That such a discrepancy should obtain is doubtless of profound though as yet imperfectly grasped significance. These authorities rightly assume that, since the kidney is practically the sole avenue for nitrogenous waste excretion, it follows that the _urea_ and _total non-protein nitrogen_ of the _blood_ must in the main be inversely proportional to the general efficiency of the _renal_ organs. Then, obviously, the same law, too, should, in lack of some other plausible explanation, govern the excretion of _uric acid_ also. But, as the above generalisation portends, it is apparently not so. Fortunately, Folin and Denis prosecuted their study still further, taking in examples of _gout_ (with and without clinically recognisable _nephritis_), also instances of _leukæmia_ and _lead poisoning_. The blood, again, in these disorders betrayed the same peculiarity, viz., that while containing an excess of uric acid, it did not contain correspondingly large amounts of urea or other waste nitrogen; in other words, the findings in the blood in gout were in full accord with the above generalisation, _i.e._, _the apparent lack of any relationship between the amount of uric acid and that of urea or total non-protein nitrogen in the blood_. Now in _leukæmia_ the cause of the _uricæmia_ is _over-production_ of uric acid, but in this instance the same is correlated with an increased _elimination_ of uric acid by the kidneys. Turning to lead poisoning, the medicinal administration of lead acetate results in a great _diminution_ of uric acid excretion, a response consistent with the view that lead inhibits the excretory power of the kidney for _uric acid_, the change, at first functional, becoming later organic; for it is held that the _uricæmia_, associated with plumbism, proves that the action of the lead is not due to inhibition of the formation of uric acid. Lastly, as to gout, opinion still wavers as to whether or not the excretion of uric acid in this disorder is appreciably _lowered_. On the other hand, it is significant that the reverse is never claimed, viz., that in gout the uric acid output is _abnormally raised_. Now, as we saw in _leukæmia_, the _high uric acid blood content_ is accompanied by a correspondingly _high uric acid output_; but, on the contrary, in gout, despite the _accumulation of uric acid in the blood_, there is _no parallel increase in its elimination_. Reflecting on the above considerations, Folin and Denis claim that “the mere fact that the uric acid may accumulate in the blood of the gouty without being accompanied by an increased elimination constitutes definite proof that the gouty kidney is damaged with reference to its ability to eliminate uric acid.”