Despite the absence of RCTs specifically evaluating fluid intake and dietary interventions for the prevention of cystine stones, the pathophysiology and biochemistry of cystinuria support several nutritional strategies that may reduce stone formation and recurrence. Cystine is poorly soluble in urine, and impaired renal tubular cystine reabsorption leads to increased urinary cystine concentration, supersaturation, crystallization, and clinical stone formation.211, 212 Preventive strategies therefore focus on reducing urinary cystine concentration, reducing cystine excretion, and increasing cystine solubility. Because cystine solubility is concentration-dependent, increasing urine volume is a central tenet for stone prevention. Very high urine output, typically 3 L/day or more, reduces urinary cystine concentration and is supported by the solubility product of cystine213 and by clinical data showing lower stone recurrence among patients who achieved this urine volume.214 Dietary strategies may also reduce cystine excretion. Cystine is derived from metabolism of methionine, which is common in animal protein sources; therefore, limiting animal protein intake may reduce urinary cystine excretion.215 In a retrospective study of patients with cystine stones, higher protein intake was associated with significantly higher cystine excretion.211 Reducing dietary sodium intake has also been shown to reduce cystine excretion, although the exact mechanism of action is unknown.213 Several observational studies support this association,216, 217 although recent observational data have questioned the magnitude and consistency of the relationship between sodium intake and cystine excretion.211 Nevertheless, increased fluid intake, moderation of animal protein intake, and reduced dietary sodium intake are accessible, low-risk interventions that are consistent with cystine solubility chemistry and renal transport physiology, and they remain foundational dietary strategies for adults with cystine stones.