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.
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.