Sodium is neither a risk nor a protective factor in urolithiasis?

The effect of changes in urinary sodium, induced by dietary manipulation in normal subjects (NS) and in stone formers (SF) was studied by observing crytalluria qualitatively and by determining calcium, oxalate and phosphate crystallization quantitatively in an experimental model. In SF the calcium crystallization was significantly higher than in NS at all the three levels of urinary sodium studied. However, no difference was observed in oxalate and phosphate crystallization rates between these two groups. Calcium and oxalate (p less than 0.05) and oxalate and phosphate (p less than 0.001) were found to be correlated in NS but were non-significant in SF. The wide changes in the urinary sodium induced by dietary changes did not influence the crystallization rate of calcium, nor of oxalate and phosphate in NS as well as in SF. The results suggested that a sodium intake with lower and upper limits of 124 mg and 6,009 mg respectively did not act as "inhibitor" of crystallization rate nor did it induce hypercalciuria severe enough to pose a "risk" of stone formation. The results did not suggest that a high urinary sodium increases the solubility of calcium phosphate.