In this place will be considered the alterations in the functions of the kidney effected by the different forms of Bright's disease, and certain other more general consequences which are liable to follow.

The functional changes in the kidneys are directly expressed by the condition of the urine, and these two are properly considered together. In Acute parenchymatous nephritis the circulation in the complex vascular system is impeded by the direct effects of the acute inflammation, and also by the pressure of the increased epithelium in the tubules and glomeruli. There is thus -a great diminution in the amount of urine. The urine also is highly albuminous, this being an expression of the fact that the special selective function of the glomeruli is paralyzed. The urine usually contains blood. The urea excreted is greatly diminished proportionately to the scantiness of the urine, and the chief danger is the possible occurrence of Uraemia.

In Interstitial nephritis the alteration in function is very different. Here there is great vascular obstruction and great loss of the secreting epithelium by atrophy, and the result is the secretion of an excessive amount of watery urine which is very deficient in urea. It is easy to understand the diminution of the urea, as in the shrinking kidney there is great atro of the epithelium, but the excess of watery urine is more difficult to comprehend in view of the fact that there is great vascular obstruction in which the glomeruli, which are the special seats of the separation of the water, are greatly involved. The dilute condition of the urine is probably to be ascribed to the loss of the tubular epithelium and the occlusion of the capillaries around the tubules. It has been pointed out that the secretion as it leaves the glomeruli is dilute and fhat it is concentrated in its passage through the convoluted tubules. This concentration is hindered by atrophy of the epithelium and capillaries, so that the urine as secreted may be regarded as virtually the secretion as it leaves the glomeruli.

Intimately related to the condition of the urine are the increased arterial tension, and organic changes in the heart and arteries, which are so characteristic of chronic Bright's disease.

Increased arterial tension or increase in the entire arterial blood-pressure is an early phenomenon in interstitial nephritis, some have even believed it to precede the kidney disease. In order to a general increase in the arterial blood-pressure there is necessary either an increase in the peripheral resistance, such as may be produced by a general contraction of the arterioles, or an increase in force of the left ventricle. In interstitial nephritis we have both of these.

Hypertrophy of the left ventricle is one of the regular phenomena of chronic Bright's disease, so that the existence of the latter may often be suggested by that of the former. The heart has the elongated form described and figured at p. 448, Fig. 216.

Thickening of the walls of the arteries generally is the other phenomenon. This has been variously described as a thickening of the external coat mainly, an Arterio-capillary fibrosis, or a thickening of the middle coat, but it really consists for the most part of a general thickening, as shown in Fig. 430, involving both coats. It is detectable most readily in the arteries of the pia mater, which are easily examined by spreading out a small part of this fine membrane, Besides these thickenings, we have frequently atheroma in Bright's disease in people advanced in life.

Fig. 430. - Arteries of the pia mater in case of granular kidney and in health In the former the middle coat and, to some extent, the extenal are thickened.

(DlCKlNSON).

These thickenings of the arteries, whilst contributing to the increase in blood-pressure, are also in part its results. The blood entering the arteries with increased force requires greater resistance in the walls of the arteries in order to prevent dilatation, and may require also an •energetic contraction to prevent an excess of blood from passing through the arteries. The arteries subjected to increased blood-pressure are probably more liable to secondary changes such as atheroma.

The increase in blood-pressure involving such considerable structural changes seems such a large result from a local disease of the kidneys that several authors (especially Gull and Sutton) have come to the conclusion that chronic Bright's disease is a general affection of the fine arteries throughout the body, and that the kidney lesion is merely a part of this more general condition. This view is expressed in the term A rterio-capillary fibrosis introduced by Gull and Sutton. As a main element in determining whether the conditions under consideration are consequences of the kidney disease, the question may be asked whether increase of blood-pressure with hypertrophy of the left ventricle occurs in cases of disease of the kidney undoubtedly local in its character. The answer to this question is that diseases of the kidney which induce obstruction to the vessels similar to that in chronic interstitial nephritis do lead to the conditions under consideration. Thus, hydronephrosis with atrophy of the kidney tissue has repeatedly been observed to lead to it. Dickinson records a case in which a stone in the pelvis of the kidney produced contraction of the kidney and led to hypertrophy of the left ventricle. It may result from partial atrophy of the kidney from arterio-sclerosis, as in two cases observed by the author. Again, it has been produced in animals by inducing in them an indurative nephritis, which was done by ligaturing the renal artery for an hour and a half to two hours and then freeing the vessel.

It is obvious from these observations that the hypertrophy of the heart is related in its causation to the lesions in the kidney, and it may be said generally that, whenever there is considerable vascular obstruction in the kidneys, hypertrophy of the heart is lmble to occur, unless the health of the patient be too low to allow of such a formative process. It is not usually marked in amyloid disease of the kidney, as the amyloid condition frequently depends on lesions which seriously injure the health, and it is not nearly so common in parenchymatous as in interstitial nephritis, for the double reason that the vascular disturbance is much less, and the interference with the general health greater in the former than in the latter.

The changes in the arteries throughout the body consist in thickenings of their coats.

The explanation of the increased blood-pressure is still to be considered, and this is somewhat obscure. It is due to the condition of the kidneys but the mere vascular changes there are not sufficient to account for it. Increase of the general blood-pressure is caused by arterial and capillary obstruction such as exist in the kidneys in this disease; but, considering the means at the disposal of the vascular system for compensator dilatation of arteries, such a local obstruction is insufficient to account for a general rise in pressure.

The changes seem inexplicable on a purely mechanical theory, and the explanations of Cohnheim as amplified by Fagge seem the most probable. In all the cases in which the cardiac and vascular changes occur there is obstruction to the vessels in the kidney, chiefly the arteries and the capillaries of the tufts. In order to the secretion of the proper amount of urine the blood must circulate much more quickly through the remaining vessels. This can only be effected by a rise in the blood-pressure in the vessels concerned, which may be brought about by a relaxation of the larger renal arteries. The activity of the renal secretion seems to be largely determined by the amount of urea and other constituents in the blood, the condition of the arteries as to contraction being regulated through the nervous system (Cohnheim and Roy). But if the local dilatation of the arteries be inadequate to cause a sufficient flow of blood, and the urinary constituents still tend to accumulate, then there can only be a relief by a general rise in the blood-pressure brought about by increase in the force of the cardiac contractions. In this view of it the cardiac hypertrophy is compensatory, and is brought about in order to prevent the undue accumulation of urea in the system.

Edema And Dropsy

Anasarca or oedema of the skin is an early and characteristic symptom of acute parenchymatous nephritis. The subject has been already considered at pp. 120-121. The oedema of the skin is to be related, On the one hand, to the excess of water retained in the blood, and, on the other, to the irritation of the skin by the abnormal constitution of the blood. The irritant which acts on the kidneys will also act on the skin.

Literature

Richard Bright, Reports of medical cases selected with a view of illustrating the symptoms and cure of disease, by a reference to morbid anatomy, vol. i., 1827; Rayer, Traite des malad. des reins, 1840; Frerichs, Die Bright'sche Krankheit, 1851; Rosenstein, Nierenkrankheiten, 2nd ed., 1870; Johnson, Lect. on Bright's dis., 1873, and Med lect. and essays, 1887; Grainger Stewart, Prac. treatise on Bright's dis., 1868, and Clin. lect. on important symptoms, Albuminuria, 1888; Charcot, Lect. on Bright's dis. (transl.), 1579; Aufrecht, Die diffuse Nephritis, 1879; Weigert, in Volkmann's Sammlung, No. 162, 1879; Rirbert, Nephritis and albuminuria, 1881; Dickinson, Dis. of kidney, part ii., Albuminuria, 1877; Ralfe, Dis. of kidneys, 1885. Glomendo-nephritis and Scarlatina - Klebs, Handb. d. path, anat., i., 644, 1870; Klein, Path, trans., xxviii., 1877; Coats, Brit. Med. Jour., 1874, ii.; Friedlander, Fortschritte der Med., 1883; Langhans, Virch. Arch., lxxvi. and xcix.; Litten, Charite-Annalen, iv.; Crooke, Birmingham Med. Rev., 1886-87. Interstitial nephritis - Traube, Gesammelte Beitrage, ii., 1871; Leyden, Zeitschr. f. klin. Med., ii. and iii.; Ziegler, D. Arch. f. klin. Med., xxv.; Ebstein, (Gout) ibid., xxvii.; Pedell, (Lead) D. med. Wochenschr., 1884; Jacob, ibid., 1886; Saundby, Path, trans., xxxi., 1880; Greenfield, ibid. Cardiac and Vascular changes - Traube, Zusammenhang v. Herz- und Nierenkrankheiten, 1856; Gull and Sutton, Med. chir. trans., Iv., 1872, and Path, trans., xxviii., 1877; Sotnischewsky, Virch. Arch., lxxxii.; Lemcke, D. Arch. f. klin. Med., xxxv.; Holsti, ibid., xxxviii.; Mahomed, Guy's Hosp. Reports, 1885; Cohnheim, Allg. Path., ii., 349, 1882; Fagge, Prin. and Prac. of Med., ii., 447, 1886; Cohnheim and Roy, Virch. Arch., xcii., 1883.