Kristina L Penniston1, Stephen Y Nakada. 1. Department of Urology, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin 53792-3236, USA.
Abstract
OBJECTIVES: To test the hypothesis that patients with hyperoxaluria, who modified their dietary calcium intake, would reduce their urinary oxalate excretion without raising their urinary calcium excretion. Diet is a major factor in idiopathic calcium oxalate urolithiasis, yet controversy exists regarding the ideal clinical recommendations. Approximately 20% of patients with calcium oxalate stone formation have hyperoxaluria (> or = 45 mg oxalate/d). Calcium supplements to bind dietary oxalate have been suggested, but clinical evidence of this therapy is lacking. METHODS: Of 144 adult patients with stone formation seen by a registered dietitian from September 2006 to September 2007, 26 (18%) had hyperoxaluria on > or = 1 24-hour urinalyses. Of those with > or = 2 complete 24-hour collections and whose hyperoxaluria was observed before their last visit with the registered dietitian, 22 patients were identified. The patients were retrospectively separated into 2 groups according to whether they had been advised dietary changes alone (diet group, n = 10) or calcium citrate with meals, in addition to the dietary changes (supplement group, n = 12). The mean follow-up time was 317 and 266 days for the diet and supplement groups, respectively. Statistical comparisons within and between groups were made for urinary risk factors. RESULTS: Urinary oxalate excretion decreased from 56 to 43 mg/d and from 60 to 46 mg/d in the diet and supplement groups, respectively (P = .003 and P = .038, respectively). Calcium oxalate supersaturation decreased from 3.48 to 1.83 and from 2.37 to 1.52 in the diet and supplement groups, respectively (P = .043 and P = .002, respectively). Urinary calcium excretion did not change in either group. CONCLUSIONS: Gastrointestinal binding of oxalate by calcium is an effective clinical strategy for hyperoxaluria, whether mediated by calcium citrate with meals or by inclusion of calcium-containing foods with meals.
OBJECTIVES: To test the hypothesis that patients with hyperoxaluria, who modified their dietary calcium intake, would reduce their urinary oxalate excretion without raising their urinary calcium excretion. Diet is a major factor in idiopathic calcium oxalateurolithiasis, yet controversy exists regarding the ideal clinical recommendations. Approximately 20% of patients with calcium oxalate stone formation have hyperoxaluria (> or = 45 mg oxalate/d). Calcium supplements to bind dietary oxalate have been suggested, but clinical evidence of this therapy is lacking. METHODS: Of 144 adult patients with stone formation seen by a registered dietitian from September 2006 to September 2007, 26 (18%) had hyperoxaluria on > or = 1 24-hour urinalyses. Of those with > or = 2 complete 24-hour collections and whose hyperoxaluria was observed before their last visit with the registered dietitian, 22 patients were identified. The patients were retrospectively separated into 2 groups according to whether they had been advised dietary changes alone (diet group, n = 10) or calcium citrate with meals, in addition to the dietary changes (supplement group, n = 12). The mean follow-up time was 317 and 266 days for the diet and supplement groups, respectively. Statistical comparisons within and between groups were made for urinary risk factors. RESULTS: Urinary oxalate excretion decreased from 56 to 43 mg/d and from 60 to 46 mg/d in the diet and supplement groups, respectively (P = .003 and P = .038, respectively). Calcium oxalate supersaturation decreased from 3.48 to 1.83 and from 2.37 to 1.52 in the diet and supplement groups, respectively (P = .043 and P = .002, respectively). Urinary calcium excretion did not change in either group. CONCLUSIONS: Gastrointestinal binding of oxalate by calcium is an effective clinical strategy for hyperoxaluria, whether mediated by calcium citrate with meals or by inclusion of calcium-containing foods with meals.
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