Oliver[48], Charcot[49], Gombault[50], Hoffer[51], and others, found a certain amount of parenchymatous degeneration. Von Leyden[52], however, was able to produce a granular condition of the kidney with glomeruli shrunken and an arterio-capillary fibrosis. Gayler[53], on the other hand, thinks that the arteritis of the smallest arteries is the preliminary effect upon the kidney, whereas more recently Glibert[54] published plates of the kidney showing definite sclerosis as well as interstitial nephritis.
Cornil[55] and Brault[56] think the vessels are affected only secondarily, and that parenchymatous changes are the primary lesion. Hoffer[57], by feeding guinea-pigs with lead, produced very definite obliterative arteritis. Klemperer[58] claims to have produced inflammation and definite necrosis of portions of the kidney substance.
The whole of the kidney is not necessarily affected. Only portions of it may show changes, while Kleinenberger[59] notes that in chronic lead poisoning, at the time of acute exacerbation of the disease, granular casts as well as red blood-cells are found; and, further, that in cutting through them crystallized masses are occasionally found, consisting of urates, and sometimes containing lead.
Gayler[60] considers that the effect on the kidney commences in the muscular coats of the smaller vessels, in which endarteritis followed by obliterative arteritis is set up.
Practically all observers, therefore, are in agreement that the kidney suffers to a very considerable extent in chronic poisoning, and the majority of observers are also in agreement that the bloodvessels themselves are the primary seat of the change. Further, the presence of blood in the urine is exceedingly rare in chronic lead poisoning, despite Kleinenberger’s[61] statement to the contrary. It certainly may occur during a very acute attack, but we have never seen this symptom.
Circulatory System.
—Arterio-sclerosis occurring in lead-workers has been known for some time, and the anæmia of saturnism has been known for an even longer period. For some time no definite type of anæmia was associated with lead cachexia, and the anæmia was generally regarded as one arising from general malnutrition. Here and there through the literature of the pathology of lead poisoning are to be found remarks which suggest that the action upon the bloodvessels may be a primary instead of a secondary effect. Obliterative arteritis is described by Uhthoff[62], Pflueger[63], Oeller[64], and Pal[65], and in other cases obliterative retinitis has been considered to be associated with the action of the lead upon the vessel walls.
Heubel[66], and later Rosenstein[67], found that, in dogs poisoned with lead, definite cerebral anæmia was produced, due to vaso-constriction, and consider it to be due to the direct action of lead upon the intima of the vessel walls. Associated with such poisoning were symptoms of eclampsia and uræmia, and the latter author considers that the uræmia is due to vaso-constriction of the kidney vessels.
Oliver[68] and others have also pointed out the alteration in the pulse-rate associated with exacerbations of colic, and a number of observers have noted that certain drugs, such as atropin and amyl nitrite, which are known vaso-dilators, have a distinctly calming effect upon the paroxysms of pain.
One or two other observers have actually noted the presence of hæmorrhages in the lesions; thus, in the case quoted by Mott[69] definite yielding of the vessel walls and signs of old hæmorrhage are described amongst other lesions in the brain. Seifert[70] also describes the presence of hæmorrhages amongst the ganglion cells in the anterior columns of the cord, both in the case of persons who have died of lead poisoning and animals to which lead had been given experimentally. In addition, Sajous[71] describes a case of paralysis of the superior laryngeal nerve, associated with hæmorrhages, in the region of the abductor muscles of the larynx. Mott’s case also showed this laryngeal hæmorrhage.