Abstract
Having endeavoured to fulfil the intention
expressed in the Introduction to collect, and to give
a complete and orderly description of all that is of
importance in the work and conclusions of investigators
on the subject of "uraemia" from its earliest
days up to the present time, and also to discuss the
modern theories in the light of recent researches
with a view to indicating in which direction future
investigation is most likely to prove profitable, I
propose, in conclusion, to recapitulate concisely the
main opinions expressed in the course of the Thesis.
1. The terms "Uraemia" and "Latent Uraemia"
should be discarded, and, as at present conceived,
there is no necessity for the continued description
of "uraemia" as a separate entity.
2. "Anephrexia" is suggested as a name for the
syndrome which may occur as the result of suppression
of urine unassociated with active disease of the
kidneys. The symptoms are due to the retention in
the body of the substances normally excreted in the
urine - "urinary poisoning."
3. "Dysnephrexia" is suggested as a term to
indicate the state of the kidneys in all conditions,
whether primarily renal or not, in which their excretory
functions are impaired, but in which the disability is only partial. This state and that of "Anephrexia
"' should be clearly differentiated, and no
attempt should be made to attribute them to a common
cause.
4, Many of the described symptoms of "uraemia"
may be explained as being due to efforts at vicarious
excretion. The "uraemic syndrome" may be restricted
to the Cerebral and Respiratory groups of symptoms.
5. General vascular changes and chronic renal
disease, probably the result of the simultaneous
action of a toxin, occur concurrently, though not to
the same degree. Clinical "uraemia" may thus occur
in two forms. In the first form, cardio-vascular
changes are marked and renal function is but little
impaired; the acute cerebral symptoms are due to
mechanical causes of vascular origin, the chronic
symptoms to changes in the cerebral vessels, and the
paroxysmal dyspnoea to changes in the vessels of the
respiratory centre in the medulla oblongata. In the
second form, impairment of renal function is predominant;
the cerebral symptoms are due to unidentified
toxins, and the paroxysmal dyspnoea to acidaemia; as
vascular change is also present this may be an additional
factor.
6. The residual nitrogen of the blood in
"uraemia" contains toxic products of abnormal - metabolism capable o`f producing "uraemic" symptoms, although
none of the suggested substances can be regarded as
the specific toxin of "uraemia." The liver may be
concerned in the production of these toxins but their
origin cannot be entirely attributed to hepatic
insufficiency.
7. It would appear to be quite possible for
the manifestations of "uraemia" to be produced, in
certain cases, by the known nitrogenous substances
which the kidneys have failed to excrete. Further
investigations are required as to the effects of
substances maintained in the blood for long periods at
the concentrations found in "uraemia."
8. There is no reason to suppose that either
the loss of an hypothetical internal secretion of the
kidney, or the production of nephrolysins, is in any
way concerned in the causation of "uraemia."
9. In view of the varied symptomatology of
"uraemia," it is highly probable that several causes
may act in combination. In one case there may be a
toxic factor, which in another may be complicated by
the effects of acidaemia or of high blood pressure;
the diminished calcium content of the blood may increase
the excitability of the nerve cells, or the retaine3
products of metabolism may reduce the impermeability
of the cerebral vessels to toxins. All possible
variations of co- operating influences may be expected
to occur in the varied circumstances which lead to the
"uraemic state."
