Intake of vitamin C has long been associated with an increased risk of kidney stone formation. The most common component of kidney stones is primarily calcium oxalate crystals. Vitamin C is metabolized to oxalate, which, with increased intake, could lead to higher rates of oxalate excretion and increased risk of stone formation. However, studies have yielded contradictory results. Curhan et al. reviewed subjects consuming 1,000 mg or more of vitamin C (normal for men is 90 mg/day and women 75 mg/day) and found no increased risk for stone formation. In fact, those consuming a normal daily amount showed a 10% reduction in stone formation [40].

A recent well-designed prospective randomized trial was conducted by Traxer et al. to further evaluate possible risk of vitamin C supplementation. In this study, 12 normal subjects and 12 stone formers were randomized to either 1,000 mg of vitamin C twice daily or placebo. Diets were strictly controlled. They found a statistically significant increase in urinary oxalate in the vitamin C group versus placebo for both normal subjects (34.7 vs. 28.5 mg, P = 0.008) and stone formers (41 vs 30.5 mg, P = <0.001). Overall, urinary oxalate increased by 20% in normal subjects and by 33% in stone formers. Calcium oxalate relative saturation ratio was also significantly higher in the vitamin C versus placebo group. Based on these findings, they recommend limiting vitamin C use to less than 2 g per day in calcium oxalate stone formers [41].

It would appear that there could be an increased risk of stone formation in the setting of vitamin C supplementation as extremely high levels of vitamin C intake (>1,000 mg/day) may increase urinary oxalate excretion, but reports on actual stone formation are conflicting. It has been concluded that an intake of 90–100 mg per day is required for optimal chronic disease prevention [42]. Therefore, it is currently recommended that intake not exceed the daily reference intake for vitamin C, 75 mg/day for women and 90 mg/day for men [4].

Cranberry juice has long been recommended for its potential beneficial effects in preventing urinary tract infections. Cranberries contain two compounds with anti-adherence properties that prevent fimbriated E. coli from adhering to uroepithelial cells. There have been several trials to test this effect, and although data is conflicting, there is at least some good evidence to recommend cranberry juice for prevention of UTIs [43]. However, many in the lay public also perceive cranberry juice to be beneficial in preventing kidney stone formation. Cranberry juice does contain citric acid, and, therefore, it has been assumed that cranberry juice’s ability to increase urinary citrate may potentially prevent stone formation. However, there is little data to support the use of cranberry juice for the prevention of renal stones. Most studies have produced mixed results. Indeed, the most recent data seem to suggest the same. Cranberry juice may increase the propensity for crystallization of calcium oxalate from enhanced urinary saturation of calcium oxalate. It reduces urinary pH, thereby increasing the propensity for uric acid crystallization, although it does partly offset this by decreasing urinary uric acid levels. Overall, it is unlikely that cranberry juice does anything to substantially affect the risk of renal stone formation [44]. As such, it should not be recommended as a preventive strategy for recurrent stone formers.

The major source of sodium in the American diet is sodium chloride (salt). Thus, the terms “sodium” and “salt” are largely interchangeable in the common vernacular. The relationship between salt intake and stone risk has been well established. Studies have examined the effect of a low-sodium diet on the crystallization of stone-forming salts in urine. When comparing a low- to a high-sodium diet, it was observed that high sodium intake increased urinary sodium, calcium, and pH while decreasing urinary citrate, thus causing an increased tendency for the crystallization of calcium salts in urine. For this reason, stone-forming patients, particularly those with hypercalciuria and/or who are prone to forming calcium stones, should reduce their dietary sodium intake to 1,500 mg, 35% below the daily recommended value (2,400 mg) [45]. The problem, however, is that most patients far underestimate their intake, in large part because they fail to consider the sodium content in many foods. Patients tend to believe simply not adding salt to food is enough. In fact, however, many foods contain large amounts of sodium. These can include, but are not limited to, canned foods, fast food, frozen foods, bread, and especially cheese. Penniston et al. evaluated dietary sodium intake among 83 stone formers, and the results were striking. Mean sodium intake was high (3,300 mg/day), exceeding the recommended intake of 1,500 mg/day for recurrent stone formers, despite the fact that most patients had previously been instructed to reduce sodium intake. This study also found that greater than 85% of total sodium intake was from foods, most commonly processed meats (15%), bread and baked goods (14.1%), canned and pickled goods (8.5%), various condiments (8.4%), cheese (7.2%), and snacks (6.8%) [46]. This demonstrates the importance of counseling patients such that they fully understand the many potential sources of excess sodium in their diet.

Foods of animal origin, particularly their protein component, are known to lower urinary pH and increase urinary uric acid [47, 48], both of which are risk factors for uric acid and calcium stone formation, and multiple studies have shown a correlation between increased animal protein intake and stone formation [10, 49]. Most physicians and patients are aware that diets which are more carnivorous are associated with increased risk of stone formation but may not be clear on specifically which types are most contributory. A common myth, for example, is that the protein from all animal foods, including dairy, is the same. This has been shown to be not true with respect to both acid load of diet [50] and to uric acid production [51]. Another myth is that “red meats” are somehow more lithogenic than fish or poultry. In truth, all meats appear to be equally lithogenic. Tracy et al. compared the effects of three different animal protein sources (beef, chicken, and fish) on renal stone risk. They performed a 3-phase randomized cross-over metabolic study with a total 15 subjects. Each phase was 1 week, during which patients consumed a standard diet containing either beef, chicken, or fish. Serum chemistry and 24-h urine samples were obtained after each phase. They found that beef was associated with lower serum uric acid than chicken or fish and that fish was associated with higher urinary uric acid levels than either beef or chicken. There were no differences in other urinary parameters such as pH, calcium, citrate, oxalate, or sodium [52]. Based on this, patients with relatively high intakes of meats should limit the intake of all animal tissue, including fish. Conversely, dairy sources of protein, such as yogurt and milk, do not increase renal acid load or uric acid production, and patients should have no need to limit dairy intake.

To expound further on how animal tissue contributes to stone formation, one must consider urinary acid load. Uric acid becomes less soluble as urine becomes more acidic which leads to precipitation and formation of uric acid stones as well as nucleation of calcium oxalate crystals, hence promoting formation of calcium oxalate stones [53]. High-protein, low-carbohydrate diets are associated with a significant increase in net acid excretion by approximately 50 mEq/day [54]. There are two possible mechanisms by which this occurs. First, the protein component of animal-derived foods tends to be rich in sulfur-containing amino acids, and oxidation of sulfur to sulfate generates protons [55]. Second, severe carbohydrate restriction results in production of keto acids [56]. Reddy et al. evaluated this by enrolling ten subjects in a prospective metabolic study. Patients initially consumed their usual diet, followed by induction regimen of high protein, severely carbohydrate-restricted diet for 2 weeks, and then maintenance regimen of a moderately carbohydrate-restricted diet for 4 weeks. Twenty-four-hour urine and serum studies were performed for each phase. They found a significant increase in net acid excretion and urinary calcium levels, and urinary saturation of uric acid increased twofold. Urine pH decreased to an average in the 5.6 range, and urinary citrate levels decreased significantly as well [54].