Brian H Eisner1, Michael L Eisenberg, Marshall L Stoller. 1. Department of Urology, University of California-San Francisco, San Francisco, California 94143, USA. eisnerbh@urology.ucsf.edu <eisnerbh@urology.ucsf.edu>
Abstract
PURPOSE: Increased sodium intake is thought to promote nephrolithiasis by dietary sodium hypercalciuric effects. However, equivocal data exist on whether increased urine sodium actually increases the nephrolithiasis risk. We examined the relationship between urine sodium and urine risk factors for nephrolithiasis. MATERIALS AND METHODS: We retrospectively reviewed the records of 880 patients evaluated at a metabolic stone clinic to determine the relationship between urine sodium and urine calcium, volume and calcium oxalate supersaturation. Patients were separated into sodium excretion quintiles. Tests of linear trend were performed by examining the linear contrast in coefficients and using Cuzick's nonparametric linear trend test. Multivariate linear regression with urine sodium as a continuous variable was done to assess the relationship between urine sodium and other urine variables. RESULTS: Tests of linear trend showed that urine calcium and volume increased with increasing urine sodium (each p <0.01) but urine calcium oxalate supersaturation decreased with increasing urine sodium (p <0.01). Multivariate linear regression was adjusted for age, sex, body mass index and urine constituents. Urine sodium was positively associated with urine calcium (beta = 0.28, 95% CI 0.15 to 0.41, p <0.001) but negatively associated with urine calcium oxalate supersaturation (beta = -0.013, 95% CI -0.016 to -0.011, p <0.001). There was a trend toward a positive association of urine sodium and volume (beta = 0.001, 95% CI -0.00019 to 0.002, p = 0.10). CONCLUSIONS: Increasing urine sodium does not appear to increase the risk of calcium oxalate nephrolithiasis. Global sodium restriction may not necessarily alter the risk of stone formation, ie cause changes in calcium oxalate urine supersaturation, in patients with a history of nephrolithiasis.
PURPOSE: Increased sodium intake is thought to promote nephrolithiasis by dietary sodium hypercalciuric effects. However, equivocal data exist on whether increased urine sodium actually increases the nephrolithiasis risk. We examined the relationship between urine sodium and urine risk factors for nephrolithiasis. MATERIALS AND METHODS: We retrospectively reviewed the records of 880 patients evaluated at a metabolic stone clinic to determine the relationship between urine sodium and urine calcium, volume and calcium oxalate supersaturation. Patients were separated into sodium excretion quintiles. Tests of linear trend were performed by examining the linear contrast in coefficients and using Cuzick's nonparametric linear trend test. Multivariate linear regression with urine sodium as a continuous variable was done to assess the relationship between urine sodium and other urine variables. RESULTS: Tests of linear trend showed that urine calcium and volume increased with increasing urine sodium (each p <0.01) but urine calcium oxalate supersaturation decreased with increasing urine sodium (p <0.01). Multivariate linear regression was adjusted for age, sex, body mass index and urine constituents. Urine sodium was positively associated with urine calcium (beta = 0.28, 95% CI 0.15 to 0.41, p <0.001) but negatively associated with urine calcium oxalate supersaturation (beta = -0.013, 95% CI -0.016 to -0.011, p <0.001). There was a trend toward a positive association of urine sodium and volume (beta = 0.001, 95% CI -0.00019 to 0.002, p = 0.10). CONCLUSIONS: Increasing urine sodium does not appear to increase the risk of calciumoxalate nephrolithiasis. Global sodium restriction may not necessarily alter the risk of stone formation, ie cause changes in calcium oxalate urine supersaturation, in patients with a history of nephrolithiasis.
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