Lead in the urine is by no means so common nor so definite a symptom of lead poisoning as might be supposed, considering the extreme manner in which the kidneys suffer in old-standing cases. Of particular importance in this respect is the case referred to by Zinn[43], where a woman aged thirty-three received 20 grammes of lead acetate in error. After the first acute symptoms had passed off, the case drifted on to one of chronic poisoning, with the usual symptoms of colic, anæmia, and cachexia. During the whole period of the disease, both acute and chronic stages, examinations of the urine for lead were made, using the method of Fresenius Babo[44]; yet lead was only detected in the urine during the early stages, and directly the acute symptoms had passed off no further lead could be detected. This point is of some importance, particularly when taken together with the experiments quoted by Blum[45], who, injecting animals with lead iodide, was unable to recover lead from the urine. The iodide only passed through the kidney, the lead being retained in the body. Jaksch[46] states very definitely that lead is not found in the urine in chronic cases, but only in the acute cases, and then quite early. With regard to the kidney two views are held--the one regarding the disease of the kidney as primarily affecting the bloodvessels, and the other as an initial parenchymatous change causing secondary obstruction and alteration in the vessels themselves. There is therefore much evidence to show that, whether the bloodvessels be primarily or secondarily affected, almost all observers are in accord in the opinion that at one time or another, either sooner or later, the bloodvessels become affected through the action of lead. Kobert[47] points out that in no case was distinct cirrhosis of the kidney produced in experimental lead poisoning in animals; inflammation certainly was to be seen, either interstitial or parenchymatous, but apparently the poisoning had not progressed a sufficient length of time for definite cirrhosis to be produced. On the other hand, kidney changes have been found of various types, all of which may be the precursors of the ultimate cirrhotic and fibroid change occurring in the kidneys seen in chronic poisoning by lead as well as in chronic alcoholism. Particular stress must be laid on the fact that cirrhotic kidneys are so frequently the direct result of long-continued alcoholic excess, and, from what has been demonstrated in the experimental researches on predisposition to lead caused by alcohol, the condition of cirrhosis of the kidney in a lead-worker is by no means indicative of lead poisoning, as it may be an old alcoholic effect long antedating that due to lead.