CHRONIC BRIGHT'S DISEASE. 15 



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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 Button, 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 uriniferous 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 

 in the tubules, and in many instances proliferation of the interstitial 

 connective tissue occurs. Atrophy of the kidney, which sets in 



