Indeed, in view of this, as hitherto ascertained, _absence of uricolytic enzymes_, there can, as Wells says, “be little doubt that the fundamental reason for the existence of uric acid gout in man lies in the inability of the human organism to destroy uric acid. Consequently, inasmuch as man, unlike other mammals, cannot destroy uric acid rapidly by oxidation, he is always a potential victim of uric acid retention and deposition.” Now we have, we hope, shown that there is no evidence that the _uric acid retention_ in gout is due to functional inability on the part of the _kidney_ to excrete uric acid. This being so, we have, as Von Noorden rightly says, no right to do violence to the facts by assuming that, in a case lacking any other evidence of _nephritis_, a condition of “latent nephritis” is the cause of the uric acid retention and deposition. Similarly, there is at present no evidence forthcoming that the retention of uric acid is due to _abnormal purin combinations_ in the _blood_. Nay, according to Wells, on the best evidence obtainable, uric acid exists in a _free_ state in the blood, and not combined, as has been urged by many workers in this sphere. But if the cause of _uric acid retention_ lies neither in the _kidneys_ nor in the _blood_, there must exist something abnormal in the gouty individual which renders impossible what may be termed a _compensatory uric acid excretion_. Now, as disclosed in the previous chapter, experimental research, in diseases other than gout, has shown that the _bodily tissues have an appreciable capacity for retention of uric acid_ (Fine). This, moreover, gains probability from the fact that Wiechowski, in his prolonged studies as to the possibility of uric acid decomposition in the human body, was never able to detect any evidence of _uricolysis_. Furthermore, on the clinical side, the fact that _intravenous injection of uric acid_ does not produce a corresponding degree of _uricæmia_ seems, as Bass and Herzberg suggest, to indicate that in gout the _retention capacity of the tissues for uric acid is augmented_. Lastly, in the precipitation and anchoring of urates in the tissues in gout, we have objective proof, _i.e._, tophi, that the uric acid is actually held in the tissues. Does not this seem to indicate that there are _peculiarities of tissue in the gouty_? What, then, the subtle change that determines the _retention and deposition_ of urates in the tissues in gout? May we not, with Walker Hall, hazard the reflection that there may be differences between the _nucleotides_ of normal and gouty tissues? For, doubtless, if there be peculiarities of tissue in the gouty, these will be reflected in abnormalities of _tissue function and metamorphosis_.