The central role of body weight in determining stone risk is clearly described in scientific literature. BMI, weight, abdominal circumference are independently associated with kidney stone risk (14). Nevertheless, the mechanisms underlying this relation are still unknown. Data exist in literature to suggest that body weight can affect the excretion of many promoters or inhibitors of crystalline aggregation. For example, some population studies in the United States have demonstrated how urine pH is inversely correlated to body weight and how urinary excretion of calcium, oxalate and uric acid increase as body weight increases (15,16). Notwithstanding these data, the effects of body weight on the excretion of many urinary stone risk factors remains partly unknown; this is due to the limited weight categories, the low number of obese people in the study populations, the absence of a control group with "non stone formers" and the failure to record food intake in the studies published. In addition to this, as regards urinary excretion, the evaluation of excess weight solely on the basis of BMI values and abdominal circumference may seem somewhat reductive. It would appear to be more useful to assess body composition, lean mass, fat tissue mass and mineral mass. In this way, by better stratifying obesity classes, it might become simpler to understand the intricate endocrine/metabolic changes that occur in obesity (hyperinsulinism, hyperestrogenism etc.) and establish better correlations with the urinary excretion of stone risk factors. In fact, some studies (16) have demonstrated a slight increase in the total incidence of stone disease in female obese patients compared to males, with a slightly higher mean age in the females and, in any case, ages being equal, with a lower number of recurrences in the females compared to the males. These phenomena are probably affected by the concentration of serum estrogens and by the transformation in the fatty tissue of the adrenal androgens into estrogens; nonetheless the effects of serum estrogens on the urinary excretion of calcium are unknown. Finally, some studies have demonstrated that body weight also affects the composition of the stones. In fact, it has been demonstrated how the incidence of uric acid stones is higher in overweight/obese patients than in normal weight patients; some studies have highlighted that patients with idiopathic uric acid nephrolithiasis have a higher BMI than hyperuricosuric patients who form calcium oxalate stones. The pathophysiological link should be sought in hyperinsulinism: in fact insulin resistance is associated with a decrease in the production of renal ammonia leading to a consequent decrease in urinary pH, characteristic of uric acid stone disease (17). This theory is indirectly corroborated by the aforementioned indirect relationship between BMI and 24-h urine pH and the finding that also age-related reduced urinary acidification capacity increases the risk of uric stone disease, irrespective of body weight. On the basis of the above, it is clear how the presence of excess weight/obesity, uric acid or mixed stone disease could raise suspicions of a Metabolic Syndrome: there are, however, no conclusive studies on this, and neither have the effects on stone risk and arterial blood pressure of water therapy and a low-salt diet in a population of overweight/obese stone formers been sufficiently studied.