Volume 2
A text-book of practical medicine : with particular reference to physiology and pathological anatomy / by Felix von Niemeyer ; translated from the eighth German edition, by special permission of the author, by George H. Humphreys and Charles E. Hackley.
- Date:
- 1880
Licence: Public Domain Mark
Credit: A text-book of practical medicine : with particular reference to physiology and pathological anatomy / by Felix von Niemeyer ; translated from the eighth German edition, by special permission of the author, by George H. Humphreys and Charles E. Hackley. Source: Wellcome Collection.
Provider: This material has been provided by the Royal College of Physicians of Edinburgh. The original may be consulted at the Royal College of Physicians of Edinburgh.
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![remain only the stage of inflammatory swelling and that of atrophy and shrinkage. But even the connection between these two stages has been denied by certain authors—Johnson and other English writers—who maintain that these conditions, instead of being phases of one and the same disease, are the products of totally different pathological processes. The very great diversity of opinion regarding the histology of Bright's disease may be summed up as follows : For some authors the essential primary lesions in all forms of the malady originate in the renal epithelium {Johnson) ; for others, the disease begins only in the interstitial connective tissue (Traube). Others again believe that it may commence in both or either of these tissues. Hence they recognize an intertubular or interstitial, and an intratubular or parenchymatous form of the malady ; but they admit the coex- istence of the two forms. Johnson first pointed out a hypertrophy of the muscular coat of the small arteries, not only of the kidney, but of other organs, and showed that under such circumstances the epithelium cannot remain intact; and he traces back the hyper- trophy of the left ventricle of the heart, so often met with in Bright's disease, to the greater resistance opposed in that affection by the hypertrophied vessels. Latterly there has been great controversy upon the views of Gull and Sutton, according to whom, in the con- tracting form of the disease, the primary lesion is not in the kidney at all, but the atrophied kidney is merely one of the lesions which accompany a general disorder of the minute arteries and capillaries, and which consists in a deposit of hyaline lymph in the adventitia of the arteries (seldom in the intima), and in the outer coats of the capillary walls. It must be admitted that shrinking of the kidney and degeneration of the arterial walls often coexist; but further research has shown that such coexistence of the two lesions is by no means constant.] In Bright's disease the epithelium of the uriniferons tubules exhibits the alterations which we have repeatedly described as char- acteristic of all parenchymatous inflammations. Its cells first in- crease considerably in bulk, through imbibition of an albuminous liquid ; their contents then undergo fatty metamorphosis, by which the epithelial cells gradually become converted into cells of fatty granules. Finally, the cell-membrane perishes, and the fat-globules emerge free into the urinary tubules. While these are the essential changes which the kidney under- goes, in the majority of cases coagulating exudations are also formed m the tubules, and in many instances proliferation of the interstitial connective tissue occurs. Atrophy of the kidney, which sets in](https://iiif.wellcomecollection.org/image/b21981772_0002_0029.jp2/full/800%2C/0/default.jpg)
