distress often comes on so insidiously that its existence is not even suspected until swelling in the feet and ankles, gradually increasing upwards, and a little puffiness of the eyelids, cause attention to be directed to the urine. But it is this form which so frequently terminates in Bright's disease.

The inflammatory condition of the organ becomes gradually, and in some instances slowly, transformed into the stage of fatty degeneration, which produces the enlarged, pale, fatty kidney of Bright. In this stage the kidney is very much enlarged, and increased in weight; its capsule is readily separated, and its surface is smooth with occasional depressions, it is of a pale yellow colour, with a peculiar mottled appearance from the intermingling of some healthy tissue with the great mass of diseased. On a longitudinal section of the organ being made, the medullary cones generally present a healthy appearance, and no alteration in size. The cortical substance is observed to be greatly increased in diameter, and to have a pale yellowish white colour. This increased bulk and altered colour are produced by distention of the convoluted tubules, by the deposit and gradual accumulation of fatty matter within their lining, glandular, epithelial cells. This fatty matter is deposited in the shape of globules and granules of various

sizes, and distends the cells to such a degree that many of them burst or fall to pieces, and their contents accumulate within the tubules, and block up their channel, so that the tubules, in their turn, become swollen and distended, and in some instances ruptured; the accumulation of fat within them being facilitated by their length and tortuous arrangement; the diseased epithelial cells and their débris are generally cemented together into casts by a fibrinous matrix. Under the microscope the tubules present an opaque black appearance. It is necessary to mention that the swollen tubules compress the distal capillaries distributed between and around them to such a degree that the circulation of the blood through these minute vessels is retarded and very greatly diminished; it is this condition which imparts to the surface and cortical substance of the enlarged fatty kidney its peculiar exsanguine appearance.

The whole of the tubules are never equally affected by fatty degeneration: in the worst cases some are left in a more or less healthy condition and capable of discharging their secreting function.

When the disease runs its full course, the stage of fatty enlargement is succeeded by atrophy; the size of the organ is considerably diminished; its surface

becomes very uneven, numerous elevations alternating with depressions; and when a section is made, the cortical substance is observed to be wasted, this being effected by absorption and washing away by the urine of a large proportion of the fatty degenerated epithelium, and consequent shrivelling, atrophy and even closing of a large proportion of the tubules. The malpighian corpuscles are less conspicuous, many of them being reduced in size, the fibrous matrix is relatively increased, and the arteries are thickened and much more prominent. When the kidneys have reached this phase of disorganisation, they are no longer able to discharge their function, and death from uræmia is the usual result.

When fatty degeneration is established the urine becomes more abundant, much paler, and less albuminous than during the inflammatory period; it contains no blood corpuscles, nor granular epithelium, nor tubule-casts containing them; it throws down a light coloured, flocculent deposit, in which are found an abundance of tube-casts containing fat globules and granules (fatty casts), and some that are hyaline; also free epithelium loaded with fatty particles. The urine is still highly albuminous, this condition being persistent throughout the whole progress of the disease.

The specific gravity of the urine in this stage varies considerably, according to the extent to which the kidneys are involved, and the quantity of albumen. But when the density is low, notwithstanding the addition of albumen, and the urine at the same time is scanty, it indicates greatly diminished secretion of the solid urinary excreta and their consequent retention in the blood to a highly dangerous degree; so that, under such circumstances, the invasion of uræmic coma may be dreaded.

The morbid condition of the kidneys, just described, is productive of three exceedingly important conditions, which it is necessary to study separately, namely: 1. Albuminaria. 2. Retention of water in the blood. 3. Retention of the solid excreta of the urine.

Albuminuria is the earliest and most persistent symptom, being the last to disappear, even in cases terminating in complete recovery. It is not only a symptom of great interest pathologically, but the mechanism of its production, concerning which there has been much difference of opinion, supplies one of the most important indications of treatment in Bright's disease. In the inflammatory stage this symptom and the accompanying hæmorrhage are undoubtedly caused by the hyperæmia or active con

gestion of the vascular system of the organ, producing distention of the malpighian capillaries, and the escape of blood serum, and of blood through their walls; similar to what occurs in the inflammation of other parts, but with this difference that the serum, instead of accumulating in the surrounding tissues is, in consequence of the peculiar position of the vessels from which it escapes, poured into the tubules and discharged in the urine. I may add, that it is the peculiar position and arrangement of these vessels which cause hæmorrhage from them in renal inflammation. It is necessary to state that by the blocking up and distention of the tubules by solid fibrinous casts, and the pressure thereby exerted on the distal capillaries, passive congestion becomes superadded to the primary, active hyperæmia, so that the effusion and hæmorrhage give no relief to the distended malpighian vessels, and the albuminuria is maintained.

The albuminuria of the fatty stage, when blood corpuscles have disappeared from the urine, is produced by a mechanism similar, in character, to that which gives rise to dropsy, from obstruction of the venous circulation, as in heart disease. To understand this mechanism, it is necessary to bear in mind the anatomical relation subsisting between the