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Clinical Investigation Unit, Department of Endocrinology and Department of Nephrology and Hypertension (to C.J.D.), University Hospital Leiden, The Netherlands
Address correspondence and requests for reprints to: Socrates E. Papapoulos, M.D., Department of Endocrinology, Building 1, C4-R, University Hospital, Rijnsburgerweg 10, 2333 AA Leiden, The Netherlands.
Dietary excesses in animal protein and/or salt have been implicated as risk factors in calcium oxlalate urolithiasis. The underlying physicochemical mechanism is, however, not known. Eight healthy men were given four different diets varying in animal protein and in sodium content for 1 week each. On a high protein intake (2 g/kg-day) significant changes in urinary calcium, uric acid, and citrate excretion rates were found. Similar changes in calcium and citrate were induced by a high sodium intake (310 mmol/day). The changes were more pronounced when a high protein was combined with a high sodium diet. Urinary calcium increased from 3.79 ± 0.31 to 6.42 ± 0.61 mmol/24 h and urinary uric acid from 4.69 ± 0.26 to 8.0 ± 0.47, whereas urinary citrate decreased from 3.93 ± 0.53 to 2.79 ± 0.34 mmol/24 h. All three dietary regimens induced a significant decrease in the ability of urines to inhibit calcium oxalate monohydrate crystal agglomeration, which was most marked during the combined diet (from 345 ± 39 to 205 ± 28 min). The ability of urines to inhibit crystal agglomeration was related to their citrate content (r=0.69, P<0.0001). These results show that high animal protein and/or sodium intake decrease the ability of urines to inhibit the agglomeration of calcium oxalate crystals and provide a possible physicochemical explanation for the adverse effects of dietary aberrations on renal stone formation.
* These studies were supported by Grant C-87.0683 from the Dutch Kidney Foundation.
Received November 20, 1989.
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