Bright's disease is not primarily a kidney disease, lint is really a circula tory disturbance. The brain and kid neys, the end-organs of the circulation, suffer most. It may well happen that death comes on from brain-lesion at a when the kidneys are yet in rea sonably good condition. Details of a case in which, by careful dieting and avoidance of extremes of temperature or other hurtful factors, the kidneys were spared, yet the fatal issue came through the brain. The brain is a very sensitive organ, and may show signs early in the ease. The kidneys are in sensitive, and may not react until late in the progress of the arterial changes.
The first symptoms of Bright's disease may be those of increased arterial ten sion. There may he, because of this. increased frequency of urination or oc casional nose-bleed or persistent head ache. A very early symptom may lie functional gastric disturbance from in creased blood-pressure. These gastric symptoms must not be confounded with the nausea and vomiting of later stages of a epliritis. The prenephritie condition of Bright's disease may be detected in the irregularities of the circulation. These may give rise to clumsiness m the use of limbs or to actual paresis of one or more members. There may be tem porary aphasia, and this symptom may recur several times, passing off com pletely in the interval. The earliest symptoms of Bright's disease if carefully looked for will nearly always be found in the brain. L. Faug,eres Bishop (Pro ceedings Amer. Med. Assoc.; Medical sews. June 21, 1902).
Pathology. — The reduction in size and weight is about equal in both organs in genuine primary contraction of the kidneys. The two kidneys may together weigh not over two ounces, and they may be only one-half or one-third the normal size. They are frequently imbedded in thick, adipose tissue, and the capsule is thick, opaque, and very adherent; so that, on stripping it off, portions of the renal cortex come away at the same time. The outer surface of the organ is red, irregularly granular, or finely nodular, and occasionally small cysts are present. The tissue is firm, dense, and resistant to the knife. The cut surface shows a thin, atrophied cortex, with dark-reddish streaks alternating with pale portions.
Anxieties, worries, and the high nerv ous tension required by modern business activity and by social life (the latter, particularly, in elderly ladies) favor the development of chronic Bright's disease. Associated with these causes are usually to be found an overindulgence in rich foods and sedentary habits.
The cold, moist climate of New Eng land and the Middle States seems, to Purdy, to predispose to contracted kid ney. Hydronephrosis, chronic pyelitis, and chronic congestion of the kidney (of cardiac origin, etc.) may cause a chronic productive nephritis without exudation, though never the true "con tracted and red-granular" kidney.
The pyramids are darker than the cortex, and are also diminished. In the gouty contracted kidney they show fine stria tions of sodium orate or of uric acid, or crystals representing uric-acid infarc tions. The principal changes are seen microscopically to be an increased pro duction of connective tissue, especially in the cortical substance, and a more or less proportionate degeneration and atrophy of the renal parenchyma. The destruction of the latter is due to the circulation of noxious agents, but it is replaced by cicatricial fibrous tissue (Weigert). This new tissue is not uni formly distributed in the cortex, but appears in irregular masses around the shrunken glomeruli or between the tubules. In the pyramids the distri bution is more general. The glomeruli are, in many instances, very small and fibrous in advanced cases; in the earlier cases the cells of the tufts and capsules are swelled and multiplied and a small celled infiltration may be seen around the glomeruli and tubules. This cellular infiltration later becomes fibrillated and ends in thickening. The changes in and the growth of the capillary and infra capillary cells and of those around the tufts are partly responsible for the glomerular atrophy, as are also the cap sular thickening and hyaline or waxy degeneration and the thickening and occlusion of arterioles. The tubules show decided changes, some being in cluded in masses of connective tissue, with resulting compression-atrophy and even obliteration of the lumen. Others show constriction by the intertubular connective tissue, the lumen eleswhere thus being increased; this is especially prominent in the granules on the outer surface of the kidney, and little cysts may be seen here and there by the naked eye, as the result of damming back the urine in the tubules thus affected. The epithelium lining these tubules shows granular, fatty, or waxy degeneration, and may be either flattened, cuboid, or swollen in variety. The tubes may con tain fatty or granular debris and tube casts.