Again, as modern investigations show, the variations in the uric acid content of the _blood_, _re_ the incidence or intensity of attacks, are most _erratic_. Far from its being essential that uricæmia be present, acute attacks may occur with even a _sub-normal_ uric acid blood content; in short, the variations are so erratic as to seem quite out of keeping with the assumption that the uricæmia in gout is primarily of _renal_ origin. If it were so, one would expect no such vagaries in the uric acid content of the blood. One would rather, given the existence _ab initio_ of a _renal functional defect_, look for not only a permanent _uricæmia_, but further, from time to time, augmentations and diminutions thereof, synchronising with the rise and wane of gouty paroxysms; in other words, that in gout the clinical course and crises of the disorder would be linked up with harmonious variations in the degrees of uricæmia. URICÆMIA DOES NOT NECESSARILY PORTEND GOUT If it were so, why does not every case of nephritis develop gout? The researches of Myers and Fine have shown that _uric acid_ is the nitrogenous metabolite that first _accumulates_ in the _blood_ in _early_ interstitial nephritis. Only in its _later_ stages do urea and other waste nitrogenous products undergo like retention therein. Now let us review these findings, _re_ nephritis, in light of another statement by Folin and Denis, which runs as follows:— “In pure gout, unaccompanied by any abnormal urea retention in the blood, the kidney is damaged (so far as we yet know) only with its function of removing down to the normal level the uric acid of the blood.” Is it not clear, then, that in the _early_ stages of _nephritis_, viz., prior to retention of urea and other waste nitrogen, we have precisely that isolated functional renal disability, _i.e._, _inability to excrete uric acid_, that we postulate to be in operation in the _initial_ stages of _gout_? Yet, notwithstanding this similitude in the blood content of the two disorders, cases of nephritis do not necessarily develop gout. Indeed, as a matter of fact, examples of nephritis, of all grades and intensities, may run to their full end without manifesting any symptoms even remotely reminiscent of gout. Even Magnus Levy, ardent advocate as he is of the primary renal origin of gout, could not but admit that this salient clinical obstacle barred the way to acceptance of his otherwise plausible view. However, he fails to proffer any other solution of the problem.