will result in a decrease in the fraction of free-ionised calcium, which is the species thermodynamically important for the saturation of calci­um forming salts.

The effect of potassium citrate upon the skeleton is shared by other alkaline salts, such as potassium bicarbonate. In fact, in postmenopausal women, the oral administration of potassium bicarbonate, at a dose sufficient to neutralise endogenous acid, improved calcium balance, by reducing calcium excretion, through a reduction of bone resorption and an increase in the rate of bone formation. In a prospective short-term study, alkaline mineral water induced a significant reduction in the biochemical markers of bone resorption. There also are re­cent reports of a specific effect of potassium intake on calcium excretion, because it has been found that potassium deficiency increases, whereas potassium supplementation as either cit­rate or bicarbonate or chloride salts, decreases calcium excre­tion. Potassium citrate, given to healthy menopausal women decreased net acid excretion and concurrently de­creased markers of bone resorption (Figure 2). Percent varia­tions of urine citrate were inversely related to those of de- oxypyridinolines and hydroxyproline, whereas calcium excre­tion exhibited only minor decreases .


Figure 1 – Dependence offree ionised calcium on citrate in urine specimens at two different total calcium concentrations.


Figure 2 – Effetcs of a three-month course of potassium citrate on bone metabolism and calcium excretion in post-menopausal women. Treated women (panel A) are compared to untreated ones (panel B) (**p<0.001 vs baseline; **p<0.01 vs baseline).

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