(2) Some individuals with granular kidney never develop gout. Also we have to recall that— (1) Paroxysms of gout often occur for many years before the symptoms of interstitial nephritis develop. (2) In persons of gouty stock acute attacks may ensue at an age at which nephritis is practically unknown. Apart from the difficulty of reconciling these disparities, we cannot overlook the fact that both gout and granular kidney are very common diseases, sufficiently common, as Samuel West pointed out, to be not infrequently associated accidentally, without any cause or connection. Again, both affections, be it observed, are prone to develop in the middle and later decades of life. In light of this, is it not readily conceivable that both may arise independently, mere coincidences, both evidences of _pre-senilism_? Hastings Gilford, indeed, classes gout with syphilis, lead, and alcohol as amongst “the chief promoters of pre-senility.” Again, certain toxic agents which predispose to or initiate renal mischief also favour apparently the incidence of gout, _e.g._, _lead_ and _alcohol_. Samuel West, discussing the relationship of both gout and lead to granular kidney, maintains that, though each may produce chronic change in the kidney, neither of them _causes_ granular kidney. But the presence of granular kidney, he holds, greatly enhances the liability of the victim to gout on the one hand and plumbism on the other; also, to both together and in each affection alike markedly increases the gravity and the risk. Sir William Roberts, too, has some wholly relevant observations on this point. Thus all will agree with him that “it is difficult to conceive that plumbism induces the same constitutional diathesis as that which obtains in true gout.” He held that gout and plumbism, though they differ in all other respects, yet have one point in common, a tendency to uratic deposition. But such precipitation, he contended, was the outcome of a gouty tendency, reinforced by lead poisoning; or if, on the other hand, uratic deposits occurred in plumbism, the same had but accentuated a pre-existing gouty diathesis. In this connexion, too, it should be recalled that the frequent association of gout and lead poisoning which exists in London is not seen in the North of England or in North America. Is it not clear, then, that reflection on the broad clinical affinities exhibited by gout and granular kidney does but emphasise the essential distinctness of the two morbid entities? Inferentially, too, it lends no colour to the assumption that gout is of primary _renal_ origin.