Again, given _intravenous_ injection of uric acid into a _normal_ man, its excretion occupies several days, and it fails to appear _quantitatively_ in the urine. But if administered during a course of _atophan_, then the _whole_ amount injected is excreted within twenty-four hours. If the same procedure be followed in a _gouty_ individual, precisely the same results are obtained; in other words, both normal and gouty kidneys react in identical fashion to atophan. Given an inherent functional defect, _quâ_ uric acid excretion, in the _gouty kidney_, one would scarcely expect a wholly _normal_ reaction thereto. Surely some disparity would be disclosed, some aberration in response as compared with _normal_ renal organs. Again, while McLester and others claim that atophan exerts “a selective stimulating influence on uric acid excretion,” it is quite possible that its _rôle_ may be otherwise explained. May it not influence the actual _formation_ of uric acid, or, failing this, the _form_ in which it is presented to the kidneys for excretion? Nicolaier and Dohrn, indeed, believe that _atophan_ influences in some way purin metabolism within the _muscles_ and so leads to _increased formation and excretion of uric acid_. At any rate, whatever be the explanation of the action of atophan, the fact that _healthy_ and _gouty_ kidneys react _alike_ thereto cannot be interpreted as proof of defective capacity for uric acid elimination in gouty subjects, indeed the reverse. Moreover, in all our attempts to saddle the kidneys with the responsibility for the delay in exogenous purin excretion, we are for ever hampered in that we know not whether the alleged renal impairment is _primary_ or _secondary_ to the gout. That the kidneys are frequently functionally inefficient in the _later_ stages of gout may be conceded. But what of the _initial_ phases of the disorder? Some talk very glibly of subjects who are, they say, “potentially gouty.” But has the rate of disposal of ingested purins been investigated in persons suffering from so-called “goutiness,” or, perhaps more pertinently, in those individuals, not uncommon, who, while exhibiting _auricular tophi_, have yet experienced no frank attack of gout?