Hypertension and obesity are also widespread social diseases with important epidemiological similarities to nephrolithiasis. These affinities have, over the years, led investigators to seek interconnections between the three diseases in order to find a common pathogenic moment. As far as hypertension is concerned, various studies have demonstrated that urinary excretion of calcium is greater in hypertensives than in normotensives. A linear association between the excretion of 24-h calcium and arterial blood pressure has been demonstrated in numerous studies, including INTERSALT (6). In 1999, after following up 132 hypertensives and 135 controls for 5 years, our group published a paper which reported the onset of stone disease in the hypertensives in significantly higher percentages compared to the controls, with an RR of 5.5 (7). Moreover, a year earlier, Madore and Curhan published two studies (8,9) conducted on a large cohort of Americans in which they demonstrated that patients with a past history of nephrolithiasis without hypertension were more prone to become hypertensive during the follow-up than non stone formers. These results, further confirmed by many subsequent studies, did not however succeed in clarifying the doubt as to whether it is the hypercalciuria of hypertensives that predisposes them to the development of stone disease or whether it is the renal damage, albeit microscopic, caused by stone disease that triggers the development of hypertension. Scientific literature has, however, identified, for hypertensives, stone formers and controls alike, a linear relationship between the excretion of calcium and the excretion of sodium, where calcium is the dependent variable and where the slope of the straight line, i.e. the increase of calcium for each mmol of sodium, is much greater in both stone formers and hypertensives than in controls. Moreover, as far back as the '80s, it was demonstrated that a reduction in kitchen salt intake from 10 g to 4 g per day, has the capacity to reduce calciuria more than a reduction in calcium intake from 1000 mg to 500 mg (10,11).