Cornil remarks that the expression of Bright's disease applied to the kidney has nowadays no more value than the expression of dyspepsia applied to the pathology of the stomach or of asystolie applied to the pathology of the heart. He distinguishes : 1. Granular alteration of the renal epithelium, —a common lesion found in different forms of hyperaemia, especially in those symptom atic of the infectious diseases.
2. Fatty degeneration, which is secondary to the chronic diseases.
3. Chronic congestion of the kidney, due to mechanical disturbances of the circulation.
4. Diffuse nephritis, in which all the anatomical elements of the kidney are involved.
(a) Acute nephritis with predominance of congestive and inflam matory phenomena.
(b) Acute nephritis with predominance of diapedesis.
(c) Acute nephritis with predominance of degenerative lesions.
(d) Nephritis with predominance of the lesions of the glomeruli.
(e) Nephritis with predominance of lesions of the epithelium.
(f) Nephritis with predominance of lesions of the stroma.
5. Systematic nephritis, in which from the first the lesion involves exclusively one of the elements of the kidney.
(a) Epithelial cirrhosis of the kidney. A chronic degeneration of the renal epithelium with atrophy of certain systems of tubes and glomeruli.
(b) Vascular cirrhosis—a true interstitial inflammation of the kidney with endarteritis of the renal arteries.
All of Cornil's anatomical descriptions are very true to nature, but his classification is not one adapted to clinical purposes.
As we look back over the history of the disease, it is easy to rec ognize the points of difference and the progress which has been made.
From the very first we find authors looking at the disease from two points of view : that of the symptoms and that of the lesions. So that, while some regard Bright's disease as a nephritis with its attendant symptoms, others regard it as a disease of the blood, or of the arteries and capillaries, with which a nephritis may or may not be associated.
At the time when Frerichs wrote, it was customary to regard a great many morbid conditions as of an inflammatory character, and to think that every inflammation went regularly through three stages. So we find Frerichs arranging all the lesions of Bright's disease as belonging to the stages of congestion, exudation, and contraction of a nephritis, and teaching that all the forms of acute and chronic Bright's disease were different stages of one and the same morbid process.
Then we find in England, first Johnson, and then Dickinson, re ferring most of the kidney lesions to changes in the epithelium of the tubes. Here, again, it soon became evident, that although changes in the epithelium exist 4ud are of importance, yet Johnson and his school had taken too one-sided a view of the subject.
That iu some cases of Bright's disease there is waxy degeneration of the walls of the arteries and Alalpighian tufts was early recognized by Rokitansky. As these kidneys have been more studied, it has been found that there may be : 1. Waxy degeneration of the arteries and glomeruli, without any change in the other parts of the kidneys or any disturbance of its functions.
2. Waxy degeneration of the arteries and tufts, followed by chronic changes in the rest of the kidneys.
3. Waxy degeneration of the arteries and tufts, forming an unim portant part of a chronic nephritis.
The next step forward was the recognition by Traube of the con dition of chronic congestion of the kidney, its dependence on heart disease, and its termination in changes in the structure of the kidney.
Then we find an attempt by Grainger Stewart to go back to Fre richs' classification of an inflammation in three stages, but separating the waxy and the cirrhotic kidneys.
Among English writers we find a disposition to class the kidneys according to their gross appearance, and to speak of the large white kidney and the contracted kidney, and to regard the cirrhotic kidney as not inflammatory. In England, also, we find especial attention drawn to the condition of the arteries and capillaries in the kidneys and in the rest of the body as a cause of the kidney lesions and of the symptoms.
The next step forward was the recognition of the changes in the glomeruli, first by Kiebs, then by Cohnheim, Friedlander, and others.
At the same time there has been an attempt, especially in Ger many, to class together the changes in the epithelium, the exudation of inflammatory products, and the formation of new connective tissue under the one head of parenchymatous inflammation, teaching that the morbid process originates in the epithelium, and that the other changes are secondary to this.