A STUDY 
OF THE 
Arteries and Veins in Bright's Disease 
BY 
ARTHUR V. MEIGS, M.D. 
PHVSICIAN TO THE PENNSYLVANIA HOSPITAL, PHILADELPHIA 
Reprinted from The Medical Record, July 7, 1888 
NEW YORK 
TROW'S PRINTING AND BOOKBINDING CO. 
201-213 East Twelfth Street 
1888 A STUDY 
OF THE 
Arteries and Veins in Brights Disease 
BY 
ARTHUR V. MEIGS, M.D. 
PHYSICIAN TO THE PENNSYLVANIA HOSPITAL, PHILADELPHIA 
Reprinted from The Medical Record, July 1888 
NEW YORK 
TROW'S PRINTING AND BOOKBINDING CO. 
201-213 East Twelfth Street 
1888 A STUDY OF THE ARTERIES AND VEINS IN 
BRIGHTS DISEASE.1 
For some time past my clinical observations made annu- 
ally in the wards of a large general hospital have led me 
to feel how unsatisfactory is our present understanding of 
the cause of many forms of heart disease, and of the 
mode of origin of Bright's disease, and at the same time 
how difficult it is to arrive at a satisfactory understanding 
of a case in which these two apparently far apart diseases 
are, as so commonly happens, coexistent. The intimate 
relation of disease of the two organs is so well known that 
for some years medical literature has been filled with va- 
rious theories to explain how the one is dependent upon 
or caused by the other. As a result of the observations 
of Bright it soon became well known that hypertrophy of 
the heart-and it was said of the left ventricle in particu- 
lar-was very commonly associated with disease of the 
kidney; and naturally enough it was thought, as the clin- 
ical history of such cases demonstrated the existence of 
kidney disease long before that of the heart became known, 
and often the heart disease was not suspected at all be- 
fore the autopsy was made, that the heart disease was 
entirely dependent upon, and caused by, that of the kid- 
ney, and complicated theories were brought forward to 
explain how the train was set in motion, and the various 
steps from its inception to its final development. Soon 
clinical medicine demonstrated that in many cases in 
which the coexistence of heart and kidney disease was un- 
1 Read before the College of Physicians of Philadelphia, Tuna 6, 
1888. 4 
deniable the history occasionally proved beyond perad- 
venture that heart disease had existed before there was 
any suspicion, much less evidence, of disorder of the kid- 
ney. New theories were required to explain this con- 
dition, and they were soon found, principally in the re- 
sults of congestion of the internal organs, and of the 
kidneys in particular it was assumed, which was a neces- 
sary result of disordered action of the heart. Another 
step was the observation that the two organs-heart and 
kidney-are connected by an immense vascular highway, 
the arterial system, which was found in many instances to 
partake in the disease; for atheroma of the arteries, more 
or less extensive, is a common accompaniment of com- 
bined heart and kidney disease. Parenthetically it may 
be observed here that it is curious that comparatively little 
is to be found in medical literature in regard to the state 
of the venous system, either in the form of study of its 
physical condition, or of theory in regard to what might 
be expected to happen to the veins, though the rest of the 
subject has been from many points of view somewhat 
overloaded with theories. This is strange, when it is rec- 
ollected that the venous highway connecting the two organs 
is just as large and fully as important as the arterial. The 
observations of Dr. George Johnson of the hypertrophy 
of the muscular coat of the arteries of the kidney, and 
later of the same hypertrophy in various other tissues 
and organs in cases of red granular contracted kidney, 
and those of Virchow of the state of the arteries in amy- 
loid disease, constitute important landmarks in the devel- 
opment of our knowledge of the whole subject, and this 
though there has been, and is, great difference of opinion 
in regard to the interpretation of the various facts ob- 
served. The paper of Gull and Sutton upon the so-called 
arterio-capillary fibrosis was the first systematic attempt to 
show that many cases which had previously been called 
Bright's disease of the kidney were, in truth, due solely to 
changes which had their origin in the arteries and capillaries, 
and in the connective tissue in which they lie. This was 5 
a bold step in advance, and has done much toward leading 
to a clearer comprehension of the complaint by ridding 
the minds of pathologists of the idea that the disease was 
Bright's disease of the kidney, and that in that organ alone 
must they dare to seek for the original source of the path- 
ological train. The observations of Gull and Suttor, 
though of great value in thus clearing the atmosphere of 
this old doctrine, have not been borne out in other re- 
spects by subsequent and more extended observations. 
Their assertion that the origin of the vascular changes is 
to be looked for in the adventitia of the arteries and in 
the capillaries can hardly be considered to have been 
substantiated. With regard to capillaries our present 
means for their study are not satisfactory, and little has 
been even asserted, up to the present time, of their dis- 
eases, except that in some cases it has been considered 
that the walls of the Malpighian tufts of the kidneys were 
thickened, and again, that there was in various organs in- 
crease of the perivascular connective tissue. So far as 
the first assertion is concerned-that the walls of the 
Malpighian capillaries are thickened-it cannot be con- 
sidered as having been proved, though it is exceedingly 
likely; and for the increase of connective tissue it yet re- 
mains to be demonstrated that this is a part of, or even 
due to, the capillaries, with regard to the real physical 
condition of the walls of which we are still somewhat in 
ignorance. No attempt to study the condition of the 
capillaries in dead tissues, further than to trace their 
course, has as yet yielded any conclusive results. Nor 
has it by any means been demonstrated that the changes 
so extensively found in the arteries and arterioles have 
their origin in the adventitia. 
The present state of knowledge of the complaint seems 
to be about as follows : It has long been known that in 
cases of albuminuria certain physical changes take place 
in the kidney, and that very commonly there is enlarge- 
ment of the heart, and further, often there is atheroma of 
the larger arteries, which is more or less extensive as the 6 
case may be. It has, besides, been demonstrated that 
other changes, chiefly of a degenerative or atrophic nature, 
are found in many of the various organs and tissues of the 
body-namely, disease of the cerebral arteries, and of 
the arteries and substance of the spinal cord,1 emphysema 
and slow inflammatory processes in the lungs, calcareous 
and allied forms of disease of the heart valves, degenera- 
tions of the coronary arteries, and fibroid change of the 
muscular substance, and various forms of disease of the 
liver and spleen. Such being the case, quite a number of 
the medical minds that have bestowed attention upon the 
subject have been struck with the idea, and have enun- 
ciated the belief that this hydra-headed disease, or collec- 
tion of related diseases, as the event may prove it to be, 
had its origin in the arteries or capillaries, or both, though 
no one has as yet shown what the mode of origin is; Dr. 
Johnson, and those of his school, believing it to be one of 
the so-called blood-diseases which produces its first physi- 
cal change in the secreting cells of the kidney, while Gull 
and Sutton, and their following, equally strenuously up- 
hold the opinion that the disease has its origin in the 
adventitia of the arterioles, and in the capillaries and 
perivascular connective tissue. 
The utter inadequacy of a diagnosis of valvular disease 
of the heart, or Bright's disease of the kidney, in cases of 
this nature, as at all descriptive of the real conditions, has 
pushed itself upon me so forcibly of late years that I have 
been in the habit of saying, and recording in my clinical 
histories, that these cases were of vascular origin. Some- 
times it seems like the natural result of the advance of 
years, the machinery wearing out simply because it is too 
old; or, again, it is as if premature old age came upon the 
patient, or perhaps he is worn out by dissipation, or be- 
cause he has earned his livelihood by some physical labor 
1 Gull and Sutton : On Changes in the Spinal Cord and its Ves- 
sels in Arterio-capillary Fibrosis, Trans. Path. Soc., London, vol. 
xxviii., 1877. 7 
SO severe that it necessarily speedily exhausts his vital 
forces and produces the physical disorganization. The 
absurdity of the old practice of endeavoring to elicit a 
history of rheumatism, and then, if the slightest account 
of joint pains during the past life could be had, of attribut- 
ing the disease to that, I have long looked upon as the 
weakest explanation. It is now well known that rheu- 
matism, instead of being, as was formerly thought, almost 
the sole cause of valvular disease of the heart, is but one 
of many, all of which are equally capable of producing it. 
Dr. Allbutt1 long ago, in an able article, expressed his 
opinion that, in the large manufacturing town in England 
in which he lived, heart diseases in hospital practice were 
much more common among young men as the result of 
overexertion of the body than of acute rheumatism. 
As clinical study has seemed to do little for me in the direc- 
tion of showing what is the original physical change or patho- 
logical basis of the disease, but has merely taught me to be 
able to predict, with a good deal of accuracy, that, in addi- 
tion to the well-known lesions in the heart and kidneys, 
other very widely diffused changes will be found if sought 
for after death, I have turned from the wards to the post- 
mortem room in the hope that thus some light might 
be shed upon the subject. In this way I have been 
led to the observation of facts which, I trust, may be 
worthy of the consideration of the profession. It is with 
a profound sense of the wisdom of Sir James Paget's ob- 
servation,2 that " medicine and surgery are eminently a 
science of observation; deductions from facts are always 
unsafe; I believe that they have done far more harm than 
good; and, for the most part, when sufficient facts have 
been collected and arranged, the general conclusions that 
may justly be drawn from them are nearly manifest," 
that I attempt to describe what I have seen. If I should 
1 The Effects of Overwork and Strain on the Heart and Great 
Blood-vessels, St. George's Hospital Reports, v., p. 23. 
a Address at Owen's College, Lancet, October 15, 1887. 8 
be led into making deductions, and few men can resist the 
inclination, which seems a natural one to thinking beings, 
the already quoted wise saying must be remembered, and 
a sharp line drawn between that which is a result of ob- 
servation and therefore fact, and what is merely theory or 
deduction. 
The first things that strike one who reflects upon this 
combination of heart and kidney disease is the intimate 
connection there is between the two organs by the 
vascular system, the arteries and veins, and that if the 
disease begins in one organ and extends to the other, this 
must be the channel of communication ; or that perhaps it 
does not originate in either, but in the blood-vessels, and 
secondarily extends to the organs. This latter preconcep- 
tion is rendered still more probable when it is remembered 
that degenerative changes parallel to those found in the 
heart and kidneys exist in many other organs and tissues, 
and it therefore becomes much more easy to believe that 
the vascular change is the cause and not the consequence. 
In pathological investigation, therefore, with a view to 
further elucidation in regard to the original cause, my 
mind has been occupied with the preconceived idea that 
the search must be prosecuted by study of the physical 
conditions of the arteries and veins, and perhaps the 
capillaries. This statement is made with the knowledge 
that wherever blood-vessels go they are accompanied by 
nerves, and that it is possible, and from a purely theoretical 
stand-point as likely, that the pathological lesions under 
discussion originate in the nerves as in the blood-vessels. 
Drs. Da Costa and Longstreth1 have asserted that in 
Bright's disease there is a constant lesion of the renal 
nerve plexus, and have expressed their opinion that this 
lesion is the cause of the kidney disease, and have further 
suggested that a similar lesion may exist in other ganglia 
1 Da Costa and Longstreth : Researches on the State of the Gan- 
glionic Centres in Bright's Disease, American Journal of the Medical 
Sciences, July, 1880. 9 
producing parallel effects, as, for instance, in the cardiac 
plexus, causing the hypertrophy of the heart. Though 
this is of course an explanation which may be correct, it 
has been by no means proved, and even if extended in- 
vestigation should show nerve-lesions to be as constant a 
feature as are the blood-vessel changes, it remains to be 
discovered which, if either, is the real original cause, for 
upon purely hypothetical grounds the two are perhaps 
equally acceptable.1 
In making somewhat extended post-mortem investiga- 
tions the lesion I have found to be most constant and 
most extensively distributed throughout the tissues is 
disease of the arteries and arterioles, a condition in which, 
so far as my observations have carried me up to the 
present time, though I confess that the study has not as 
yet been exhaustive, the veins seem to participate. In 
regard to the condition of the capillaries I have nothing to 
say, for, as already stated, there is no known satisfactory 
method of studying their physical condition in dead 
tissues. It is a commonly recognized fact that in cases of 
the so-called Bright's disease there is ordinarily present a 
greater or less amount of atheroma of the larger arteries; 
and Johnson upon the one hand, and Gull and Sutton on 
the other, and when these names are mentioned it must be 
understood that all other observers who have either preceded 
or followed them in the same lines of investigation are in- 
cluded, have made extensive observations in regard to the 
state of the minute arteries in many of the organs and 
tissues of the body. Their conclusions have been quite 
different from those reached by me, though in the course 
of my investigations I have fallen upon appearances 
1 Since the above was written Dr. Da Costa has published another 
paper upon this subject, giving the results of microscopic examination 
of the cardiac ganglia in cases of Bright's disease, and announcing 
that extensive organic changes were found-The Middleton Gold- 
smith Lecture on the Relation of the Diseases of the Kidney, espe- 
cially the Bright's Diseases, to Diseases of the Heart-Medical Neus, 
May 5, 1888. 10 
similar to those they have described. I have made sec- 
tions from the brain, spinal cord, lungs, heart, liver, spleen, 
kidneys, and of various of the larger arteries and veins, 
and in all of them-except the spinal cord, and with regard 
to its condition my examinations have not been sufficiently 
numerous to be conclusive-have found quite constantly 
present an irregular overgrowth and thickening of the intima 
of the arterioles. This thickening varies very much in its 
anatomical characters and its extent, and often when it is 
present in high degree there is involvement of the other 
coatings, though ordinarily they have undergone no 
change. The morbid appearances will be better under- 
stood from an examination of the plates than would be 
possible from any written description. The condition ap- 
pears to be nothing but that which is described in text- 
books of pathology as the various forms and stages of 
atheromatous change, but observers do not seem to have 
connected its existence with this disease further than to 
have noted that it was commonly present in the larger 
arteries. The appearances found differ much in accord- 
ance with the size of the vessel in which they are observed, 
and in different organs. In larger-sized vessels the more 
commonly understood atheromatous changes will most 
usually be found-misshapen vessels, calcareous deposits, 
loss of substance of intima, thickened patches upon the 
inner surface (these being often so extensive as to cause 
great obstruction to the blood-current, sometimes the 
lumen of the vessel being a mere chink at one side; see 
plate, Fig. 5), and where the condition has progressed to 
its full development, more or less destruction or alteration 
of the entire thickness of the walls. In smaller ones the 
changes are most commonly confined to increased thick- 
ness of the intima, which is not usually so irregular in 
degree at different portions of the circle as is the case in 
large arteries, though it is seldom absolutely uniform. 
The intima in such vessels, when examined in cross sec- 
tion, often has a thickness which will be half as great as, 
or even equal to, that of the muscular coat, but it may 11 
vary to almost any extent. This tissue, when examined 
under the microscope, appears to be composed of fibrous 
material, the fibres of which, when the vessel is viewed in 
cross section, appear to be circular, and in longitudinal 
sections to run lengthwise ; there are, therefore, probably 
abundant fibres running in all directions, thus giving the 
tissue considerable strength. Contrary to what is com- 
monly stated, I have usually found this morbid tissue to 
contain here and there numerous nuclear elements. In 
the larger vessels in particular, and where the patches of 
atheromatous thickening are large, they are often composed 
of a well-organized tissue containing numerous cells, which 
in their appearance and arrangement resemble granulative 
tissue, seeming disposed to arrange themselves in nests, as 
is common in young and rapidly growing tissues. 
The well-organized cellular outgrowth of the intima in 
these cases is identical with that which has been most fre- 
quently described as syphilitic endarteritis, and yet I have 
seen it in a number of cases in which there was neither a 
history of syphilis nor reason to suspect the existence of 
that disease. Examination of the endocardium and valves 
of the left heart often shows a condition precisely parallel 
to, and seemingly a part of, the same process, the evi- 
dences of which exist so extensively in the arteries. It 
seems positive that the endocardial and endarterial 
changes are but part of the same disease, and that this is 
the cause of the valvular changes which so frequently 
arise, complicating the trouble, and, when they exist, much 
hastening the inevitably fatal result. In examining the 
thickened patches of endocardium, and in sections of aortic 
valve flaps, thickened and distorted by the disease, there 
were found the same nest-like arrangements of cells de- 
scribed as existing in the intima of the arteries. 
While the above-described conditions are those I have 
usually seen as a result of examination of the arteries, I 
have not, as a common thing, found the increased thick- 
ness of the muscular coat which is described by Johnson, 
and called by him a hypertrophy, to be present in such 12 
degree as to render its existence undoubted. Arteries 
may often be found in which it could be said that the 
middle coat was unduly thick, and, again, others, in re- 
gard to the state of which there might be dispute, but in 
most instances I have failed to find an increase so great 
that its existence could be considered to be beyond doubt. 
It is a much easier matter to be sure that the appearances 
described of the intima are morbid; for, in th©" natural 
state, in small vessels certainly, it constitutes hut a very 
thin layer, and besides, when it is seen to be many times 
thicker, as happens in many instances, upon one side of 
transverse section of an artery than upon the other, there 
cannot be a shadow of doubt that such an appearance is 
pathological. This is very different from what -is found 
in regard to the muscular coat, which, if at all thickened 
by disease, is uniformly so, and there is, therefore, nothing 
to contrast it with, and its state can be merely estimated 
as a matter of judgment. It is curious that in one case in 
which I made many sections (case of J. K ) of different 
organs and vessels, the only artery in which there was un- 
doubted thickening of the muscular layer was one of the 
primary branches of the renal. In this vessel the intima 
was thickened to a slight degree, but much more so at 
some parts of the circle than at others, and the plicated 
membrane very distinctly visible around the entire circuit; 
the muscular coat, however, which was probably*of twice the 
ordinary thickness in a vessel of such size, did not present 
the appearances which could be called those of true hy- 
pertrophy; for, although the muscle bands and nuclei 
were present and numerous, there were also visible very 
many other cells which were exactly like those described as 
so commonly found in the overgrown intima. These cells 
were, so to speak, wedged in between the muscle elements, 
and many of them were undergoing pigmentary degenera- 
tion. Sections of the abdominal aorta in this case, and of 
the minute arterioles in the renal substance itself, did not 
show any indisputable increase of the muscular coat, 
though there was in both overgrowth of the intima. To 13 
anyone who would wish to advocate Dr. Johnson's view, 
that increased thickness of the muscular layer is a true 
hypertrophy, and that it increases what he calls the " stop- 
cock" power of the arterioles, does it not seem strange 
that the only artery that showed undoubted increased 
thickness of the middle layer in this case should, in that 
very layer, present the marked evidences of a degenera- 
tive process, and that the vessel affected should be a very 
large one, to which, ordinarily, is attributed elasticity and 
not much contractility, while the minute arterioles of the 
kidney, the very citadel of the supposed condition, should 
present none of it, and all the vessels in the neighborhood 
should have plainly thickened intimas? 
Fig. 9 represents two views of a minute artery removed 
from a kidney under a dissecting microscope. The upper 
one is intended to produce the same effect as Johnson's 
(" Medical Lectures and Essays," by George Johnson, 
1887) picture, from the appearances of which he makes 
his assertion of the existence of hypertrophy of the muscular 
coat. The vessel was carefully dissected out, then split open 
with scissors, and mounted with the inner side up, thus 
showing half of the internal surface of the vessel and the 
thickness of its walls at the cut edges. No fibrous coat is 
distinguishable, and the same holds good in Johnson's fig- 
ures, but the muscular coat and intima are very well 
shown. Whether the muscular coat is increased or not I 
think might well be disputed, as this layer in the walls of 
an artery o'f such size is always a marked feature in a 
picture; that the intima is increased in amount, and, as 
represented in the picture, irregularly so, there can be no 
doubt, though it might be said that this is due to the 
crude method of preparing the object, to dissect it out 
and then cut it with scissors. That such is not the case, 
however, and that the intima is actually thickened, and 
irregularly so, is made very plain by the other picture. 
This is a bit of the same artery, and the section was pre- 
pared by cutting off from the end, before it was split open, 
as thin a section as could be made with a pair of scissors, 14 
and it very well shows the thickened intima lying within 
the plicated membrane, which latter is not distinguishable 
at all in the longitudinal section. To my mind it becomes 
evident from the contrast presented in these two pictures 
that the change of the intima is a much more positive and 
unmistakable one, and one which in tire nature of things 
is capable of producing quite as grave effects as that of 
the muscular coat, upon the existence of which in this 
vessel doubt may be cast; a change also which, even if in 
other vessels its existence is undeniable, is accompanied 
by degenerative processes so extensive as to render its 
proper classification as a true hypertrophy uncertain. 
So far as the " fibrosis and hyaline-fibroid " condition 
described by Gull and Sutton is concerned, I have failed 
to discover it in its full development. They declare their 
belief, and try to prove, that the vascular changes have 
their origin in the fibrous coat, and describe a high degree 
of thickening of the adventitia as being usually present. 
There can be no doubt that there is great increase of 
fibrous tissue, and it is found more extensively developed 
around the blood-vessels, the place in which connective 
tissue exists more abundantly than elsewhere in all organs; 
but its appearances are more those of a general increase 
of perivascular connective tissue than of the adventitia of 
arterioles alone. And for the matter of that, how is it pos- 
sible to decide, in any section examined with the micro- 
scope, where the fibrous material lying outside the muscular 
coat of an artery ceases to be adventitia and becomes 
perivascular connective tissue ? The two structures are 
identical and shade into each other without any defined 
boundary. Nothing that answered the description of 
hyaline-fibroid change of arterioles has come under my 
notice except certain appearances presented by the vessels 
in sections of the spinal cord ; in the thoracic and abdom- 
inal viscera I have failed to find it, and cannot compre- 
hend why this should be unless it is, as stated by Johnson 
(" Medico-chirurgical Transactions," vol. Ivi.), that their 
methods were faulty and that the use of glycerine and 15 
camphor in mounting produced the appearances described. 
In the spinal cord I have found arteries with walls that 
looked entirely structureless except for a few nuclei 
lying at the edge of the lumen of the vessel, and answered 
exactly to the appearances described and figured by Gull 
and Sutton (" London Path. Soc. Trans.," loc. cit.'). It 
might be well to mention here, as a matter of interest, 
though I have no explanation to offer, and do not know 
if it had any bearing upon the condition, that in this same 
case, which was one of marked Bright's disease, the olivary 
body, and nucleus dentatus within it upon the right side, 
was much larger than the left, though no morbid condition 
of the tissue itself could be discovered upon either side. 
In two cases in which I made extensive microscopic ex- 
amination of the tissues, and they are the two from which 
the vessels represented in the plates were taken, I found 
morbid changes in the veins as well as the arteries. 
Atheroma of veins so extensive as that of the femoral, 
which is shown in Figs. 7 and 8, is not usually described 
as being common, though the occasional occurrence of 
the disease in veins is sufficiently well known. After 
the section from which the picture is made was prepared, 
it was found impossible to determine with certainty, from 
the microscopic appearances alone, that the larger vessel 
of the two was really a vein, so great is the thickening of 
the intima and fibrous coats, and it was only by a careful 
examination of the piece of tissue from which the section 
was cut, and the discovery of a well-marked valve in the 
vein, that an absolute conclusion was reached. The two 
vessels, which were removed from the upper part of the 
thigh together, were found to be rigid, like bony tubes, 
and it was only after decalcification that sections of them 
could be cut. The process of disease in this vein appears 
to have been exactly the same as takes place in arteries, 
some thickening of all the coats, perhaps, for when con- 
sidering the state of the muscular layer it must be re- 
membered how thin it is in a natural condition in veins, 
and of the intima in particular. It is a noticeable fact 16 
that the thickening of the intima varies very much at dif 
ferent parts of the circle of tire vessel, in this respect be- 
ing precisely parallel to what has already been so much 
emphasized as occurring in arteries. The structure of the 
intima also appears to be similar in character to that found 
in arteries. How the two inner coats became loosened 
from the fibrous one, as appears in the plate, cannot of 
course be known; but it may be that the breakage oc- 
curred in removing the vessels from their position in the 
thigh, for so rigid were they that it required the exercise 
of some force to remove them. 
Fig. 12 represents a portion of a vein lying in the adi- 
pose tissue covering the front of the heart, and presents a 
condition of which I have never seen any description. In 
most of it the walls are very thin and the tissue of a very 
loose texture, but in the intima there are two spots oppo- 
site each other in which marked cellular outgrowth has 
taken place and the cells have in the most distinct way 
arranged themselves in nests precisely like those described 
as existing in the arterial system. When this is examined 
with a higher power the arrangement of the cells can be 
still more plainly distinguished. 
In most of the veins I have examined in this disease, 
what has struck me most forcibly in them has been the tenu- 
ity of their walls and the looseness of texture of the 
material of which they were formed. This can be seen to 
some extent with the naked eye as well as by the aid of the 
microscope. I have found that it is not uncommon, if a vein 
is cut open, spread out flat, and then held up to a strong 
light, for the walls to vary much in thickness at different 
parts, and in some places to be exceedingly thin. In the 
case of J. K , sections were made transversely across 
a large branch of the renal vein, and the walls were found 
to be so thin that it seemed astonishing how it could have 
been at all an adequate container of blood. 
In regard to the structural condition of the capillaries, 
for reasons already mentioned I do not even pretend to 
an opinion. 17 
It may perhaps now be permissible to attempt to draw 
some contrast of the general features of the two cases 
from which my illustrations were taken. That of J. K 
was made the subject of a short paper read before the 
Philadelphia Pathological Society in the early part of 1888, 
and published in the "American Journal of the Medical 
Sciences" for June of the same year, and it will therefore 
not be well to do more than sketch the outlines of the 
case again. It was one of typical aortic regurgitation in 
a man fifty-four years of age. The heart disease came on 
late in life and without the occurrence of any attack of 
rheumatism more than some vague joint pains, which 
never confined him to bed, and he died gradually of heart 
failure, without dropsy or anything to point to involve- 
ment of the kidneys, except that when he first came under 
notice there was a trace of albumen in the urine, without 
casts, which, however, soon disappeared never to return. 
After death there were found brown atrophy of the heart, 
fibroid degeneration, thickening of the endocardium and 
of the aortic valves, and in both of these the existence of 
the peculiar cell-growth which has been described. The 
arteries and veins of the heart presented appearances 
already mentioned (Figs. 11 and 12). The lungs gave 
evidence of some catarrhal inflammation and their arteries 
of thickening of the intima. The liver-cells were much 
degenerated, and the arteries as in the other organs. The 
kidneys exhibited evidence of parenchymatous disease, 
there were casts in the tubules, and the arteries showed 
the same change as found in vessels elsewhere (Figs. 9 and 
10). The condition of the renal artery and vein, and of 
the abdominal aorta, vena cava, and a small branch of the 
cava have already been mentioned. There were large in- 
flammatory bands in one of the iliac veins, causing ob- 
struction in that vessel. 
The case of J. C presented in many respects a con- 
trast. He was fifty-one years of age, and had suffered with 
some shortness of breath and palpitation for three years. 
When admitted to the hospital, about two months before his 18 
death, there was great dyspnoea, amounting to orthopnoea, 
and of this he never got rid. Dropsy and difficulty of 
breathing increased, and his sufferings became worse and 
worse ; nothing seeming to afford him any relief until, 
finally, he died, having suffered what was almost agony. 
The conditions were in all respects those usually regarded 
as typical of Bright's disease, except that no casts were 
found in the urine, though albumen was always present. 
Post-mortem examination showed that the heart and all 
its openings were much enlarged, there was extensive brown 
atrophy of the muscular substance and calcareous deposit 
in the base of the aorta and valve-flaps. The minute 
veins exhibited irregular thickening of the intima, and the 
condition of one of the arterial branches is shown in 
Fig. 5. The pleura was thickened and the lungs adherent; 
there was emphysema and some catarrhal infiltration, and 
the condition of a minute arteriole is represented in 
Fig. 3. The liver was in a state of fatty and granular de- 
generation, and the hepatic arteries and portal veins were 
much thickened and diseased. There had been inflam- 
mation around the spleen, binding it to the surrounding 
organs, and on section it showed marked fibrosis, and the 
arteries were much thickened, the intima markedly so. 
There was parenchymatous disease of the kidneys, the 
capsules were thickened, and there were infarctions, and 
the arteries diseased (Fig. 4). The radial artery and femoral 
artery and vein were atheromatous and calcified (Figs. 6, 7, 
and 8). The abdominal aorta presented distinct irregular 
thickening of its intima. In the spinal cord there seemed 
to be some degeneration of the nerve-fibres, particularly 
of the peripheral nerves, and the arterioles presented the 
characters described and figured by Gull and Sutton ("Lon- 
don Path. Soc. Trans.," loc. tit.} as hyaline-fibroid degen- 
eration. The walls were composed of a material which 
under the microscope appeared structureless, except that 
a few nuclei lay at the inner edge. In the medulla ob- 
longata, as already mentioned, the right olivary body and 
its contained nucleus dentatus was much larger than the 19 
left. The large artery running along the front and that 
upon the posterior surface both presented in marked de- 
gree the irregular thickening of the intima. Figs, i and 2 
show the condition of the intima of one of the middle cere- 
bral arteries. Sections of this vessel higher up, or rather 
of its branches after it had divided into three, exhibited 
irregularly thickened intima in two of them, while the 
third presented an appearance quite natural. 
In these two cases the mode of death and the picture 
presented by the history of the last few years of life were 
as dissimilar as could well be, though in many respects 
the pathological lesions found were singularly parallel. 
Though in the first case the man died what would com- 
monly be considered a typical heart death, and in the 
second an equally typical kidney death, and there should 
have been, reasoning from analogy, a great difference in 
the pathological lesions, such was not the case. It would 
be difficult, if not impossible, for anyone, from a study of 
the pathological lesions alone in these two cases, to say 
that the modes of death would have been in anywise dif- 
ferent. The most important of these lesions, perhaps, 
were the changes in the heart and kidneys, and in respect 
of these the two cases were not materially unlike, and in 
both were found besides extensive changes in the arterial 
and venous systems, which, though presenting many points 
of difference, were yet only varying features of what seems 
to be primarily the same disease. 
The disease seems- to be very wide-spread in its early 
effects even, and may first reveal itself clinically by a 
cough if it takes possession first of the lungs, or by the 
symptoms of apoplexy, if the brain arteries are the earli- 
est to suffer injury, or by epistaxis perhaps, which has al- 
ways seemed to me to betoken just as positively a physi- 
cal change of the arterioles of the nares, though of this 
there is no pathological evidence as yet, as does the apo- 
plexy show that the brain-arteries are diseased. Often 
have I found, by the most careful inquiry into the clinical 
history in cases of typical Bright's disease, that the first 20 
symptom with which the patient has suffered has been 
cough, and it is a fact well known how often persons dy- 
ing of apoplexy are found to have had Bright's disease, 
and it is equally well known how often epistaxis is the 
first warning given of the existence of kidney trouble. 
There is, however, no reason, except that Bright first 
drew attention to the existence of changes in the kidneys 
(and this is no reason at all), to suppose that the diversi- 
fied lesions were all caused by the changes in either the 
secreting substance or in the arteries of the kidneys.. 
The fact that cerebral hemorrhage and epistaxis are 
such common accompaniments or symptoms of chronic 
Bright's disease seems to me the strongest proof that it 
should not properly be considered to be one of the kid- 
ney, for there exists at the present time no evidence to 
show that the kidney disease which sometimes, but not 
always, exists in such cases, originated before the blood- 
vessel change which was their direct cause, nor is there 
even a very plausible theory to strengthen such a hypo- 
thesis. 
In conclusion, it may be stated that my desire has been 
to make clear, by language and pictures, the view that in 
the so-called chronic Bright's disease, we have to deal 
with one which is wide-spread in its effects; that the 
most characteristic and probably most important changes, 
so far as at present known, are those of the intima of the 
arteries, in which probably the veins always participate ; 
that changes in the muscular coat and adventitia, though 
often present, are by no means so important in their ef- 
fects, and probably are secondary to those of the intima; 
that the process seems to be coextensive with, and prob- 
ably is a part of, the change in the large arteries which is 
so common and so well known as atheroma; and finally, 
that it seems likely, in the absence of proof that changes 
in the nerve-substance are a necessary accompaniment, or 
even if such were proved to be the case, the lack of 
knowledge that antedated the disease of the blood- 
vessels, that the earliest of the now known pathological 21 
lesions to make its appearance is the change in the intima 
of the blood-vessels. 
My paper must not be closed without an acknowledg- 
ment of my great indebtedness to Dr. B. A. Randall for 
the beautiful illustrations I have been enabled, through 
his skill, to present. 
/ m.m. 
Fig. i.-Case of J. C . Middle cerebral artery, showing irregular out- 
growth of intima. The accompanying vessels are somewhat enlarged ; the adven- 
titia and muscular coats are normal. The plicated membrane shows very dis- 
tinctly around the entire circle. The intima is seen within the plicated membrane, 
and is thickened in the entire circuit; but at one side, and occupying about one- 
third of the circumference, the thv kness is very great. At one portion of this 
mass there are numerous blood-corpuscles, entangled in the tissue, while at an- 
other there is distinct cellular structure, x 20 diameters. 22 
0.3 m.m. 
Fig. 2.-A portion of the same artery as Fig. i, and showing the cell-growth 
and entangled blood-corpuscles, and that the general character of the structure of 
the most thickened portion of the intima is a fibrous material. The open spaces 
are probably due to tearing of the tissue in mounting, x 35 diameters. 23 
9. to m. m. 
Fig. 3.-Case of J. C . Minute arteriole from lung, showing great thicken- 
ing of the intima, which contains a few scattered cells, though most of it consists 
of a homogeneous, structureless-looking material, quite different from the appear- 
ances seen in Figs. 1 and 2. The muscular coat and adventitia cannot be very 
satisfactorily differentiated, but they do not appear to be at all thickened. The 
plicated membrane is a marked feature of the picture, x 220 diameters. 24 
0. S' mm. 
Fig. 4.-Case of J. C . Minute arteriole from the kidney, showing great 
thickening of t e intima, which is almost structureless, containing only a few scat- 
tered cells; there being in addition merely a few fibres running around the circle 
of the vessel, x 60 diameters. .* 25 
tm.rrt. 
Fig. 5.-Case of J. C--. Branch of coronary artery from anterior surface of 
heart, showing almost the entire lumen of the vessel filled with an outgrowth, the 
opening being a mere chink. When seen with the amplifying power used in mak- 
ing the picture, this morbid material has, as represented, merely a fibrous appear- 
ance ; more magnified, the deposit is seen to contain a great many cells and to be 
a well-organized fibrous growth, x 28 diameters.  
Fig. 6.-Case of J. C . Radial with two accompanying arteries. It was so 
much hardened by mineral deposit that it had to be decalcified before sections 
could be cut. The differentiation of fibrous and muscular coats does not show 
well, perhaps owing to the soaking in acid to remove the salts, but more likely to 
the extensive atheromatous degeneration. The plicated membrane is a marked 
feature around the entire circuit, and the intima within it is much thickened. 
The atheromatous degeneration has extended deeply into the muscular layer, 
x 15 diameters. 
■S' n?.rn. 
Fig. 7.-Case of J. C -. Femoral artery and vein. Both vessels were con- 
verted into rigid bony tubes by calcareous deposit and had to be treated with acid 
for its removal before sections could be cut. The artery shows ordinary atherom- 
atous changes, the intima being irregularly thickened and spots of degeneration 
existing in the muscular coat. The vein shows an intima very greatly and irregu- 
larly thickened. At one place this coat and the muscular layer are broken loose 
from the adventitia. This probably occurred in removing the vessels from the 
thigh, for they were so rigid and firmly fixed in their position that some violence 
was necessarily used in cutting and tearing them loose, x 5 diamet .rs. 27 
f m. n. 
Fig. 8.-One-half of same vein as in Fig. 7, more highly magnified, and therefore bet- 
ter exhibiting the minute structure, x 22 diameters. 28 
Fig. 9.-Case of J. K . Views in longi- 
tudinal and transverse section of an artery 
from the kidney, which was removed under a 
dissecting microscope, and then split in hall 
with scissors lengthwise, and mounted with the 
inner side upward in imitation of Dr. John- 
son's pictures ("Medical Lectures and Es- 
says," by George Johnson, 1887). There are 
visible the inner surface of the artery and the 
edge of the intima and muscular coats. The 
fibrous coat does not show at all, and this 
is the case in Johnson's figures also. The in- 
tima is thickened, and in various degrees at 
different areas ; this might be said to be due to 
irregular cutting of the vessel, but is disproved 
by what is seen in the transverse section. 
The circular view is of the same vessel, but cut 
transversely with a pair of scissors. This 
shows marked thickening of the intima and its 
irregular distribution, and the plicated mem- 
brane is a marked feature of the picture, though 
not visible at all in the longitudinal section. 
The question whether the muscular layer was 
thickened in this vessel is one which might 
well be disputed, though there can be no 
doubt of the thickening of the intima and its 
difference in degree at different positions, x 
68 diameters. 
0. S' m.m. 29 
Fig. io -Case of J. K. . Minute arteriole from the kidney, showing marked 
irregular increased thickness of the intima, x 100 diameters. 30 
/. mm. 
Fig. ii.-Case of J. K . Third descending branch of left coronary artery 
(runs down front of heart in or near interventricular septum), exhibiting, most 
beautifully, extensive atheromatous degeneration. In two positions there is slight 
imperfection in the mounting, the outer portions of the section being folded over. 
There was no calcareous matter deposited in this vessel. The fibrous and 
muscular coats exhibit no extensive changes, there being merely slight inva- 
sion of the latter by the degenerative processes, and this is visib'e in the lower 
portions of the figure. The plicated membrane has been destroyed every- 
where except in the portion of the artery figured at the right-hand side of the 
picture, and there it forms a marked boundary between the muscular coat and 
intima, which latter, throughout its entire area, is most markedly and irregularly 
thickened. In the lower part of the picture, at the junction of the intima and 
muscular coats, atheromatous degeneration and softening is shown to have taken 
place, and extended into both the layers. The state of the intima of this vessel is 
typically characteristic of the diseased condition which it has been desired to de- 
scribe and represent, x 12 diameters. 31 
0.5 mm 
Fig. 12.-Case of J. K--. Of a vein and artery, contained in the adipose tis- 
sue, from the anterior surface of the heart, near the interventricular septum. The 
walls of the vein are generally thin and of loose texture, but there are two masses 
lying in the intima upon opposite sides of the vessel which are made up of tissue 
which evidently has a cell-like arrangement. More magnified, this is plainly seen 
to be composed of cells arranged in nests, and is pi ecisely similar in structure 
to what is found in the intima of arteries, and in the endocardium and heart- 
valves. x 40 diameters. 
Note.-These ar« from pen-drawings by Dr. B. A. Randall, and the plates 
were made by photographic process, and reduced from the original size by about 
one-quarter to one-half.