A brief resume of the pathological aspect of
Bright's disease is given. The interpretation
usually put on the pathological findings is that the
various types of Bright's disease represent different
stages of one continuous process which is initiated
by the primary glomerular lesions in the first or
acute stage. hence the use of the terms first, second
and third stage nephritis. The continuous process is
usually regarded as a progressive degeneration of the
renal elements brought about by the obstruction to
blood flow through the glomeruli.
The clinical course of Bright's disease is
briefly reviewed. It is pointed out that only a
minority of cases pass through the three stages or
types. Subacute or "second stage" nephritis is often
encountered apparently arising independently. The
explanation of this phenomenon by assuming a preexisting
"subclinical" acute nephritis is discussed.
The functioning power of the kidneys in the three
stages or types of Bright's disease is described.
It is pointed out that acute glomerulo- nephritis and
chronic glomerulo- nephritis are associated with
impairment of excretion of nitrogenous end products
by the kidneys and that the blood pressure is raised,
while in subacute glomerulo- nephritis excretion of
nitrogenous end products is adequate, and the blood
pressure is normal.
An investigation is described which attempts to
establish the presence or absence of a "subclinical"
acute glomerulo- nephritis. The limitations of the
investigation are pointed out. No evidence was found
to favour the presence of such an entity.
The view that Bright's disease is a condition
which inevitably progresses from the acute stage
through the subacute to the chronic stage, or ends
in cure after the acute or subacute stage, is criticised.
It is pointed out that the fact that renal
function improves when a case passes from the acute
to the subacute type is not in keeping with the view
that the change is due to a further progression of
damage to the nephrons initiated in the acute phase.
That the tubular degeneration which is so marked in
subacute glomerulo-nephritis, is due to vascular
obstruction of the glomeruli is shown to be false. It is
demonstrated that the tubules have their own direct
blood supply which is quite adequate even although
glomerular circulation is abolished entirely. If the
acute stage initiates a chain of events which leads
inevitably to a small granular kidney with failing
function, why do not all cases show this progression?
A point is made of the fact that the glomerulitis
seen in Bright's disease is not pathognomonic for
that condition. It is a non -specific response which
can result from a variety of stimuli or toxins of
varying intensity. Such glomerular changes are seen
in focal embolic nephritis, syphilitic nephritis, in
diphtheria and typhoid etc. That tubular degeneration
can occur with little or nothing in the way of coincident
glomerular changes is evidenced by such conditions
as lipoid nephrosis, nephroses due to chemical
An alternative view is suggested. The micro -
pathology of the various types of Bright's disease
are regarded as reactions which vary in tempo in
accordance with the intensity of the irritant, so
that acute, subacute, and to some extent chronic, reactions
take place. The similarity between the process
and that which occurs in acute, subacute yellow
atrophy, and healed yellow atrophy of the liver is
mentioned. In this way cases of acute and subacute
glomerulo-nephritis can arise de novo. It is suggested
that the response evoked in the kidney (the
type of nephritis) depends on the intensity of the
circulating toxin. The toxin may be the same for all
types of Bright's disease or may differ. Chronic
focal sepsis would appear to play a part in the
aetiology of some cases of subacute glomerulo-nephritis.
The method by which the toxin intensity may vary
is discussed. Partial breakdown of immunity mechanism
is suggested as a cause, and is linked with the low
blood complement and proteins observed in some cases
The possibility of aglomerular tubular function
in sub -acute and chronic glomerulo- nephritis is
mentioned. This is not regarded as being the sole
mechanism by which the kidneys function but may well
play an important part.
From these reflections it is felt that the
"accepted view" rests on very slender evidence,
namely, that some cases do progress through the
various stages, and that the glomerular changes can
be traced through these stages. As we have seen
there is nothing pathognomonic about "glomerulitis".
It can result from a variety of causes.
The known facts would appear to be explained by
the alternative view more satisfactorily. The evidence
suggests that subacute nephritis is due to a
toxin of less intensity than is encountered in acute
nephritis, and as such may arise independently or
follow an acute attack. Chronic glomerulo- nephritis
is probably a stage of healing with perhaps some mild
irritant action superimposed, and is therefore a
sequence of repeated attacks of acute glomerulonephritis,
or of subacute glomerulo-nephritis.
The necessity for more numerous and extended
investigations into the question of "subclinical
nephritis" is appreciated.