Epithelial

casts.

of fibrine which has escaped from the malpighian vessel. While pursuing its course towards the exit it has reached a wider channel, from the walls of which fibrine is poured out in sufficient quantity to surround and imbed it in a larger cylinder. In cases where I have seen such double casts in the urine I have found after death that the outer investment has evidently been supplied by the straight tubes which have been dilated and bared of epithelium, and have contained large fibrinous plugs. (See plate 3.)

Though as a rule fibrine forms the basis of urinary casts, and often is their only constituent, yet it sometimes happens that cylinders are found in the urine which appear to consist entirely of compacted epithelial cells, or of epithelial cells held together by fibrine so small in amount as to be barely perceptible. Not only do epithelial cells enter into the composition of casts, but, as has been stated, casts may contain anything which traverses the tubes. They therefore give an insight into what is going on in the gland, while by their diameter they show the calibre of the cavity in which they were moulded. If epithelial cells are imbedded, there is a catarrhal or inflammatory state of the tubes, which promotes Pus casts. the growth and detachment of cells. If pus cells are included, the inflammatory or catarrhal state has taken such hold of the tubes that the epithelial cells are replaced by pus globules. Blood globules will show that there has existed enough congestion to rupture the malpighian capillaries.

Granular casts.

Diameter of casts.

Amorphous granular matter will vary in its indication, according to its origin. It appears that such granular matter is of two kinds, one sort produced by the breaking up of detached epithelial cells, and generally associated with a late stage of tubal inflammation; the other sort belonging to granular degeneration, and apparently consisting of comminuted and altered fibrine.

The diameter of the casts will give indications of a certain kind. If the casts are of small size, not more than 1000 of an inch in thickness, they have come from tubes which retain their epithelial lining. If they are of large size, 500 or thereabouts, they have been moulded in tubes which have

lost their epithelial lining. If of larger size still, they may even be nearly double the width last mentioned-they have come from tubes which, in addition to the loss of their cellular lining, have become dilated. Casts of the largest sort may be always regarded as having been formed in the straight tubes, while the smaller varieties may come from the straight or convoluted tubes indifferently.

CHAPTER III.

Change

limited to tubes.

PATHOLOGY OF TUBAL NEPHRITIS.

Ir appears that, as regards inflammation of its secreting structure, the kidney bears an analogy with the mucous membranes, especially with such as are bestowed in a tubular form. When the bronchial membrane is inflamed, if the disease be violent enough to destroy life in a short time, we find that the membrane is injected, and that the tubes contain an excess of secretion, which is more or less altered from its natural state. If the patient die later in the disease the excess of vascularity is less evident, and but for the alteration in quantity and character of the fluid which the tubes contain, there is no very legible record of the morbid action which has proved fatal.

In the kidney the inflammatory change is also strictly limited to the inner surface of the tubes, and the product of inflammation, as in bronchitis, is an excessive growth of epithelium, of which the cells may be natural, or may, particularly if the disease has lasted any time, be changed in several particulars. They may become fatty, or may become changed into pus globules. The narrowness and contortion of the secreting tubes renders it very difficult for the epithelial growth to make its way out, when, as in this disease, it is superabundant. The consequence is that the ducts become packed to distention, and the organ is proportionally increased in size.

It will be convenient to consider the morbid anatomy of the disorder first in its acute, and then in its chronic form. It is not always easy to make the distinction, for the changes are the same in their nature in either case, although the

well-marked examples of each sort are sufficiently unlike each other.

ACUTE TUBAL NEPHRITIS.

and

The inflammatory action, in its early stage, is accompanied Acute by a great increase of blood in the gland, which becomes form. perhaps more than double its usual weight. The surface remains perfectly smooth, but there is a remarkable increase of vascularity. The vessels which divide the surface into lobules, and in health are but faintly seen, become intensely injected, sometimes so as to give an almost uniform redness Kidney ento the surface. The stellate veins which are seen in a later larged period of the disease are as yet absent. as yet absent. The capsule is injected. loose and thin, as in health. On section the inside presents a red or chocolate colour, and drips with blood. The pelvis is injected. Underneath the blood by which the tissue is obscured, a light-coloured or buff deposit exists, which does not belong to the healthy kidney. This becomes more evident when the surface has been washed. The malpighian bodies stand out as red dots. It may happen that though the disorder be no less acute, the congestion will be less conspicuous than the increase of bulk. The colour may be whiter than in health, though the cut surface exudes blood freely, and the whole organ is obviously injected. But the vascularity is masked by the opaque white epithelium which distends the tubes; and the cortex, which is greatly increased, looks as if it consisted of two materials: a red and a buff, coarsely intermingled. The cones are less changed than the cortex, being simply congested. Plate 1 represents a kidney in an early stage of nephritis, the result of scarlatina.

Under the microscope the cortical tubes are seen to be stuffed with an opaque brown material, which so long as it remains in the tube does not display any structure, but looks uniformly granular. Spread out on the glass it is seen to consist of cells of epithelium, not changed excepting that they may be stained of a brownish colour, beside blood corpuscles and indefinite granular matter; the latter probably

Tubes stuffed

with epithelium, granular

fibrine.

resulting from disintegration of the epithelial cells. This condition is most marked in the convoluted tubes, but the straight usually contain more or less of the same material. Beside the cell growth, there is usually fibrinous exudation in the tubes. In some cases (Vallance, p. 69) this is very abundant.

The malpighian bodies stand out prominently, and their vessel is seen to be distended with blood corpuscles. There are no other changes in the organ. The tubes are everywhere matter,and in contact with each other. There is no interstitial effusion, and, excepting the distention of the tubes and blood vessels, the organ is natural. The disorder-the desquamative nephritis of Johnson-is essentially a renal catarrh. It depends upon a too prolific epithelial growth, not upon any change in the nature of the cells, which, taken singly, present no tangible departure from their normal state.

Tendency

to

recovery.

The variations in the appearance of the organ depend upon the relative proportions of blood and of epithelium. It seems that the more congestive varieties are produced by exposure to cold, while those in which the epithelial formation is most evident are generally due to scarlatina (see plate 1). In the latter case the tubes contain little or no blood, but a profusion of natural gland-cells, with some granular material, probably derived from a breaking up of others.

It may be, if the attack is recent and slight, such as often occurs in the course of continued fever or diphtheria, that unless looked at with some care nothing might be noticed but that the cortex is more bulky than usual. The kidney is thick, heavy and rounded. The cortex often shows a sort of coarse grain, as if a buff-coloured formation had been packed in a minute vascular network.

The disease has a natural tendency to recovery. The vascular excitement in which it commences usually depends upon some transient cause, and will subside as it expends. itself in secretion, if the circumstances are such that free epithelial growth can take place. This process, however, in the kidney is fraught with peculiar danger, from the narrow