Further observations on the waxy or amyloid form of Bright's disease / by T. Grainger Stewart, M.D.

  • Stewart, Thomas Grainger, 1837-1900.
Date:
1864
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Licence: Public Domain Mark

Credit: Further observations on the waxy or amyloid form of Bright's disease / by T. Grainger Stewart, M.D. Source: Wellcome Collection.

Provider: This material has been provided by The University of Glasgow Library. The original may be consulted at The University of Glasgow Library.

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    directly from tlie branches of the renal arteiy into the vasa recta of the medullary portion, and from thence into the capillaries, without passing into tlie cortical portion at all. From this it is evident tliat not only in the waxy degeneration, but in other forms of disease of the kidney, where there is an obstruction of the jjassage of blood through the vessels of the cortical portion, an increased collateral pressure would be exerted on the vessels of the medullary portion, from whicli, in consequence, an increased flow of watery urine would take place, and the whole quantity passed might be above, or, at least, not below the average. But the amount of blood sent directly to the medullary portion is very much less than that sent to the cortical substance, and no one can conceive that a shutting off of the latter from functional activity could be more than compensated by increased activity in the former. To say that a set of vessels, not amounting to more than one-fifth of another set, are capable of performing all their functions, seems to me extremely unsound, and, especially in this case, untenable, seeing that the vasa recta of the medullary portion are themselves very often the seat of this degene- ration, and yet tlie polyuria is present. The explanation seems quite inapplicable to tliis fbrm of disease. Besides, it is by no means proved that merely the amount of blood in a vessel bears relation to the amount of fluid transuding through its walls; the state of these walls themselves may probably influence these transu- dations in a manner and to a degree that we by no means under- stand. I do not wish to commit myself to any theory on this point, but it seems to me that the probabilities are more in favour of my explanation than of the other. An increase of thirst and of drinking cannot be regarded as the essential cause of the polyuria, seeing that in some cases I distinctly ascertained that the amount of urine was equal to, or even surpassed, the total amount of fluids consumed. Character of the Urine.—The pale colour, and low specific gravity, and the presence of albumen, do not require special notice. The quantity of urea I hope soon to make the subject of special inquiry. The Tubecasts.—In the amyloid degeneration we may meet witli tubecasts of various kinds, the delicate transparent casts, which were formerly called waxy, and are now better termed hyaline ; these hyaline casts with occasional epithelial cells in a state of fatty degeneration enclosed in their substance, others with a larger number of fatty cells, and occasionally finely or coarsely gi-anuhu casts. Occasionally we see casts containing individual cells in a state of amyloid degeneration, and presenting its peculiar reaction. The occurrence of casts, such as these last mentioned, and which may be termed the amyloid casts, would- of course establish the diagnosis of amyloid degeneration of the kidney; but none of the others afford any special evidence on one side or other, for they occur in all forms of Bright's disease. Thus, the hyaline casts con- stantly occur in the late stages of'that degeneration which follows upon acute nephritis, and are thus evidently derived from uriniferous