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Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate
interpreted cautiously because the food-frequency questionnaire used in these studies did not measure sodium intake either accurately or precisely (Subar et al., 2001). In this study (Curhan et al., 1993), the incidence of kidney stones correlated directly with meat intake. In a 12-year prospective study of an even larger number of female nurses, the incidence of stone formation was inversely associated with dietary potassium (2.0 to 4.7 g [52 to 119 mmol]/day) (Curhan et al., 1997). In a study conducted in Finland where the dietary potassium intake is greater than in the United States, risk for kidney stones appeared to decrease with an increased intake of potassium (3.8 compared with 4.6 g [97 to 118 mmol]/day) (Hirvonen et al., 1999). However, higher intakes of potassium did not appear to further reduce risk, and the relationship between potassium intake and kidney stones, overall, was nonsignificant.
Role of Acid-Base Balance, Urinary Citrate, and Relationship with Sodium
An increased intake of meat has long been recognized as a risk factor for kidney stones, presumably because of the resultant acid load and the well-documented impact of that load on urinary calcium excretion (Lemann, 1999; Lemann et al., 2003). By increasing the acid load and slightly reducing the plasma bicarbonate concentration, an increased intake of animal protein also induces a decrease in the urinary excretion of citrate (Breslau et al., 1988), a major risk factor for the formation of kidney stones (Coe et al., 1992; Pak, 1987). Urinary citrate chelates urinary calcium in a soluble form (Bisaz et al., 1978; Meyer and Smith, 1975; Pak, 1987). Both hypocitraturia and hypercalciuria occur with even modest potassium deficiencies (Hamm, 1990; Simpson, 1983). Administration of either potassium bicarbonate or potassium citrate induces an increase in the urinary excretion of citrate (Pak, 1987; Sakhaee et al., 1991; Simpson, 1983), as well as a reduction in the urinary excretion of calcium (Lemann et al., 1989, 1991). Neither the citraturic effect of potassium citrate nor its hypocalciuric effect is greater than that of potassium bicarbonate, presumably because these salts induce similarly small increases in the plasma concentration of bicarbonate (Sakhaee et al., 1991).
One clinical trial tested the effects of potassium citrate in preventing recurrent kidney stones (Barcelo et al., 1993). In a double-blind, placebo-controlled trial of 57 patients (25 men and 32 women) with kidney stones and hypocitraturia conducted over 3 years, 1.2 to 2.3 g (30 to 60 mmol) of potassium citrate were administered in addition