To our mind, albeit, the disparity carries with it the inevitable postulate that in gout some other factor intrudes, some _tertium quid_, something vital, something biological, haply an _infection_. For even if we grant, for the sake of argument, that _renal retention_, if it were proved, might explain such anomalies in the excretion of uric acid and other nitrogenous metabolites as occur in gout, yet, nevertheless, no one could possibly contend that this factor alone could explain the nature of gout, could adequately account for its dramatic and protean phenomena. TO WHAT MAY BE ASCRIBED THE DEFICIENT ELIMINATING CAPACITY OF THE KIDNEY FOR URIC ACID? Naturally the advocates of the renal theory had to account in some way for the alleged functional disability of the kidney. Thus, Sir Dyce Duckworth, recalling the occasional occurrence in hysteria of _anuria_, held that, judging from the general phenomena of acute gout, “the influence of the _nervous system_ ... must not be left out of account as a possible determining factor for renal inadequacy.” Others, with whom Duckworth disagreed, propounded the view that the deposition of urates in the renal tissues was essential for the initiation of a nephritis in the gouty. Duckworth, on the other hand, held that nephritis could develop in their absence. Croftan considers the renal changes in gout identical with those of chronic plumbism. From experiments with hypodermic injections of _xanthine_ and _hypoxanthine_ over a prolonged period, he concludes that the presence of minute quantities of purin bases in the circulation is capable of producing _marked renal changes_. On the other hand, _uric acid_, injected into the circulation of healthy animals for a period of over three months, produced _no renal change_ whatever. As to this possibility, viz., that the _circulating uric acid_ might lead to _nephritis_ in the _gouty_, some reflections of Folin and Denis are instructive. Normal blood, according to these observers, contains not less than from 1-2 or 2-5 mg. per 100 grams, while that of _gouty_ blood does not, in their experience, exceed 6 mg. Continuing, they observe, “There is, however, no reason to suppose that a uric acid concentration of 4-6 mg. per 100 grams of blood is very much more irritating or stimulating to the kidney than the somewhat more dilute solution represented by normal blood. Disregarding the insolubility of uric acid, the elevation of its threshold of elimination from 2-4 or 6 mg. (per 100 grams of blood) is certainly a small one. Kidneys in which the threshold of elimination for urea has risen by 10-20 mg. (per 100 grams), or even more, are extraordinarily common.”