The question of the acid-base factor in the etiology and pathogenesis of rickets is one that has long excited interest. The experimental results have, however, been conflicting and the controversial discussions have failed to clarify the situa tion. Summaries of the earlier work have been given by Shelling ('25), Hess ('29), Gyà ¶rgy ('29) and Goldblatt ('31) and in our earlier papers (Shohl et al., '28, Shohl et al., '32). That rickets is associated with an acid metabolism and tetany with an alkaline, has been strongly advocated by Freudenberg and Gyà ¶rgy ('22). The role of acidosis in the pathogenesis of rickets has recently been reviewed by Morris, Ford and Graham ('36) who could find no evidence that acidosis was "either a causal or associated factor in infantile rickets." The acid-base equilibrium of the blood shows little or no variation from the normal in either clinical rickets or infantile tetany, or, except in special cases, in experimental rickets (Shohl et al., '31). Therefore, efforts to show changes in metabolism have been directed toward studies of the ex cretion of acid and ammonia in the urine. With regard to the effect of ingestion of acid our previous experiments have tended to confirm Gyà ¶rgy's thesis, with 69