So far as the experiments on animals are concerned they seem merely to show that urea in the blood does but little harm, and that abolition of the functions of the kidneys causes death.
It was to escape from some of these difficulties that Frerichs pro posed the explanation that the cause of uraemic symptoms was poi soning by carbonate of ammonia. He taught that urea in excess in the blood did no special harm, but that if by the action of some fer ment the urea was changed into carbonate of ammonia, then symp toms of intoxication would regularly follow. This theory, at one time popular, is now so entirely abandoned that it is not necessary to state the objections to it.
A modification of the theory of intoxication by urea is that of in toxication by urea and the other excrementitious substances of the urine together. The same affirmative and negative facts are to be found for this theory as for that of poisoning by urea alone. Normal uncontaminated urine injected into the veins of animals seems to do little harm unless the kidneys of these animals are injured by opera tion. If the kidneys are operated on, the animals die.
In human beings there are the patients with unemic symptoms and an excess of excrementitious substances in their blood and tissues; the patients with urvemic symptoms, but without any excess of excre mentitious substances; and the patients with anuria, an excess of excrementitious substances, and no ura3rnic symptoms.
A very important modification of the chemical aspect of the ques tion is that made by Oppler and others. They hold that it is an error to think that urea or any other constituent of the urine acts as a blood poison. Rather an interference with the functions of the kid neys must lead to a disturbance of the regular chemical changes in all parts of the body. Such an interference is followed by a change in the nutrition of the tissues which shows itself in loss of weight, in anaemia, and in disturbances of the functions of the brain. This way of looking at the subject is certainly a very rational one.
The opposition to all the chemical explanations of uraemia looks to changes in the blood pressure as the exciting cause of urnaic at tacks. The most complete theory of this kind is that of Tranbe.
This theory explains the occurrence of urmic attacks as follows : The disease of the kidneys causes thinning of the blood serum, hyper trophy of the left ventricle of the heart, and an excess of blood pres sure in the arteries. If by any accidental circumstance the blood
tension is suddenly increased, or the blood serum still further thinned, oedema and anoemia of the brain are produced. The form of the uroc mic attack will vary with the portion of the brain which is rendered or cedematous. If the cerebral hemispheres alone are in volved the patient simply becomes comatose ; if the central portions of the brain alone are affected there will be convulsions without coma; if both the hemispheres and the central portions of the brain are anmmic and cedematous, both convulsions and coma are developed.
Traube also states : That he never saw an attack of uremia in renal disease where the left ventricle of the heart was not hypertrophied, and where an in crease of tension in the aortic system could not be demonstrated; That the diluted state of the blood serum can be recognized by the pallor of the skin and mucous membranes, and the presence of dropsical effusions; That in every instance in which he examined the brain after death he could confirm the existence of anminia and oedema; That the presence of blood effusion within the cranial cavity in many of these cases confirms the suspicion that the abnormally high arterial blood pressure to which these effusions owe their origin has also something to do with the production of the cedema which is pres ent at the same time.
Experiments on animals have also shown that by ligating the ureters, then the jugular vein on one side, and then injecting water into the carotid on the same side, general convulsions and coma can be produced. After death cedema of the brain without extravasation of blood is found.
The objections to Traube's theory are obvious : In patients who exhibit well-marked cerebral symptoms the specific gravity of the blood serum is not always lowered; the arterial tension is not always increased; neither anoemia nor cedema of the brain can always be demonstrated after death. These are facts which are soon ascertained by any one who sees much of kidney disease.