BRIGHT demonstrated the existence of a morbid species characterized by inflammation of the kidney, albuminuria and oedema. He deemed the different clinical forms which this disease presents different phases of the same morbid condition. Physicians, after him, struck by the difference which these forms assume, subdivided Bright’s disease into two distinct diseases: parenchymatous nephritis and interstitial nephritis.
There is, then, a dualist school opposed to the unicist school of Bright. It is represented principally by Lancereau. Is there really a single malady, of different characteristics, according to the phases which it goes through, or do there really exist several affections of different nature, incorrectly joined together by the single name of “Bright’s disease?”.
This question is difficult to answer. On the one hand is a fact impossible to contest, namely, that when parenchymatous nephritis ends neither by recovery nor by death, either in the first weeks or the first months of the disease, but pursues a slow and chronic course, it is soon accompanied by the symptoms and the lesions of interstitial nephritis, so that as a consequence in such a case, the interstitial nephritis, with ultimate renal atrophy, is indeed, the last phase of the parenchymatous nephritis; and that in such a case the theory of Bright is absolutely true.
On the other hand, it cannot be denied that there are cases in which the disease begins in an insidious manner, progresses very slowly, with more or less complete periods of remission, and with periods of aggravation characterized by a symptomatic complexus which has no resemblance to that of parenchymatous nephritis, and in which the kidney, throughout all periods of the disease, shows the lesions of interstitial nephritis, and ends fatally in renal atrophy.
In such cases the nephritis is interstitial in the outset, and rightly distinguished from Bright’s disease proper. To this must be added that interstitial nephritis is always joined of gout, of syphilis and of lead-poisoning; that it is accompanied, in consequence, by the hepatic, pulmonary, encephalic, and, especially, cardiac lesions common to arterio-sclerosis.
Physicians who, like Lecorche and Talamon, defend the unicist doctrine of Bright’s disease, strive to show that in acute cases, designated by the name of parenchymatous nephritis, there is always an affection of the heart and of the vessels analogous to that which is always observed in interstitial nephritis. They affirm that every nephritis is always accompanied by considerable increase in arterial pressure, and consequently by dilatation and then by hypertrophy of the heart.
Traube has explained these cardiac and vascular phenomena by the obstacle which the arterial circulation meets in the kidney in consequence of inflammation there. This explanation is questionable, but, what is more important, dilatation of the heart is by no means always found in all cases of Bright’s disease. (Lecorche, page 419.).
Thus, Bamberger’s statistics show 807 cases of primary Bright’s disease to be accompanied only 344 times by hypertrophy of the heart.
The statistics of Galabin cover 101 cases and show only 34 cases of hypertrophy. Upon autopsies made at the Charity Hospital and Berlin, Vais remarked that in 20 cases of parenchymatous nephritis, hypertrophy existed in 14 cases.
Labadie-Lagrave, in the Dictionary of medicine and Surgery, says, word for word, “that, if a certain degree of dilatation of the ventricles, together with fatty degeneration of the myocardium, is the rule in chronic parenchymatous nephritis, hypertrophy of the left ventricle is wholly foreign to the symptomatology of this nephritis.” (Article on “The Kidney,” page 783.).
Experiments made upon animals are not sufficiently unanimous in results to show that hindrance to the circulation determines cardiac hypertrophy and elevation of arterial pressure.
Ludwig tied the renal arteries without causing either elevation of arterial pressure or hypertrophy of the heart. Grawitz and Israel, contracting the renal and removing one of the kidneys, produced hypertrophy of the left ventricle, but did not increase arterial pressure.
Lewinski alone produced hypertrophy of the left heart and an increase in the arterial tension by contracting the renal arteries in dogs. (Leorche, page 407.).
The conclusion from the total of these experiments, and also from clinical facts, is that hypertrophy of the left ventricle, instead of being closely united tote existence of the parenchymatous nephritis, is only an exceptional occurrence in the course of this disease. Lecorche and Talamon, and those who uphold the doctrine of absolute unity, plainly exaggerate when they speak of hypertrophy of the heart as a constant lesion in this disease.
Increase of arterial tension, which, according to Huchard, has always for its corollary chronic inflammation of the arteries and hypertrophy of the heart, is the constant lesion of interstitial nephritis, for the reason that this latter form of disease is joined to the existence of gout, or of lead-poisoning, which has for its lesion general arterio-sclerosis.
It is difficult to say whether interstitial nephritis, supervening as terminal phase of parenchymatous nephritis, is accompanied by general arterio-sclerosis or not. It is difficult to say, because we have not yet studied this question of pathological anatomy, nor distinguished sufficiently simple interstitial nephritis from the interstitial nephritis which follows parenchymatous nephritis, and which constitutes Bright’s disease in its last stage.
Upon the whole, then, we hold that there is such a thing as an interstitial nephritis which, from beginning to end, has always the characteristics of sclerosis; that this nephritis is accompanied always by intense thirst, by polyuria, by albumin in the urine, usually in small quantity and sometimes but intermittently present, by pale urine of low specific gravity, with notable diminution of urea. Let us add, as a characteristic of this form of nephritis, that it is not usually accompanied by oedema, except in the period of cachexia.
Interstitial nephritis is, in symptoms and in lesions, absolutely distinct from parenchymatous nephritis. It is also distinguished by an extremely chronic course, a very long duration, and a constant termination by uraemic accidents.
Interstitial nephritis is, plainly distinguished from parenchymatous disease by its relations with gout, plumbism, and the general arterio-sclerosis accompanying these two latter conditions.
We shall, therefore, take chapters for the consideration of our subject: one for Bright’s disease, a morbid species; the other for interstitial nephritis, a disorder depending on arterio-sclerosis.
CHAPTER FIRST.-bRIGHT’S DISEASE.
Bright’s disease is characterized by anasarca, albuminuria, and inflammation of the kidney, first parenchymatous, but finally interstitial, if the disease lasts long enough.
Bright’s disease has two forms-one markedly acute in its beginning, the order of insidious origin and chronic course.
1. Acute Bright’s Disease.-This may begin when the patient is in full health, or, on the contrary, by way of complication, in the course or at the end of acute diseases: scarlet fever, diphtheria, typhoid fever, pneumonia, etc.
An intense febrile movement, vomiting and headache mark the beginning of the disease. The patient usually feels a dull pain in the region of the kidneys, while at the same time the urine is diminished to quantity, although micturition is frequent; the urine often contains blood, is always high-colored, of specific gravity lower than normal-falling to 1010 or even 1006, together with, at the same time, a great diminution of urea, which falls as low as 9 grammes to the litre; but the characteristic feature is the presence of albumin in quantity habitually considerable (4, 6, 8, 12, grammes or more): sometimes the urine, when heated, solidifies in the tube.
At the same time the dropsy shows itself. It begins almost always in the face, in the eyelids or in the subconjunctival tissue. There is then observed what full of tears, and there is shown the raising of the ocular conjunctiva by a layer of liquid. OEdema increases over the face, the natural lines disappear, and the face-immobile, pale and shining-appears like marble. Dropsy spreads over the rest of the body and anasarca becomes general. The disease, thus established, progress rapidly, and terminate in some days or some weeks by death or recovery.
Death takes place customarily either fro internal oedema (oedema of the lung, oedema of the glottis, pleuritic effusion, pericarditis, encephalic dropsy); often general anasarca, diarrhoea and progressive enfeeblement characterize the last days of the disease; at other times uraemic accidents, of which the most frequent are eclampsia and coma, come to put an end to the sufferings of the patient.
When the disease is to terminate by recovery, the first symptom is the increase of the urine, which rises rapidly to 1,2,3, and 4 litres. At the same time the febrile movement disappears and anasarca diminished in proportion to the increase of the urine.
