In the experiments on animals, subjected to poisoning over considerable periods, the condition of the kidney in every instance showed distinct histological changes; and the longer such animals had been subjected to the poisonous effects of the metal, the more advanced were the signs of degeneration in its structure. In the earliest cases the disease partook much more of the nature of an interstitial nephritis, and it was in the later and more chronic stages only that changes in the glomeruli and fibroid degeneration were to be found, but in even these earliest cases of poisoning definite minute interstitial hæmorrhages were to be found scattered about the kidney. These minute hæmorrhages did not cause symptoms of hæmaturia, as in none of the experimental animals was bloody urine observed. On the other hand, besides definite small areas of hæmorrhage, patches were discoverable, indicative of hæmorrhage which had undergone fibroid change. Even in the illustrations given by Glibert[5], there appears to be evidence that hæmorrhage had taken place and had undergone fibroid degeneration, and there is very little doubt that in cases of kidney disease, the preliminary action of the poison determines small local yieldings of the vessel walls, with leakage, often hardly amounting to true hæmorrhage, at such spots. There is nothing opposed to the theory in the findings of other observers; in fact, if the preliminary gross effect be leakage of the description given, all the other lesions described by various observers follow as a corollary. In the kidney, as in the other regions of the body, the venioles rather than the arterioles appear to be the preliminary site of destruction, and microscopical observation of the sections leads to the view that the intima of the vessels and not the media or the muscular coat is the one affected in the first place. Capillary hæmorrhages under these conditions are easier to understand than if the arterioles themselves or their muscular or middle coats were primarily affected. As degenerative changes progress, the whole of the vessel--external and middle coats and intima--undergoes change, ultimately resulting in the extreme narrowing and consequent blocking of the vessels themselves. Further shrinkage taking place in this area produces the shrunken sclerosed kidney. Zinc in the form of oxide behaves in very much the same way upon the kidney as does lead. An experimental animal, which was given 0·2 gramme of zinc oxide per kilogramme body weight by hypodermic injection in the muscles of the back, died in fifteen days, and the kidneys showed extensive hæmorrhages--not merely the minute and capillary hæmorrhages found in lead poisoning, but hæmorrhages extending right through from the cortex.