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rence of kidney stones in both sexes is directly related to the urinary sodium:potassium ratio (Cirillo et al., 1994). In a pre-post, uncontrolled study of children with idiopathic hypercalciuria, reducing the dietary sodium:potassium ratio greatly reduced urinary calcium excretion (Alon and Berenbom, 2000). Hypercalciuria is generally accepted as a major risk factor for calcium-containing kidney stones (Coe et al., 1992). The incidence of kidney stones has been shown to increase with an increased sodium:potassium ratio (Stamler and Cirillo, 1997).

In a longitudinal study of 51,529 men conducted prospectively over 4 years, the incidence of symptomatic kidney stones, while not correlating with dietary sodium, did correlate strongly and negatively with dietary potassium as measured by a food-frequency questionnaire over a broad range of intake (2.9 to 4.0 g [74 to 102 mmol]/day) (Curhan et al., 1993) (see Table 5-8). The absence of a relationship between dietary sodium and kidney stones should be

TABLE 5-8 Epidemiological Studies on Potassium Intake and Risk of Kidney Stone Formation

Reference

Study Design

Potassium Intake,a g/d (mmol/d)

Relative Risk for Kidney Stones

Curhan et al., 1993

Health Professionals Study, 45,619 men, 4-yr follow-up

Q1

< 2.9 (74)

1.0

Q2

3.1 (79)

0.88

 

Q3

3.4 (87)

0.74

Q4

3.8 (97)

0.69

Q5

> 4.0 (102)

0.49

 

p trend < 0.001

Curhan et al., 1997

Nurses’ Health Study, 91,731 women, 12-yr follow-up

Q1

2.0 (52)

1.0

Q2

2.7 (69)

0.86

 

Q3

3.2 (81)

0.75

Q4

3.7 (95)

0.67

Q5

4.7 (119)

0.65

 

p trend < 0.001

Hirvonen et al., 1999

Prospective cohort, n = 27,001 Finnish male smokers

Q1

3.8 (97)

1.0

Q2

4.6 (118)

0.76

Q3

5.1 (131)

0.85

 

Q4

5.7 (146)

0.79

 

p trend = 0.34

a Q = quartile or quintile of intake.



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