Tiziana Meschi, MD, Antonio Nouvenne, MD, PhD, Loris Borghi, MD*
Kidney stones are a disorder that could be termed social because of its vast diffusion and growing incidence in wealthy industrialized countries.1 Many international studies have shown that this condition affects just less than 10% of the population, constituting an expense of approximately 2 billion dollars a year in hospital admissions in the United States alone.2 Insome cases, it is the consequence of specific hereditary or acquired diseases, such as cystinuria, primary hyperoxaluria, medullary sponge kidney, primary hyperparathyroidism, and infections or anatomic malformations of the kidneys and urinary tract. However, the most common form is idiopathic calcium nephrolithiasis (ICN), with the formation of calcium oxalate stones, sometimes mixed with calcium phosphate and with a prevalence of approximately 80%. The distribution by sex shows the frequency to be slightly higher in men.3 The pathogenesis of ICN includes genetic and acquired factors that interact to cause biochemical urinary abnormalities that lead to the formation of kidney stones. A high rate of supersaturations of calcium oxalate and/or calcium phosphate leads to the formation of crystalline nests that can grow and join together to form a stone. The urinary elements and compounds, both inhibitors and activators, involved in the crystallization process are known as lithogenic urinary risk factors. For calcium oxalate, the lithogenic urinary risk factors are low urinary volume (<2 L/d), hypercalciuria (>250 mg/d), hyperoxaluria (>40 mg/d), hyperuricosuria (>600 mg/d), hypocitraturia (<320 mg/d), and hypomagnesuria (<50 mg/d). For calcium phosphate, in addition to the above, the most important factors are hyperphosphaturia (>1000 mg/d) and urinary pH. A pH more than 7 favors the formation of kidney stones primarily comprising phosphates, whereas a pH between 6 and 7 associated with a urinary volume of less than 1 L/d can dangerously increase the supersaturation of calcium phosphate and lead to the formation of mixed Ca-oxalate and Ca-phosphate stones. Last, in the case of uric acid–induced stone disease, another common form with a frequency of 10%to 15%, the factors involved are hyperuricosuria and pH less than 5.5. Of the various lithogenic urinary risk factors, the most commonly observed in patients with ICN is hypercalciuria, with a prevalence of approximately 50%. Regarding the age of onset, there are 2 peaks: between 20 and 30 years and between 50 and 60 years.4 The presence of a genetic substrate does not, however, detract from the role of lifestyle: dietary habits and lifestyle have a direct effect on the lithogenic urinary risk factors and the pathogenesis of this condition. This article examines the role of lifestyle in the prevention and treatment of calcium and uric acid kidney stones. This article specifically analyzes the relationship between (1) kidney stones and dietary habits, (2) kidney stones and body weight, (3) kidney stones and exercise, (4) kidney stones and stressful life events, and (5) particular causes.