But this, be it noted, is neither so marked nor so constant as the subsequent _increase_; in short, at the zenith of an acute attack, _an augmented output of uric acid_ ensues. At the very time when presumably the alleged functional renal impediment would be most pronounced, the impermeability of the organs for uric acid accentuated! Surely such behaviour seems scarcely compatible with the supposition that there is even a temporary diminution in the capacity of the kidney to excrete uric acid. Does it not in truth constitute strong proof of the reverse? Moreover, the said vagaries that herald the oncoming and that chequer the course of the paroxysm are not _invariable_, an obvious _caveat_ against hasty _etiological_ inferences therefrom. Any tendency thereto should also be curbed by the reflection that, viewing the character of the uric acid excretion in gout as a whole, the variations therein are not more extensive than in _healthy_ individuals, and assuredly, _on the mere basis of the fluctuations in uric acid excretion_, no diagnosis of gout is possible. _Retarded Purin Elimination._—The mainstay in argument, however, as advanced by more modern advocates of the renal theory of gout, is that a _retarded output of exogenous purin_ is typical of this disorder; but, here, again, there is no room for dogmatism. Thus Walker Hall reminds us that “the quantity of purins present in the food does not overstep the solubility of urates in the blood-stream, for once the material is metabolised and ready for removal the amount of blood, so far as solubility goes, places the whole amount of purins within the reach of the renal cells in less than twenty-five minutes.” We see, therefore, as far as _rapidity of transport_ to the kidneys is concerned, there is no delay in presentation of the opportunity for the excretion of exogenous purin. While the alleged tardiness of output is attributed to defective action of the _kidneys_, it is at least equally possible that the delay, as Walker Hall states, “may be due to a defective or idiosyncratic nuclear metabolism, which results in the formation of isomeric purins or incomplete purin combination, and which makes greater demands upon the selective activities of the renal cells;” for it must be recollected that as yet we are ignorant as to the exact form in which uric acid circulates in the blood-stream, whether as _sodium mono-urate_ or in _organic_ combination. Moreover, experimental _injections of uric acid_ into the _tissues_ or _veins_ show no impairment in the elimination capacity of the kidneys for uric acid. Thus, Wells cites evidence that “the kidney in gout shows no lack of ability to excrete uric acid injected into the tissues.”