Gout, with a section on ocular disease in the gouty

by Llewellyn J. Llewellyn

Gout and Nephritis

The association between gout and renal disease is admittedly intimate, in so far as gouty subjects often have granular kidneys, while gout is a frequent complication of this type of renal disorder. Nevertheless, the clinical relation between the two diseases is ill defined and, moreover, somewhat erratic. In most instances the renal defect is engrafted upon the antecedent gout, or the sequence is reversed; and, again, the two conditions may arise contemporaneously. Lastly, in sharp and disconcerting contrast to this mutual overlapping of the two disorders, we have the awkward fact that more commonly gout and granular kidney run to their fell end quite independently of each other.

Thus, Sir William Roberts observed: “It is quite common to see articular gout, even of chronic and inveterate character, run its entire course without any accompanying signs of structural disease of the kidneys.” The same, to be sure, is equally true of granular kidney, which may pass to its close without any suspicion of gout.

Now, as we have seen, the primary renal origin of gout fails of demonstration. Is gout, then, causally related to granular kidney, or is there some less direct relation between them?

As to this, to begin with, it is extremely rare that a “gouty” subject develops acute nephritis. In the exceptional instances when it does occur it is either purely accidental or else the outcome of an exacerbation of a previously existing interstitial nephritis.

The question then arises, Can gout when long continued originate per se the condition we are pleased to term “gouty kidneys”? As seen above, such renal lesions are by no means an inevitable sequel or concomitant of long-standing gout. Moreover, there is nothing specific of gout in the so-called “gouty” kidney. It is an interstitial nephritis, which may assume the appearances of the ordinary “contracted kidney” or the “arterio-sclerotic” type. There may be uratic deposits at the apex of the pyramids, or even an uric acid calculus; but even so that of itself constitutes no proof of the renal changes being “gouty” in origin. In short, the prefix “gouty” as applied to these types of renal lesion is just as unscientific and unwarrantable as used in regard of “phlebitis,” “eczema,” and so forth.

Nor, quâ gout as a causal factor, are we in better case if the renal disorder be of the “arterio-sclerotic” type. No direct relationship is established between gout and arterio-sclerosis beyond the fact that both are usually met with in middle-aged or elderly people. Moreover, a man may develop arterio-sclerosis and arterio-sclerotic kidneys, yet never have any vestige of gout.

There being nothing specific of gout in the lesions of so-called “gouty” kidneys, we must revert to the clinical findings to refute or establish any causal connection between gout and the renal disorder. Now, gout is a disease of middle and late life, and rarely of itself proves mortal. On the other hand, it appears increasingly probable that the seeds of granular kidney are laid in earlier life, and, on the average, its course is shorter than that of gout. Also the two disorders have clinical facies absolutely distinct the one from the other.

From the above considerations it is, I think, clear that, whatever the hidden nexus between gout and “granular kidney,” it is neither essential nor constant. It is rather, I believe, of the nature of a coincidence. Furthermore, as applies to so many problems pertaining to gout, and, for that matter, to “granular kidney” also, we labour under the grave disability that both terms are, especially “gout,” very vaguely applied and when used are often a matter of personal opinion. Consequently, as Samuel West shrewdly observes, “it is difficult to discuss satisfactorily the relation of two conditions to each other when neither condition admits of precise definition, for some authorities are more easily satisfied in the diagnosis of gout than others; and, while some place all forms of chronic interstitial nephritis in one and the same category, others are not so comprehensive, and regard granular kidney as a definite clinical disease, of which the interstitial nephritis is only a part.” Under these circumstances, the need for further and more exact researches in this sphere is but too obvious.

Meanwhile, accepting the general opinion as to the frequency of the co-existence of gout and granular kidney, is there any explanation thereof? For myself, I am inclined to believe that the common overlapping of the two disorders is in large measure due to this, that the factors, i.e., excess in alcohol, overeating, etc., that make for the eruption of gout, are largely identical with those that promote the development of granular kidney. Hastings Gilford holds “there is very little doubt that syphilis, lead, and gout do not so much originate Bright’s disease as excite it into activity when it already exists in a smouldering or latent condition.”

With this view I feel much in accord, and if to the malign effects of gout be superadded the effects of alcohol or, haply, lead also, how incalculably greater the chances of fanning into flame any latent tendency to nephritis—a legacy, perhaps, of some long bygone infection.