The effect of Ascorbic acid ingestion on the risk of calcium oxalate kidney stone formation

Master Thesis


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University of Cape Town

This study was undertaken to investigate the effect of prolonged megadose ingestion of ascorbic acid on the risk of calcium oxalate kidney stone formation. Ten healthy male subjects (ages 20 to 30 years) participated in the study. Each was required to ingest a daily dose of 4 g ascorbic acid per day for a period of 5 days. Twenty-four hour urines were collected at various times prior to, during and after this protocol. During each 24 hour collection, aliquots were withdrawn and stored in the presence and absence of an EDTA preservative. Other aliquots were withdrawn for immediate ascorbate analyses. Urine samples were analysed for sodium, potassium, magnesium, calcium, citrate, oxalate, urate, phosphate and creatinine. A new flow-injection method was designed, developed and tested for the analysis of urinary ascorbate. Analytical data obtained from this method were compared with results obtained from a manual titration method using 2,6 dichlorophenolindophenol. While the accuracy of both methods was found to be similar, results obtained by the flow-injection were more repeatable. All urine samples were analysed for ascorbate by both methods. In vitro crystallization experiments were performed on each urine to determine the limit of metastability and the rate of calcium oxalate crystallization. All data were statistically compared using the method of least-squares. Prolonged ascorbic acid ingestion had no effect on urinary calcium and oxalate nor on several other biochemical risk factors including urinary citrate, sodium, chloride and creatinine. Calcium oxalate metastable limits and crystallization kinetics were also unaffected, as were values of the Tiselius risk index and calcium oxalate relative supersaturation. While risk-reducing changes in urinary magnesium and pH occurred, these were offset by risk-increasing changes in urinary potassium and phosphate. The investigation showed that in vitro conversion of ascorbate to oxalate occurs but that this can be prevented by the presence of EDTA in the collection vessel. The study also demonstrated that ingestion of large doses of ascorbic acid probably commences with high percentage absorption of the vitamin but that saturation is achieved within 24 hours. Continued ingestion results in less absorption with excess ascorbic acid being excreted unchanged in the urine. In a separate case study, prior to the commencement of the investigation described above, a healthy male participant was given a daily dose of 8g ascorbic acid in a protocol which was planned to last 9 days. Significant crystalluria and haematuria developed on the 8th day after which further ascorbic acid ingestion was immediately suspended. In this individual, several risk factors changed significantly. These were urinary oxalate excretion, metastable limit, Tiselius risk index and calcium oxalate relative supersaturation. This study shows that prolonged ingestion of large doses of ascorbic acid does not increase the risk of calcium oxalate kidney stone formation. However, the results of the special case study highlight the fact that in some individuals, renal handling of ascorbic acid may be impaired, leading to undesirable consequences.

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