The Role of Diet in Kidney Stone Pathogenesis and Prevention

The origin of kidney stones is multifactorial, involving a complex interplay of genetic, metabolic, and environmental factors. This review aims to detail the relationship between the molecular pathogenesis of kidney stone disease and the impact diet can have on stone formation and patient outcomes.

Diet is an important part of managing kidney stones at a molecular level. Oxalate can be absorbed from the diet through the digestive system into the urine where calcium and oxalate can combine to form stones. Evidence supports that low dietary calcium contributes to first time and recurrent stones, and high dietary sodium elevates the risk of calcium stone formation. Diets high in animal protein cause high levels of urinary uric acid and calcium and low levels of urinary citrate. Low urine pH favors uric acid stone development, and fructose increases serum and urinary uric acid levels. Alternatively, consuming fruits and vegetables raises urinary pH and citrate excretion. Adequate hydration also dilutes urinary solutes and reduces supersaturation. Potassium citrate, magnesium, and calcium supplementation are thought to prevent stone formation. Diet and adequate hydration can manipulate the pathogenesis of stones to prevent recurrence and improve patient outcomes. Calcium oxalate stones are the most common, followed by calcium phosphate, uric acid, struvite, and cystine stones. By aligning nutritional interventions with stone type and metabolic profile, healthcare providers can offer non-invasive methods for improving outcomes.