In all deference, we doubt the legitimacy of the inference, if only for the very excellent reason that, to quote Von Noorden’s words, even to-day “it remains uncertain whether the retention of urate arises because the outlet is blocked, or because the uric acid is held fast by chemical affinities.” Apart from this, there are several objections to Folin and Denis’ assumption. URICÆMIA NOT NECESSARILY DUE TO RENAL DEFECT Thus Pratt, in some examples of his cases of gout, found that there was no apparent diminution or delay in the output of exogenous purin in the urine. On the other hand, he observes that “our study of the blood shows that _a marked increase in retention of uric acid in the blood_ may result from the ingestion of purin bases even when _no evidence of retention is found on examination of the urine_.” This would appear to indicate that the uricæmia, sequential to exogenous purin intake, ensues independently of and apparently despite the absence of any delay or diminution in uric acid elimination. Again, Walker Hall, discussing the metabolism of exogenous purins, reminds us that a gouty subject excretes an excess thereof as completely as a normal individual, with only this difference, that he takes a longer time to do so; but even this disability is removed by a simultaneous intake of atophan. His comment is that “the gouty kidney, therefore, is not poisoned beyond compensating for and responding to an extra load.” “Perhaps,” he says, “the situation may be summed up in the observation that _the uricæmia of the gouty is maintained in spite of a fair renal elimination_.” URICÆMIA NOT PECULIAR TO NEPHRITIS Again, a grave obstacle to the acceptance of Folin and Denis’ inference is that uricæmia, though incidental to nephritis, is not peculiar thereto. Thus Roy Upham and Higley noted its presence in 85·6 per cent. of their cases of _nephritis_; but, on the other hand, they found that no less than 40 per cent. of another series of clinical cases, not _suffering from nephritis_, also showed uricæmia. This would appear to indicate that, while uricæmia is an exceedingly common symptom of early chronic interstitial nephritis, it is by no means _specific_ for that disorder; in other words, its diagnostic valency as a symptom of _nephritis_ is distinctly limited. _Reverting_ now to _gout_, what evidence is there that the uricæmia therein is due to defective eliminatory capacity on the part of the kidney for uric acid? Certainly there is no proof that the kidney, at any rate in the _initial_ stages of gout, suffers from this particular functional disability. Indeed, the fact that, at the very acme of an acute attack, the output of uric acid is not only not diminished, but actually _increased_, constitutes strong proof of the reverse.