Twenty-nine kidney stone formers (mean age, 49.8 years) and 19 non-stone formers (mean age, 50.8 years) received 1,000 of ascorbic acid twice a day (with the morning and evening meals) for six days, and no ascorbic acid (control period) for another six days, in random order. A low-oxalate diet was consumed throughout the study. On day six of each treatment period, the subjects received 136 mg of oxalate two hours before breakfast. Of the 48 participants, 19 (12 stone formers, 7 non-stone formers) were identified as responders, defined by an increase in 24-hour total oxalate excretion of greater than 10% after ascorbic acid treatment than after the control period. Responders had a greater 24-hour Tiselius Risk Index (a measure of calcium oxalate saturation) after ascorbic acid supplementation than after the control period (mean, 1.10 vs. 0.76), because of a 31% increase in the percentage of oxalate absorbed (10.5% vs. 8.0%) and a 39% increase in endogenous oxalate synthesis. The authors concluded that supplementation with 1,000 mg of ascorbic acid twice a day increased urinary oxalate excretion and the Tiselius risk index for calcium oxalate kidney stones in 40% of participants, both stone formers and non-stone formers.
Comment: Opponents of nutritional therapy have long claimed that vitamin C supplementation can cause kidney stones, even though there is virtually no evidence supporting that belief (see Arch Intern Med 1998;158:2187-2191). In fact, a large epidemiological study showed that the risk of kidney stone formation was 22% lower in men who consumed 1,500 mg/day or more of vitamin C, compared with the risk in men who consumed less than 250 mg/day. Although high-dose vitamin C may induce a small increase in urinary uric acid excretion in some people, and a larger increase in a very small proportion of the population, other effects of the vitamin might be expected to help prevent kidney stones. For example, increasing urinary ascorbic acid excretion may cause a small increase in urine acidity, which could reduce calcium oxalate precipitation. Vitamin C in the urine also binds calcium, thereby reducing the formation of calcium oxalate crystals.
While the new study appears to demonstrate that vitamin C increases kidney stone risk, its experimental design does not mimic real-life conditions. The participants in this study were given a fairly large amount of oxalate on an empty stomach, two hours before breakfast. Under normal circumstances, oxalate is a constituent of a meal, and the calcium present in that meal would bind a proportion of ingested oxalate and prevent it from being absorbed. Vitamin C may increase urinary oxalate in people dosed with pure oxalate, but it is not at all clear that the same effect would occur when oxalate is ingested as part of a meal.
It is possible that vitamin C supplementation can promote stone formation in rare individuals who have a particular genetic makeup, but for the general population there is no convincing evidence that vitamin C causes kidney stones.
Massey LK, et al. Ascorbate increases human oxaluria and kidney stone risk. J Nutr 2005;135:1673-1677.
