BACKGROUND: Human calcium oxalate (CaOx) nephrolithiasis may occur if urine is supersaturated with respect to the solid-phase CaOx. In these patients, dietary oxalate is often restricted to reduce its absorption and subsequent excretion in an effort to lower supersaturation and to decrease stone formation. However, dietary oxalate also binds intestinal calcium which lowers calcium absorption and excretion. The effect of increasing dietary oxalate on urinary CaOx supersaturation is difficult to predict. METHODS: To determine the effect of dietary oxalate intake on urinary supersaturation with respect to CaOx and brushite (CaHPO4), we fed 36th and 37th generation genetic hypercalciuric rats a normal Ca diet (1.2% Ca) alone or with sodium oxalate added at 0.5%, 1.0%, or 2.0% for a total of 18 weeks. We measured urinary ion excretion and calculated supersaturation with respect to the CaOx and CaHPO4 solid phases and determined the type of stones formed. RESULTS: Increasing dietary oxalate from 0% to 2.0% significantly increased urinary oxalate and decreased urinary calcium excretion, the latter presumably due to increased dietary oxalate-binding intestinal calcium. Increasing dietary oxalate from 0% to 2.0% decreased CaOx supersaturation due to the decrease in urinary calcium offsetting the increase in urinary oxalate and the decreased CaHPO4 supersaturation. Each rat in each group formed stones. Scanning electron microscopy revealed discrete stones and not nephrocalcinosis. X-ray and electron diffraction and x-ray microanalysis revealed that the stones were composed of calcium and phosphate; there were no CaOx stones. CONCLUSION: Thus, increasing dietary oxalate led to a decrease in CaOx and CaHPO4 supersaturation and did not alter the universal stone formation found in these rats, nor the type of stones formed. These results suggest the necessity for human studies aimed at determining the role, if any, of limiting oxalate intake to prevent recurrence of CaOx nephrolithiasis.
BACKGROUND:Humancalcium oxalate (CaOx) nephrolithiasis may occur if urine is supersaturated with respect to the solid-phase CaOx. In these patients, dietary oxalate is often restricted to reduce its absorption and subsequent excretion in an effort to lower supersaturation and to decrease stone formation. However, dietary oxalate also binds intestinal calcium which lowers calcium absorption and excretion. The effect of increasing dietary oxalate on urinary CaOx supersaturation is difficult to predict. METHODS: To determine the effect of dietary oxalate intake on urinary supersaturation with respect to CaOx and brushite (CaHPO4), we fed 36th and 37th generation genetic hypercalciuric rats a normal Ca diet (1.2% Ca) alone or with sodium oxalate added at 0.5%, 1.0%, or 2.0% for a total of 18 weeks. We measured urinary ion excretion and calculated supersaturation with respect to the CaOx and CaHPO4 solid phases and determined the type of stones formed. RESULTS: Increasing dietary oxalate from 0% to 2.0% significantly increased urinary oxalate and decreased urinary calcium excretion, the latter presumably due to increased dietary oxalate-binding intestinal calcium. Increasing dietary oxalate from 0% to 2.0% decreased CaOx supersaturation due to the decrease in urinary calcium offsetting the increase in urinary oxalate and the decreased CaHPO4 supersaturation. Each rat in each group formed stones. Scanning electron microscopy revealed discrete stones and not nephrocalcinosis. X-ray and electron diffraction and x-ray microanalysis revealed that the stones were composed of calcium and phosphate; there were no CaOx stones. CONCLUSION: Thus, increasing dietary oxalate led to a decrease in CaOx and CaHPO4 supersaturation and did not alter the universal stone formation found in these rats, nor the type of stones formed. These results suggest the necessity for human studies aimed at determining the role, if any, of limiting oxalate intake to prevent recurrence of CaOx nephrolithiasis.
Authors: R Corey O'Connor; Elaine M Worcester; Andrew P Evan; Shane Meehan; Dimitri Kuznetsov; Brett Laven; Andre' J Sommer; Sharon B Bledsoe; Joan H Parks; Fredric L Coe; Marc Grynpas; Glenn S Gerber Journal: Urol Res Date: 2005-05
Authors: Nancy S Krieger; John R Asplin; Ignacio Granja; Felix M Ramos; Courtney Flotteron; Luojing Chen; Tong Tong Wu; Marc D Grynpas; David A Bushinsky Journal: J Am Soc Nephrol Date: 2019-05-17 Impact factor: 10.121
Authors: Nancy S Krieger; John R Asplin; Kevin K Frick; Ignacio Granja; Christopher D Culbertson; Adeline Ng; Marc D Grynpas; David A Bushinsky Journal: J Am Soc Nephrol Date: 2015-04-08 Impact factor: 10.121
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Authors: Kevin K Frick; John R Asplin; Christopher D Culbertson; Ignacio Granja; Nancy S Krieger; David A Bushinsky Journal: Am J Physiol Renal Physiol Date: 2014-02-26
Authors: Kevin K Frick; John R Asplin; Murray J Favus; Christopher Culbertson; Nancy S Krieger; David A Bushinsky Journal: Am J Physiol Renal Physiol Date: 2013-01-23
Authors: Saeed R Khan; Margaret S Pearle; William G Robertson; Giovanni Gambaro; Benjamin K Canales; Steeve Doizi; Olivier Traxer; Hans-Göran Tiselius Journal: Nat Rev Dis Primers Date: 2016-02-25 Impact factor: 52.329
Authors: Kevin K Frick; John R Asplin; Nancy S Krieger; Christopher D Culbertson; Daniel M Asplin; David A Bushinsky Journal: Am J Physiol Renal Physiol Date: 2013-08-07