SYMPTOMS - CHRONIC PRODUCTIVE NEPHRITIS WITHOUT The typical urine of chronic non-exudative nephritis is a urine increased in quantity, of a specific gravity of about 1.010, containing a diminished quantity of urea, without albumin or casts, or with a trace of albumin and very few casts. But exacerbations of the nephritis and changes in the circulation may for a time consider ably increase the quantity of albumin and the number of casts.
Very important modifications of the urine, however, are of ordi nary occurrence. It is quite possible with nephritis of this type far advanced to have urine not below 1.023 in specific gravity and with out albumin or casts. When one sees this urine during life and then the kidneys after death it is difficult to understand how they can be long to each other.
On the other hand there are cases in which the specific gravity of the urine falls almost to 1.000, either with or without waxy degenera tion of the blood-vessels. In some cases the quantity of urine is very much increased—several quarts in the twenty-four hours. During the attacks of contraction of the arteries, to which these patients are liable, the urine may be diminished to a few ounces or even sup pressed.
Cerebral Symptoms.—In a great many of the cases cerebral symp toms are developed at some time in the course of the disease.
Headache and sleeplessness are often present, the headache some times so severe and continuous that the patient is nearly maniacal. Instead of the headache there may be neuralgic pains in different parts of the body.
Muscular twitchings and general convulsions are much more seri ous. They may be early symptoms, or not occur until lath in the disease.
Hemiplegia, with or without aphasia, may be the first symptom to call attention to the nephritis, or may not occur until later in the disease. The invasion of the hemiplegia is sudden and is usually ac companied by coma. There is loss of motion alone, or of both mo tion and sensation. The hemiplegia, aphasia, and coma may con tinue up to the time of the patient's death, or disappear after a few hours or days. In the latter case the patient may have several such attacks. These attacks have been ascribed to localized oedema of the brain. In the cases which I have seen there were no changes in the brain tissue, but the cerebral arteries were damaged by chronic arteritis.
Delirium, mild or violent, stupor, and coma may come on in sud den attacks, or be developed slowly and gradually.
When these cerebral symptoms come on in attacks the pulse is of high tension, the temperature is raised, and the patients are said to suffer from acute Very often they recover from a number of these attacks. In the fatal attacks the pulse often loses its tension and becomes rapid and feeble; the patients die Comatose with a feeble heart.
Instead of such acute attacks of cerebral symptoms, delirium and stupor may come on gradually in persons far advanced in their ne phritis. The temperature is then apt to be below the normal and the pulse is rapid and feeble.
Temporary blindness, neuro-retiuitis, or nephritic retinitis are de veloped in a moderate number of the patients.
Chronic bronchitis and emphysema very frequently exist and their symptoms often form a large part of the clinical history.
Attention has already been called to the large share that chronic arteritis may have in the production of some of the renal symptoms.
The Heart.—The left ventricle of the heart regularly becomes hypertrophied after the nephritis has lasted for several months. The disposition to hypertrophy is, I think, rendered greater by repeated attacks of contraction of the arteries and by complicating arteritis. The hypertrophy is usually easily made out. The patient remains unconscious of its existence, or has disturbances of sensation and pal pitation. As the disease goes on the hypertrophied heart may become feeble, and then clyspncea and the other evidences of feeble circulation make their appearance.
In the same way the complicating endocarditis, which so often exists, may give no trouble until the valves are a good deal changed, or the ventricles dilated, or the heart's action altered, or the arteries contracted; then the circulation is interfered with, and the results of venous congestion of different parts of the body show themselves.
Dyspmea is a frequent symptom, often the first symptom noticed by the patient. It is a spasmodic dyspncea coming on in attacks, which last for minutes, hours, or days. It is made worse by bodily or mental exertion, or by the recumbent position. It does not resemble bronchial asthma. It is apparently due to the association of changes in the arteries and heart. It cannot be distinguished from the dysp ncea which is caused by arteritis without nephritis. With contrac tion of the arteries alone, or with a feeble heart alone, no dyspncea may exist; but if the contraction of the arteries be so great that the hypertrophied heart cannot overcome the obstruction, or if with con traction of the arteries the heart becomes dilated or feeble, then the attacks of dyspncea begin. At first the attacks are not severe and are of short duration, but if the mechanical conditions which cause them cannot be controlled, they become longer and more distressing.
The stomach may continue to perform its functions fairly well, but more often there is gastric indigestion, gastric catarrh, or spasmodic vomiting.
Dropsy as a rule is absent with non-exudative nephritis, unless it is complicated by chronic endocarditis, by cirrhosis of the liver, or by the disturbances of circulation which come on later in the nephritis.
Profuse bleeding from the pelvis of atrophied kidneys is some times seen. In all cases, after a time, the nephritis exerts its effects upon the nutrition of the patient, and the flesh and strength are diminished. On the other hand, the patients do not usually become so pale as they do with an exudative nephritis.