Again, Schade has pointed out that colloids may precipitate in reversible form or not. If in irreversible (_e.g._, fibrin) form, the concretion will remain permanent. But if the colloidal precipitate is reversible, it may be redissolved, as happens with the uric _acid infarcts_ of the infant’s kidney. In conclusion, we see, therefore, _re_ crystalloids and colloids in animal juices, that the conditions of their solubility are most complex, and though they do not explain the nature of gout, the variations doubtless stand in intimate relation to the _formation of tophi_. LOCALISATION OF URATIC DEPOSITS Uratic deposits evince a decided predilection for _cartilages_, tendons, muscles, and skin. This localised distribution of the depositions would seem to suggest their dependence on _local tissue peculiarities_. Now the presence of _sodium_ salts in a solution diminishes the solubility of urates therein. Consequently, in seeking to explain the incidence of _tophi_, it was suggested that _cartilage_ and _tendons_, being richer in _sodium ions_ than the _blood_, this might account for the fact that urates tend to be precipitated in these particular structures. Again, Almagia, working in Hofmeister’s laboratory, noted that thin sections of _cartilage_, if left for some hours in a solution of sodium urate, will take up _uric acid_. Direct inspection readily reveals the presence of white foci and diffuse opacities due to uratic deposits. The marked affinity of normal cartilage for uric acid is again attested by the fact that, given injection thereof in quantity into the peritoneal cavity of rabbits, the uric acid may often be detected by the murexide reaction in _joint cartilage_, though apparently not in other tissues. This behaviour would appear to justify the conclusion that the observed accumulation of uric acid in the cartilages in the presence of states of _uricæmia_, may be explicable on this same basis. In any case, this marked affinity of even _normal_ cartilage for uric acid seems to disprove the necessity of Ebstein’s postulate, viz., that the dissolved uric acid sets up inflammation, and that an _antecedent necrosis_ precedes the _deposition of urates_. Still, even if we concede the fact that _normal cartilage_ has a marked affinity for _uric acid_, how is it that in _leukæmics_, despite their high blood content of _uric acid_, no _uratic deposits_ ensue? Does not such disparity seem to indicate that in gout some other factor intrudes? in other words, that the excess of _sodium ions_ in particular tissues, while it may favour deposition therein, is inadequate of itself to actually determine the formation of tophi. THE CAUSATION OF TOPHI