BRIGHT’S DISEASE



The liquid undergoes considerable change in composition- diminution of albumin, increase in urea, with, at the same time, increase in specific gravity to 1018 and 1022, are what we principally observe.

When this acute of Bright’s disease terminates neither by death nor recovery, it passes into the chronic state. The febrile movement disappears and anasarca diminishes. The urine increases in quantity; the albumin is less abundant, but persists. At this time the disease presents the course and symptoms which we shall find again soon when describing Bright’s disease, chronic from the outset.

2. Bright’s Disease, Chronic fro the Outset.-This form, like the preceding, may follow an eruptive fever, typhoid fever, diphtheria or pneumonia, but in this case the beginning, instead of being febrile and tumultuous, is wholly unperceived and unrecognized; only by asking patients about their past may we succeed in connecting this chronic form of Bright’s disease to the previous existence of one of the diseases in which parenchymatous inflammation of the kidney is observed.

In other cases damp cold, long continued, is the only cause to which we may attribute the development of the disease. Lastly, there are cases in which it is impossible to find or to establish the aetiology of this form of Bright’s disease, chronic from the outset. Loss of strength, a particular kind of anaemia, with paleness of the face, puffiness of the lids, interpalpebral oedema, pale urine voided frequently, especially at night, but in volume below normal, anorexia, and pain in the head mark the beginning of this form.

If one examines the urine, one finds specific gravity diminished from 1006 to 1010; urea falls also sometimes to 9 grammes per litre, but the principal characteristic is the presence of albumen in notable quantity, reaching 4,6,8,10 grammes and more.

After several months the disease shows its character more and more. Oedema increases considerably, changing place, seizing often the face in the morning and the ankles in the evening. There is waxy pallor; loss of strength is marked, while difficulty of breathing is caused by the least movement.

The disease thus established may be prolonged for months, or even longer, but never more than three years.

The course is not regularly progressive; there are exacerbations followed by more or less complete remissions.

The exacerbations are caused usually by a chill, by overwork, by emotion, but especially by errors of diet. They are characterized by a decrease in the urine, which sometimes becomes bloody and contains always a greater quantity of albumin. Anasarca makes progress. There is sometimes vomiting, sometimes headache, and always a loss of strength, until the patient is obliged to keep to his bed.

Then amelioration takes place; it is marked by an increase in the quantity of the urine, a diminution in albumin and anasarca, return of strength and appetite. This remission which is never as complete as in interstitial nephritis, nevertheless allows the patient to resume his occupation, in port, and under the influence of intelligent treatment may be prolonged for a greater or less period of time.

From exacerbation to remission, and from remission to exacerbation, the disease, sometimes slowly, sometimes more rapidly, comes tote period of cachexia. This period is characterized by considerable dropsy. Anasarca distends the lower limbs, the skin of which becomes the seat of erythema, of fissures and sometimes of gangrenous plaques. Effusions form in the peritoneum and in the pleura. A certain degree of pulmonary oedema is usually evident. The urine becomes more more and more scanty, albumin is always present, but may diminish in quantity nevertheless, without improvement in the condition of the patient.

Anorexia, vomiting, and diarrhoea, still help to diminish the strength of the patient.

Seated usually upon a chair, because stay in bed is no longer possible, a prey to dyspnoea, resulting from dropsy of the pleura and lungs, pale and swollen, with limbs cracked and dripping incessantly with the liquid which distends them, the patient would die of exhaustion if uraemic accidents did not more usually terminate the disease. Failure of sight and headache, are the usual symptoms of this ending, which takes place either from eclampsia or from apoplexy, or from asphyxia, caused by pulmonary oedema.

In other cases, Bright’s disease assumes a form more chronic and slower. The renal lesion, from parenchymatous becomes interstitial, and the disease shows is every way the symptoms, course, and duration of the sclerotic form which we shall shortly describe.

Pathological Anatomy.-The acute nephritic lesion is essentially a glomerulitis, desquamative and with variable alteration in the tubular epithelium, infiltration of the interstitial tissue by round cells, catarrhal inflammation of the straight tubes, and inflammation of the arterioles.

The kidneys are considerably increased in size; they ar sometimes hard and tense, sometimes soft. Hyperplasia is found only in the cortical substance. Divested of their envelope the kidneys are found sometimes of uniform redness, or sometimes presenting a mottled aspect tinged with yellow. The pyramids show a more or less violet red tint.

Microscopical Examination.-More or less advanced inflammation of the glomeruli, which are not all in the same condition; some are congested, others anaemic, some normal. Albuminous and granular exudations from certain capsules take place. At other times the exudations are haemorrhagic. The tubuli are in general dilated somewhat. The epithelial cells are infiltrated with fat; sometimes pale cylinders, sometimes red globules, the result of haemorrhages, fill the loops of Henle and the straight canal. The connective stroma is not intact; it is oedematous, and shows round cells, more or less confluent, which indicate a certain degree of interstitial nephritis. Lastly, the small arterioles show cylindrical of fusiform thickening, which is the beginning of an obliteration of these arterioles.

This lesion is susceptible of complete recovery, at least if we may believe clinical experience. In other cases it ends with death. It may also end by passage into the chronic state. And in this case we have to study the evolution of a lesion which ends sooner or later in interstitial nephritis.

This conclusion is not that of authorities who allow the absolute separation of parenchymatous from interstitial nephritis, but is typical of acute nephritis, parenchymatous in character, having burst forth, either on occasion of typhoid fever, scarlet fever or some other infectious disease, or even in consequence of the effect of cold, and being terminated after several years by the symptoms and lesions of interstitial nephritis.

It is impossible to deny the morbid transformation of one of these lesions into the other.

The large red kidneys, more or less mottled with yellow and gray, soft or indurated, are transformed when the disease passes to the chronic state into the large white kidneys. Then, by a continuation of the evolution into small granular kidneys, retracted, white or red.

In the acute period the interstitial tissue is but little attacked. We find at most a few round cells interposed here and there in form of a trial between the tubules and at the openings of the arterioles. But the longer the disease the more are interstitial lesions noticed, leading by their evolution to atrophy and retraction of the kidney. Thus, facts show us that parenchymatous nephritis, when it passes to the chronic state, assumes all the characters of interstitial nephritis.

CHAPTER II.-INTERSTITIAL NEPHRITIS.

We have already said that interstitial nephritis depends upon arterio-sclerosis.

The beginning of interstitial nephritis often passes unperceived; it is characterized by polyuria and polydipsia, analogous to that of diabetes. There is perceived at the same time increase in arterial tension. It is to this increase of arterial tension that we should attribute the symptom of the “dead finger,” deemed by Dieulafoy a sign of nephritis without albuminuria.

In this first period, as a matter of fact, albuminuria shows itself often only in a transitory way, at long intervals, and in quantity estimated with difficulty. As we have already said the urine is very abundant; it is pale, of very low specific gravity, which varies from 1002 to 1012, containing a quantity of urea less than normal. he urine is slightly turbid, and may reach 2, 3 and 9 litres.

Patients are often tormented by continual headache. Anorexia, vomiting, or diarrhoea, dimness of vision, and amaurosis are observed in this form as in the preceding, but “in interstitial nephritis, amaurosis is related, not to a primitive alteration in the elements of the retina, but to a sclerotic alteration of the optic nerve and of the retina.” (Lancereau.).

OEdema may be completely lacking during nearly all the course of the disease. It is only when the nephritis has lasted for years, and when the patient becomes cachectic, that a certain degree of dropsy is evident, while at the same time albumin may reach 1,2, and 3 grammes per litre.

Clifford Mitchell