THE 
PRE-ALBUMINURIC STAGE 
of 
Chronic Bright’s Disease. 
By CHARLES W. PURDY, M. D., 
Member of the Chicago Academy of Sciences. First Vice-President, of the 
Chicago Medical Society. 
[Read before the Chicago Medical Society, May 18th, 1885.] 
CHICAGO: 
Clark & LongHiEy, Printers. 
1885. THE 
PRE-ALBUMINURIC STAGE 
OF 
Chronic Bright’s Disease 
CHARLES W. PURDY, M. D., 
Member of the Chicago Academy of Sciences. First Vice-President of the 
Chicago Medical Society. 
The more closely one studies the clinical history of chronic 
Bright’s disease, the more apparent it becomes that in its early 
stages albumen is quite often absent from the urine. 
That I may not subsequently be misunderstood by confusion 
of terms, I will here premise, that what I shall have to say 
upon this subject is intended to apply only to that group of 
clinical symptoms which are accompanied or preceded by the 
granular kidney. Such a condition of the kidney may exist; 
nay, it may even pass through all the stages of contraction, 
with its usual clinical symptoms, till death results, without 
albumen making its appearance in the urine. Such cases are 
by no means rare, as the records of post-mortem rooms in our 
hospitals demonstrate, which I shall later on amply verify. Purdy—Bright's Disease. 
[May, 
2 
Furthermore, I am convinced that a well-defined pre-albumin- 
uric stage of renal cirrhosis exists, which it is possible to make 
out, by well-defined and more constant symptoms, than that of 
the presence of albumen in the urine. This idea is by no 
means new, but has been long suspected, and is making itself 
felt with increasing force each year, if we are to judge from the 
increasing contributions to the literature of the subject, which 
have appeared within the past fifteen years. * 
It has become the dictum since the days of Bright, to hinge 
the diagnosis of all diseases bearing his name on the one 
symptom, namely, the presence of albumen in the urine. Now 
the diagnosis of Bright’s disease embraces a much more com- 
prehensive investigation of facts and data than the mere search 
for albumen, the neglect of which leads daily to very unfortu- 
nate results. 
Our life insurance companies are imposed upon frequently 
through incomplete so-called examinations of patients whose 
risks are passed as “ first-class ” (and some of them are literally 
so), upon the almost sole presumption, so far as 
the kidneys are concerned, that no disease exists because 
no albumen is present in the urine. Many of these 
cases are hurrying on to contracted renal organs, 
uremia, and death, which can at best be postponed but a short 
time. Nor is this picture an overdrawn one, as the following 
case illustrates. A year since a man made application to one 
of our leading insurance companies for insurance on his life. 
The medical officer representing the company found a slight 
trace of albumen in his urine, and he was referred to me. 
Atheromatous vessels, which had a year ago been manifest 
.through an obstinate epistaxis, showed the usual degenerative 
* Contributions on this subject, by Drs. Southy, Burdon-Sanderson, Ma- 
homed, Saundby, and others, have appeared. 1885.] 
Purdy—Bright's Disease. 
3 
changes accompanying renal cirrhosis, to have been in progress 
for some time. Fig. 1 shows his pulse tracing, which is char- 
acteristic. 
Fig. 1. 
He was put under treatment, and properly restricted dietary, 
and told that his disease was incurable, but with care he might 
live some months, or perhaps years. 
During my absence abroad, this man applied to another 
company for insurance, and was passed by the medical officer, 
and his life was insured for $8,000. His kidney disease is now 
slowly but surely advancing towards renal atrophy ; and this is 
by no means the first case of the kind which has come under 
my notice. 
In the days when I looked upon the presence of albumin- 
ous urine as the essential diagnostic symptom of renal disease, 
I have watched cases closely for years, suspecting the stealthy 
approach of cirrhotic kidneys, but was lulled into contentment 
by an occasional examination of urine, which was found to be 
free from albumen, till at length an attack of renal dyspnoea, 
or some other evidence of the disease, had pointed out that 
which I had suspected had really been going on under my very 
eyes. I have just now in mind a case which I had watched 
and suspected for nearly two years,but never could find a trace 
of albumen in the urine. Gastro-intestinal disturbances at 
length appeared, and finally a severe and prolonged attack of 
recurrent dyspnoea aroused me to the realization that my 
patient was suffering from renal cirrhosis; and subsequent 
autopsy proved the correctness of the diagnosis. Now I do 4 
Purdy—Bright's Disease. 
[May, 
not wish to be understood as underestimating the value of 
albuminuria as a symptom of renal disease; on the contrary, 
when present, I attach the greatest importance to it, under cer- 
tain conditions. But what I contend for is that when albumen 
is absent from the urine it does not prove that no renal disease 
is present. In other words, it is misleading to teach that the 
diagnosis should hinge upon this symptom alone. The form 
of renal disease under consideration is the very one in which 
albumen is most likely to be absent. 
It is to be feared that our recent rapid advance in pathologi- 
cal knowledge may have tended to incline medical thought too 
closely to the structural to the expense of the general disorder. 
In other words, the seat of disease itself is scanned most mi- 
nutely and laboriously, perhaps at the expense of less reliance 
on the good old clinical methods of investigation ; for one of 
our great teachers has said : “ After all, pathology is only a 
study of results, not'causes, of disease.” 
It was long ago noted by writers that in certain numbers of 
cases of renal disease, albumen disappeared from the urine. 
Indeed, this did not escape the attention of Richard Bright 
himself, who was the first to note this circumstance. But 
others, among them Christoson, Rayer, Rees and Malmsten, 
confirmed the observation. 
More recent authors point out that the cirrhotic form is the 
one in which this condition is noted, and pretty much all of 
them agree that in the early stages albumen is quite likely to 
be absent from the urine. 
Professor Grainger Stewart, in his admirable work on 
“Bright’s Disease,” page 188, says, referring to cirrhosis of the 
kidney : “ The early symptoms are very slight, such indeed as 
might easily escape notice. I have seen several cases in which 
the renal lesion was sufficiently distinct on post-mortem 1885.] 
Purdy—Bright's Disease. 
5 
examination, but in which there had been no albuminuria and 
no dropsy during life;” and again, page 189, he writes: “In 
the early stages (of cirrhosis) albumen is' occasionally present, 
generally in very small quantity. One day it may be distinct, 
but the next day we search for it in vain.” 
Dr. Roberts, in his last edition, says: “ But it must be 
admitted that chronic degeneration of the kidneys, not dis- 
tinguishable from some forms of Bright’s disease, does exist 
under certain circumstances, without albuminuria.” 
Bartels says (Ziemssen’s Cyclopedia, page 431, Vol. XV.) : 
“ It is these cases of genuine contracting kidney, that urine is 
occasionally excreted, which is in no way to be distinguished 
from that secreted by healthy kidneys;” and again, on the same 
page, 435-436, he adds : “ But albuminuria, as later experiences 
in this direction have taught me, is no constant symptom in 
this affection. The temporary absence of albumen, I have 
witnessed repeatedly,—for purpose of diagnosis, the matter is 
one which deserves to be detailed at greater length.” On page 
440 he cites a case which came under his care in the hospital, 
and continued under treatment, from Jan. 26th till death, March 
3rd, and though both kidneys proved to be cirrhotic and 
extremely contracted at the autopsy, he says : “ Albumen was 
entirely absent from the urine throughout.” 
Dr. Geo. Johnson, in his “ Lectures on Bright’s Disease,” page 
52, says: “The amount of albumen varies considerably. 
Absent or scanty in the early stage, it may be rather copious 
in the middle periods, and again scanty, or even entirely absent, 
in the stage of extreme degeneration of the kidney.” 
Dr. Dickinson, in his “Treatise on Albuminuria,” says, in 
referring to the urine in the early stage of granular degenera- 
tion : “ If examined in this early stage, it may be found perfectly 
free from albumen, or may contain only a minute trace, or, a 6 
Purdy—Bright's Disease. 
[May, 
trace only after food, or on getting up in the morning; ” and 
again he observes : “ Early in this disease, the urine is free, 
both from albumen and casts; later on, a trace of albumen 
appears, which may not be discoverable until the constitutional 
symptoms are such as to indicate an advanced stage of the 
disease. s So little albumen may be present, even to the end, 
that care is needed for its detection. And even that little may 
not be constant, but discoverable only after sleep, or meals.” 
Dr. Tyson, in his work on “ Bright’s Disease and Diabetes,” 
page 178, says, in referring to the urine in cases of interstitial 
nephritis: “ The albumen is small in amount, and may be 
temporarily absent, or it may be absent before a meal, and 
present after it.” 
Dr. Millard, in his treatise on “Bright’s Disease,” page 141, 
says : “The fact is, however, that in chronic nephritis, especially 
the interstitial, the appearance of albumen is often preceded 
for considerable, and even for a very long time, by morbific 
changes in the kidney, which are not recognized until the 
appearance of albumen. Indeed, nephritis may exist to such 
an extent as to produce even cirrhosis, without albumen ever 
making its appearance in the urine.” He also very correctly 
adds, (page 143): “ To rely upon albumen, solely as a means 
of determining the existence or non-existence of nephritis, is 
to rely upon an ignis fatuus. It is at best a coarse and primi- 
tive test of its presence ; insufficient in itself, and unsatisfactory 
in comparison with more searching and absolutely accurate 
means of diagnosis.” Dr. Millard cites several cases in his 
experience, wherein albumen was entirely absent from the urine, 
throughout the course of renal cirrhosis; and, indeed, he 
devotes a special chapter to the consideration of “ Nephritis 
without Albuminuria; ” which is well worthy of careful perusal. 
In “ Guy's Hospital Reports',' for 1879, (page 367) will be 1885.] 
Purdy—Bright's Disease. 
7 
found an analysis of one hundred cases of granular kidneys, 
observed in that hospital, previous to that year. Out of the 
hundred cases noted, the very large proportion of seventy-four 
were characterized by the absence of albumen from the urine. 
Dr. Saundby, on “ Occurrence of Dropsy in Granular Kidney,” 
introduces a table showing the diagnosis—which was sent down 
from the wards, to the post-mortem room, at the Birmingham 
General Hospital*—in ninety-eight cases, in all of which, the 
kidneys proved to be granular. Out of these ninety-eight, 
only twenty-two were sent down with the diagnosis of Bright’s 
disease. Hence, we may fairly assume, that in seventy-six ot 
them, albumen was not discovered in the urine. Again, Dr. 
Mahomed collected the records of sixty-one cases treated in 
Guy’s Hospital during the two years 1879 and i88o.f In 
forty-one of these, albumen was never discovered in the urine. 
Now, putting these statistics together, we have two hundred 
and fifty-nine cases of chronic Bright’s disease, in which albu- 
men was present in the urine only in sixty-eight cases, leaving 
one hundred and ninety-one cases, or about seventy-four per 
cent., in which albumen was absent. These cases can be open 
to little question, for, be it remembered, they were all hospital 
cases, subject to the usual rules for daily examinations of urine, 
and the diagnoses in all were confirmed by autopsy. 
In the light of such unanswerable testimony as the foregoing, 
I maintain that the mere absence of albumen from the urine, 
constitutes no reliable evidence of the non-existence of chronic 
Bright’s disease, and above all in its early stages. If clinical 
evidence, conjoined with post-mortem examination of our 
cases, teaches us anything, it is, that this disease may exist, 
and progress through years, without giving rise to albuminous 
*= Birmingham Medical Review, April, 1881. 
\ Guy’s Hospital Reports, Vol. XXV, 1880 and 1881, pages 304 and 305. 8 
Purdy—Bright's Disease. 
[May, 
urine; and therefore, a clinical symptom so notoriously incon- 
stant and unreliable, even in the fully formed stages of the 
disease, constitutes the most flimsy evidence upon which to 
construct the diagnosis of a disease, the most insidious and 
silent in its early advances of any with which medical science 
has to deal. 
In many instances chronic Bright’s disease is a condition in 
which its early steps have been so slow and imperceptible that 
half the lifetime of the individual has been consumed in leading 
up to it through continuous functional overtaxing of the gland 
before any marked textural changes can be made out; yet, in 
this early stage, other evidences of the disease are to be found, 
which, taken collectively, will establish the diagnosis in the 
majority of cases. 
I do not mean to say that absolutely the first departure from 
the normal condition is to be made out, for from the very 
nature of the first changes in the gland, it is probable that 
these escape detection. But I hold that during that stage in 
which no appreciable change can be made out in the renal 
epithelium (which may extend over years), albumen, as a rule, 
is absent from the urine, and yet, through other symptoms, the 
presence of the disease may often be revealed. 
I have examined, microscopically, many sections of cirrhotic 
kidneys, including those in my own collection and in the Path- 
ological Laboratory at Aberdeen, as well as in other places, 
and in the early stages of this disease I find little, if any, de- 
parture from the normal in the tubular epithelium. The ear- 
liest changes which I am able to make out, seem to be slight 
thickening of Bowman’s capsule, sparse septa of apparently 
new connective tissue creeping in at varying points from the 
capsule and between the interlobular arteries, as well as in- 
creased thickness of the coats of the small arterial vessels. I 1885.] 
Purdy—Bright's Disease. 
9 
have compared, side by side, sections of early cirrhotic kidneys 
with those of normal, with the view of ascertaining the true 
condition of the epithelium lining the convoluted tubes in the 
former, and I cannot see that it varies essentially from the nor- 
mal. It is misleading to speak of cloudiness of the renal 
epithelium. That is the normal condition, it is never clear 
unless cleared by some chemical agent. The very first change 
I am able to make out is the presence of some fat globules in 
the epithelial cells, and perhaps a slight flattening of the latter, 
so that the lumen of the tube is somewhat more open. Des- 
quamation of the epithelium, if it ever occurs in this disease, 
•certainly does not do so in this early stage. 
Bartels says : “ This much, however, I believe to be beyond 
all doubt, namely, that genuine renal contraction—the so-called 
third stage of Bright’s disease of our (German) writers, Grainger 
Stewart’s cirrhosis of the kidney, is the result of a primary 
growth or proliferation of the intertubular connective tissue.” 
Dr. Dickinson, in his treatise on “ Albuminuria,” says: “ I 
have examined these cells (tubular epithelial) in a great num- 
ber of granular kidneys, and have carefully drawn their outlines 
and dimensions, as seen through an one-eighth inch object- 
glass. The conclusion I long ago formed, one which has been 
justified by careful and continued observation, is this: In the 
vast majority of cases, in all cases excepting those in which the 
contraction of the organ has become extreme, the epithelium is 
xxactly such as is found in healthy kidneys.” 
Charcot, in his “ Lectures on Bright’s Disease of the Kid- 
neys,” describes minutely the changes found in what he terms 
the “ first stages of interstitial nephritis,” as follows : “ From 
the commencement the connective stroma is infiltrated with a 
more or less considerable quantity of small cellular elements, 
which, following the theory adopted, are called leucocytes or Purdy—Bright s Disease. 
[May, 
embryonic cells. To this cell infiltration is due the grayish 
yellow color sometimes presented by the kidney at this stage 
of the disease. Another characteristic revealed by histologi- 
cal study is, that at this period the tubular apparatus of the 
kidney presents no appreciable alteration ; the epithelium in 
the convoluted tubes is in its place, and perfectly healthy 
This, then, explains the non-appearance of albumen in the 
urine during the early stage of granular kidney, for pathologi- 
cal and clinical evidence shows that those diseases which cause 
destruction of the renal epithelium are the ones which give 
rise to the most constant and profuse amount of albuminuria. 
On this point Senator says : “ The normal functions of epi- 
thelial cells is assigned as the reason for the absence of albumen 
in the secretion of the liver, the most prominent of the second 
class of glands, and likewise in the secretions of the perspira- 
tory and lachrymal glands, supposing it to be the case that 
these latter secretions in their pure state are really non-albumi- 
nous. If the urine be regarded simply as a true non-albumi- 
nous glandular secretion, the epithelium must be credited with 
the function of preventing the escape of albumen from the 
blood. Even if the urine be regarded as a mixture of a trans- 
udation with a glandular secretion, the latter at least being the 
produce of the epithelium of the uriniferous tubes, must for the 
same reason be considered to be non-albuminous ; whatever 
view may be entertained as to the presence or absence of al- 
bumen in the transudation from the glomerular vessels. The 
conclusion is forced upon us, that when their nutrition and 
functions arejdisturbed, or when the epithelial cells of the urinif- 
erous tubes are in a state of complete decay, albumen will escape 
from the blood and lymph, and show itself in the urine hitherto 
apparently non-albuminous ; that is, that albuminuria will be- 
come developed. Observations which are alleged to prove the 1885.] 
Purdy—Bright's Disease. 
11 
contrary must be based upon error or defective investigation, 
for if not, all our doctrines with regard to specific glandular 
secretion must be thrown to the winds.” 
It may be asked, then, if the renal epithelium is not the seat 
of any degenerative change in renal cirrhosis ? How does it 
happen that albumen is present in the urine sometimes in the 
course of the disease ? 
We answer, that the latter is due to increased intra-vascular 
pressure, which is brought about as a legitimate outgrowth of 
the disease. 
It has been established, beyond doubt, that increased blood 
pressure within the vessels, will, under certain conditions, cause 
albumen to appear in the urine. J. B. Stockvis showed by 
extended experimental and clinical investigations, that altera- 
tions of the circulation which checks the afflux of arterial, or 
the escape of venous blood, causes albumen to pass into' the 
urine. In other words, over-fullness of the venous circulation, 
or slowing of the current, produces albuminuria Since, how- 
ever, other observers, and especially Senator, has pointed out 
that high pressure in the arterial vessels will also cause album- 
inuria, though to a less extent. 
Active muscular exertion is accompanied by an increase of 
the muscular power of the heart’s action by about twenty-five 
per cent., hence, the intra-vascular pressure is increased to that 
extent in the arteries, and it is no uncommon thing to find 
albumen in the urine of healthy men, who are undergoing 
active muscular exercise. Heat also causes a direct rise in the 
arterial blood pressure, as shown by the dilated, and turgescent 
vessels everywhere; as a consequence of this, we often note 
appearance of albumen in the urine during febrile conditions. 
Senator proved the proposition by the following experiments. 
He introduced rabbits into an oven, constructed for the pur- 12 
Purdy—Bright's Disease. 
[May, 
pose, previously having drawn off their urine, and testing it 
for albumen. He then slowly increased the heat in the cham- 
ber, and again tested the urine, and he states as to these exper- 
iments, many times repeated, that, “ The result in all cases 
was the production of albuminuria, when the bodily tempera- 
ture had been increased by i*5°-3°C., with sufficient rapidity, 
or the heat continued for a sufficient length of time.” 
It may be observed that heat, or any other agent, suddenly 
applied, which raises the arterial pressure, causes a contraction 
of the capillaries which resists the increased pressure, and 
albumen does not transude under such circumstances. The 
* 
pressure must be gradual to cause albuminuria. We have 
many examples of the production of albuminuria by intra- 
venous pressure. Bartels relates a case bearing on this point. 
It was one in which there was impeded escape of the blood of 
the renal vein, in consequence of thrombosis of the inferior 
vena cava, occurring in a very robust man, forty-four years of 
age. Bartels says : “ This patient passed enormous quantities of 
urine, and with a specific gravity varying from i.oi i to 1.013, 
and always containing albumen ! ” The occurrence of albumen 
in the urine as a consequence of valvular lesions of the heart, 
is another well known example of this kind, leading to what 
has been called cyanotic induration of the kidney ; a condition, 
by the way, very similar to renal cirrhosis. 
Thus it may be laid down as a rule, that intra-vascular pres- 
sure, whether arterial or venous, if only of sufficient extent, 
is likely to result in albuminuria. 
Now, in the advanced stage of granular kidney, we have at 
least two conditions which lead up to increased blood pressure, 
and especially so within the glomerular vessels. First, hyper- 
trophy of the left ventricle of the heart (almost uniformly 
present), and even before this occurs, increased power of the 1885.] 
Purdy—Bright's Disease. 
13 
heart’s action, resulting from the causes which lead up to hy- 
pertrophy. Second, anatomical changes in the kidney, which 
obstruct the outflow from the glomerular tuft of vessels. In 
order more clearly to appreciate the latter, let us first glance 
at the vascular arrangement in the cortex, and see how it is 
effected by the advancing pathological changes of granular 
degeneration of the kidney. The interlobular arteries, as they 
pass upwards towards the cortex, give off directly on either 
side lateral branches, the afferent arterioles, each one of which 
on entering a Malpighian capsule, breaks up into the capilla- 
ries composing the glomerular tuft. Now the afferent vessel 
of the Malpighian body, after uniting with the vessels of the 
tuft, pass out of Bowman’s capsule, and immediately again 
sub-divide into a network of capillary blood vessels, which 
entwine in all directions, the convoluted tubules. This net- 
work anastomoses freely also with the capillaries of the medul- 
lary rays, forming one common net-work of the whole cortex. 
Now, we have before noted that the first observable patholog- 
ical change in the cirrhotic kidney, is a proliferation of new 
connective tissue cells between and among the intertubular 
capillary plexus. New connective tissue cells, wherever formed, 
as they become old and organized, contract, and it thus happens, 
that as the disease goes on, many of the intertubular capilla- 
ries forming the plexus, become obliterated at points, while in 
others, they are in all stages of contraction, being choked off 
by the new tissue formation. It is easy to comprehend, there- 
fore, that the outward current of blood from the glomerule, is 
very seriously retarded, as it is more readily assailable from its 
large number of branches than that of the single larger affer- 
ent arteriole, coming off as it does directly from the trunk of 
the interlobular artery. We thus perceive, that the blood is 
dammed back upon the glomerular tuft, which raises the ten- [May, 
14 
Purdy—Bright's Disease. 
sion especially high within these vessels. That this is no mere 
theory, has been proven by Dr. Dickinson, who found, upon 
experiment, that the granular kidney permitted much less water 
to pass through its vessels under pressure, than the normal 
organ. 
It is likely that still another factor operates in the case of 
renal cirrhosis, to increase the intra-vascular pressure, within 
the glomerule, namely, the thickened capsule of Bowman. 
Thus we have in the advanced stage of renal cirrhosis, both 
the increased force of an extra powerful contraction of the 
heart, on the one side, of the glomerule, and counter to this, 
an impeded current on the other, exerting a backward force, 
owing to obstructed capillaries, and these two forces meet in 
the glomerular tuft of vessels, and thus we have all the condi- 
tions requisite for producing transudation of albumen as well 
as the secretion of a copious amount of urine, of low specific 
gravity, all of which are the accompaniments of advanced 
granular kidneys, but not till the disease is advanced. 
Having shown that albuminuria can never be relied upon as 
an early symptom of chronic Bright’s disease, and given at 
length the physiological and pathological reasons therefor, as 
well as referring to a large collection of clinical and autopsical 
proofs thereof, and moreover having traced it to its philosoph- 
ical and pathological cause, when it does occur; it now 
remains to ascertain, what are the symptoms which, taken indi- 
vidually and collectively, may be relied upon to establish an 
earlier diagnosis of the disease. 
So large a proportion of the profession has become wedded 
to the old teachings, that albuminuria forms the hinge upon 
which the door to renal disease has ever been opened, that I 
apprehend it will be easier to explain facts, with philosophical 
reasoning, than it will be to do away with preconceived ideas, 1885.] 
Purdy—Blight's Disease. 
15 
or break down old traditions. I am unwilling to believe, how- 
ever, that a disease so widely influencing in its pathological 
results, undermining as it does so many of the vital processes 
of the economy, can approach so silently through years of 
development, without leaving behind some imprints, which if 
properly interpreted must reveal its footsteps. 
First, then, let us glance at some of its more important etio- 
logical factors, for to know disease best is to first know its 
cause. It has been frequently pointed out that renal cirrhosis 
occurs most often in people who have lived very generously, 
partaking of highly seasoned and flavored meat diet; in short, 
they have been over indulgent in the pleasures of the table. It 
is the function of the kidneys to eliminate from the system 
nitrogenous waste, whether this be from the tissues or the 
food, or from both. We have here then a very direct cause of 
increased work thrown upon the kidneys, and the result is that 
extra activity of renal function is called for. 
Notice next, that renal cirrhosis is most often developed 
after middle age. Statistics show that the largest number ot 
cases occur between forty-one and fifty years of age, and the 
next largest between fifty-one and sixty. Thus, as a rule, it is 
a disease of middle and advancing life. Why is this ? To my 
mind, Fothergill best answered this question, when he said: 
“ The diseases incident to advancing age are those which arise 
through inability of the system to get rid of its waste pro- 
ducts.” Here then we have two powerful determining causes 
of disease, whose especial foci is the kidney: a demand for 
increased functional activity, and a diminished functional 
power. 
Gout, rheumatism, free use of alcohol, and the absorption of 
lead into the system, as well as some other factors may, and 
doubtless do, act as accelerating or predisposing causes ; but to 16 
Purdy—Bright's Disease. 
[May, 
my mind, around the two conditions, advancing age and inges- 
tion of foods which leave behind the maximum of nitrogenous 
waste, clusters most of the phenomena of the disease, in its 
causative relations, and the more closely this is kept in mind, 
the more readily will be understood what I shall have to say 
of the symptoms which accompany it. 
Heidenhain has shown conclusively by his beautiful experi- 
ments with indigo injections into the circulation, that the solid 
elements of the urine are excreted by the epithelium of the 
convoluted tubules. We have through heavily charged nitro- 
genous foods, a very material increase of work thrown prima- 
rily upon the epithelial cells of the convoluted tubules, and at 
a time when the functional power of such cells are on the wane, 
from advancing age. The cells, thus both over-taxed and 
crippled, become in time functionally impaired, and are unable 
to meet the demands made upon them. We have previously 
shown that necrosis of the cells does not result directly, but the 
impaired function is made known through the retention of 
those products in the system which it was their province to 
eliminate, and which, thus accumulating in the system, result 
in certain derangements and symptoms which we shall next 
consider. 
One of the earliest manifestations of chronic Bright’s disease 
is pallor of the skin. It is pretty uniformly present in quite 
early stages of the disease. In some well nourished individ- 
uals, it is true, the disease does not make sufficient impress 
upon the blood to cause this loss of color in the skin till well 
advanced; but taking the average of cases, as we find them 
it may be laid down as the rule that a suspicious pallor and 
unhealthy color of the skin is present, and we may often note 
this condition before albumen is discoverable in the urine. The 
THE CUTANEOUS SYSTEM. 1885.] 
Purdy—Bright's Disease. 
17 
peculiar pallor referred to is not the pronounced anaemic white- 
ness exactly which we meet with in acute Bright’s disease, on 
the one hand, nor yet the semi-bronze-like hue, due to malig- 
nant cachexia, but it is rather an intermediate tint. Dickinson 
says : “ It is somewhat of the pallor luteus somewhat anaemic 
appearance, though a sort of sun-burnt tinge upon the skin 
prevents the whiteness characteristic of the acute form, a dirty, 
faded hue.” 
Defective perspiration is also a common accompaniment of 
early cirrhotic disease, and this results in a dry, harsh state of 
the skin. This is probably due to two causes : compensatory 
elimination through renal incompetency, and perhaps later on 
to hypertrophy of the muscular walls of the small arteries of 
the skin, interfering with the nutrition of the latter. 
Other cutaneous symptoms may arise, as erythema, or acne 
rosacea, but these are more likely to occur later in the disease. 
THE MUSCULAR SYSTEM. 
One of the earliest noticeable accompaniments of chronic 
Bright’s disease, is usually diminished muscular power. The 
patient experiences an unaccountable disinclination for muscu- 
lar exertion, and is easily tired. He walks less, and rides more 
frequently than is his usual custom, when he finds it necessary 
to go about. A weary feeling is experienced in the muscles, 
and he perhaps goes to some watering place to seek rest from 
business, which latter, he imagines has over-taxed his strength, 
but he returns unimproved. 
More or less emaciation is likely also to be present, though 
this latter does not always obtain, and, in some cases, it is con- 
spicuously the opposite. 
THE DIGESTIVE SYSTEM. 
It is well known that all forms of Bright’s disease are accom- 
panied more or less by dyspeptic symptoms, at some stage of 18 
Purdy—Bright's Disease. 
[May, 
their progress. In the form under consideration, however, 
dyspepsia has been noted as one of its very earliest symptoms. 
Dr. Geo. Johnson has observed a flatulent dyspepsia, with nau- 
sea and occasional irregularity of the bowels, to precede renal 
cirrhosis so frequently, that he even regards it as one of 
the causes of the disease. He thinks the kidneys become 
deranged in such cases, in consequence of their long-continued 
elimination of the products of faulty digestion. Be this as it 
may, the fact is notorious, that flatulent dyspepsia precedes, for 
a longer or shorter time, in a large number of these cases. In 
two cases which came under my own care, it was the first 
symptom which led both patients to seek medical advice, and 
for that which they both supposed to be simple disorders of 
the stomach. In one of these cases, no albumen could be 
found in the urine till over a year after the first dyspeptic dis- 
comforts appeared, and the latter continued, off and on, till 
albumen finally was discovered in the urine in small traces.* 
In the second case, albumen was found in the urine on first 
consultation, but it has been occasionally absent in the course 
of the disease since. Loss of appetite is an early and persist- 
ent characteristic of the disease. Nausea frequently accom- 
panies the dyspepsia of renal cirrhosis, and when it does, it is 
most frequently complained of in the morning, before food is 
taken. Irregularity of the bowels completes the round of 
digestive disturbances which are the outgrowth of this disease. 
Constipation being the most frequent departure, and I have 
noted this early in those cases in which heretofore the patient 
had congratulated himself on most scrupulous regularity, 
throughout his preceding life. 
Dyspnoea is a frequent symptom of renal cirrhosis. It may 
THE RESPIRATORY SYSTEM. 
* Subsequent autopsy revealed granular kidneys. 1885.] 
Purdy—Bright's Disease. 
19 
exist in various forms, and it may be one of the first symptoms 
which attracts attention, or, it may not appear till ushering in 
oedema of the lungs, which closes the life of the patient. In 
the latter case, probably only in advanced stages of the disease. 
We may have dyspnoea coming on quite early in the disease, 
simulating asthma in many respects, especially in its more fre- 
quent prevalence at night. Some look upon it as an elimina- 
tive effort of the lungs. Others regard it as of cardiac origin, 
or at least due to cardiac disturbance. Bartels and Dickinson 
seem to regard the attacks as uremic, Rosenstein denies this, 
and Johnson speaks of them as nervous dyspnoea, of uremic 
origin. Whatever may be its cause, it simulates asthma 
closely, coming on suddenly, usually at night, accompanied by 
sibilant rales, and followed by more or less watery expectora- 
tion. 
I am aware that many authors regard this dyspnoea as a 
symptom only accompanying the advanced stages of the dis- 
ease. But that it may occur comparatively early in the disease, 
I am equally positive, as the following case has shown me. A 
case came under my observation in which the patient com- 
plained of dyspepsia, and attacks of short breathing, coming 
on at night. High vascular pressure, and other symptoms 
pointed to granular kidneys. The dyspnoea became much 
worse after a few days, indeed, in one of the spasms which I 
witnessed, I never saw more distress or anxiety depicted in 
the countenance of a truly asthmatic patient. Under diapho- 
retics and purgatives, these symptoms subsided, and the patient 
had no recurrence of them. Eight months afterwards he suc- 
cumbed from outside causes, and the autopsy revealed granular 
kidneys by no means advanced, each organ weighing slightly 
more than five ounces. In another instance, three years since, 
that of a well-informed physician, who served in his professional 20 
Purdy—Brights Disease. 
[May, 
capacity through the late war. He had noticed some declin- 
ing health, but the first symptoms which aroused his attention, 
was an asthmatic attack at night, followed by others, which led 
to to the discovery of renal cirrhosis from which he subse- 
quently died. It may be said, that there is no proof in the last 
case that the disease was not advanced, and while this is true, 
yet it was the first symptom which aroused any suspicions, 
and if no symptoms are observable till dyspnoea overtakes the 
case of a medical man, how much more likely is it to be the 
case with our patients? 
That the mucous membranes are especially prone to irrita- 
tion in the early stage of renal cirrhosis, we have already seen 
in the case of the digestive tract. It is equally so with’the 
respiratory tract. Bronchial catarrh has been frequently noted 
by various authors as preceding or accompanying the granular 
kidney. The late Dr. Mahomed regarded this as one of the 
early results of high vascular pressure, which, in some instances 
led on to pneumonia, in people of advanced age, before they 
were overtaken by the renal disease. Pharyngeal or naso- 
pharyngeal catarrh, is another evidence of disturbance of the 
respiratory tract, which may often be observed in early cir- 
rhosis ; and, lastly, I would mention, the frequent occurrence 
of emphysema of the lungs in these cases. 
Of all the disturbances which arise in the course of chronic 
Bright’s disease, those of the vascular system are among the 
earliest, most constant, and give us, when properly interpreted, 
the most important information. If the theory which we have 
advanced as to the etiology of the disease, and supported thus 
far by pathological evidence, be correct, then the first conse- 
quence which results from the disease, outside of the kidneys 
themselves, must fall upon the vascular system. And it will 
THE VASCULAR SYSTEM. 1885.] 
Purdy—Bright's Disease. 
21 
be found on following its pathology a step further, that the 
deduction will be confirmed. 
Dr. George Johnson pointed out* certain interesting and 
constant anatomical changes, which occur in the minute arteries 
in cases of granular degeneration of the kidneys, consisting of 
thickening, and hypertrophied growth of their muscular walls. 
He showed that both the circular and longitudinal muscular 
layers of the small arteries constantly participated in this 
hypertrophic development, but that the veins do not share in 
this change. Dr. Johnson regards this change in the walls of 
the small vessels as due to the resistance offered in the capil- 
laries to the circulation of abnormal blood. He says : “ The 
minute arteries, by their contractile power, under the influence 
of vaso-motor nerves, now regulate the blood supply in accord- 
ance with the diminished requirements of the glandsv This 
regulating contraction continues and increases, month after 
month, year after year, and the physiological result of this per- 
sistent over-action of the minute arteries is that their muscular 
walls become hypertrophied.” He refers the hypertrophy of the 
left ventricle of the heart (so constantly accompanying this 
disease) to a similar cause, for he adds : “ The minute arteries 
throughout the body (of course under the influence of vaso- 
motor nerves) resist the passage of this abnormal blood, and 
in consequence the left ventricle beats with increased force to 
carry on the circulation. The result of this antagonism of 
forces is, that the muscular walls of the arteries, and those of 
the left ventricle of the heart become simultaneously hyper- 
trophied.” 
Gull and Sutton, later on, claimed, ist, “That there is a 
diseased state of the arterioles and capillaries in this disease, 
characterized by increased growth in the outer fibroid coat, or 
*Medico-Chirurgical Transactions, Vol. xxxiii. 22 
Purdy—Bright's Disease. 
[May, 
tunica adventitia, which they termed arterio-capillary fibrosis.” 
2d. “That this change in the arterioles and capillaries is the 
primary and essential condition of the morbid state called 
chronic Bright’s diseases with contracted kidney.” 
3d. “ That the morbid state under discussion is allied with 
the conditions of old age, and its area may be said hypotheti- 
cally to correspond to the area vasculosa.” 
4th. “ That it is possible that this change commonly begins 
in the kidney, but that there is evidence of its beginning pri- 
marily in other organs, and finally, that the contraction and 
atrophy of the kidneys are but a part and parcel of the general 
morbid change.” 
In the light of subsequent investigation, the only one of these 
propositions of Gull and Sutton which remains tenable is the 
existence of fibroid change in the small vessels, not to the exclu- 
sion of, but in addition to, the muscular hypertrophy. 
That the cardio-vascular changes are dependent directly 
upon renal deficiency, is shown, 1st, by their constantly ac- 
companying all forms, even scarlatinal, of that deficiency, if 
only it continues long enough, or the patient survives a suffi- 
cient length of time; and this becomes another proof, that in cir- 
rhotic kidney the functional incapacity of the organ may long 
exist before it is made known by very active general symptoms. 
2d. That the occasional existence of the disease in children, 
in which cases all the typical cardio-vascular changes accom- 
pany it, completely disproves the second, third and fourth 
propositions of Gull and Sutton, and moreover, furnishes the 
very strongest evidence that the cardio-vascular changes are 
subject to the renal disease, as their primary, unvarying, and 
constant cause. 
Professor Hamilton, of Aberdeen,* has formulated the laws, 
* “On the Circulation of the Blood Corpuscles Considered from a Phys- 
ical Basis.”-—Journal of Physiology, Vol. v., No. 2. 1885.] 
Purdy—Bright's Disease. 
23 
which govern the circulation of the blood corpuscles in the 
vessels, in the most lucid manner, and demonstrated their cor- 
rectness by means of a series of interesting illustrations. These 
consist in passing a current of water, containing bodies of 
varying sizes, shapes, and specific gravity, through glass tubes, 
which thus imitate the systemic circulation. He first calls 
attention to the fact, that the blood current consists of an axial 
and peripheral stream, and that “ the colored corpuscles float 
exclusively in the axial stream, while a great many, not all, of 
the leucocytes run in the peripheral.” 
a Vessel wall 
b White corpuscles in peripheral 
stream. 
c Red corpuscles in axial current. 
He demonstrates clearly the following among other laws by 
practical experimentation : 
ist. “ That if a sphere is specifically lighter than the liquid 
i Web of frog’s foot 
2 White blood cor- 
puscles. 
After Hamilton. 24 
Purdy—Bright's Disease. 
[May, 
in which it is suspended, it will sooner or later come to occupy 
the upper strata, and will rotate.” 
Now this is precisely what the colorless corpuscles do in 
normal conditions of the blood, as may be demonstrated by 
observing the circulation in the frog’s foot, viewed horizontally 
by means of the microscope. The white corpuscles will be 
seen to roll along the upper surface of the vessels, because 
they are lighter than the blood plasma in which they move. 
2d. “ That a disc or sphere of the same specific gravity as 
the liquid in which it is immersed, moves in axial stream, 
and does not rotate.” 
This explains why the red corpuscles, as they are of the 
same specific gravity as that of the blood serum, occupy the 
axial stream of the vessels, and do not rotate as do the col- 
orless ones, but glide. 
3d. “ Spheres, or discs, whose specific gravity is greater than 
the fluid in which they circulate, move in the lowest strata of 
the tubes, and roll, or rotate.” 
Thus it will be noted, that bodies which depart from the 
specific gravity of the fluid in which they circulate, occupy 
the peripheral stream and rotate as they move; while those 
which do not depart materially from the specific gravity of the 
circulating fluid, move in the axial stream, and do not rotate, 
but glide. 
Other laws are formulated and illustrated in the same paper 
bearing on the size, weight, and rapidity of motion, as the 
bodies occupy the axial, or peripheral stream, and the fact is 
noted, that the colorless corpuscles evince a tendency to 1885.] 
Purdy—Bright's Disease. 
25 
stagnate, or clog in places, especially at the curves of the 
tubes. I have gone over these experiments with Professor 
Hamilton in his laboratory, and I know that the laws which 
he formulates do not rest on any mere theoretical basis, 
but are amply borne out by his interesting and instruc- 
tive demonstrations. Professor Hamilton thus sums up 
this matter: “The cause of a colorless corpuscle blocking the 
tube undoubtedly is, that its light specific gravity tends to 
press it upwards against the wall of the vessel, to which it may 
become temporarily adherent. From this we may learn an 
important lesson, namely, that if the colored corpuscles were 
not so balanced as to closely approach the specific gravity of 
the plasma, the circulation would become a physical impossi 
bility; for if they were specifically lighter or heavier than the 
plasma to a marked degree, there would be a constant tend- 
ency for them to obstruct the capillaries and to hinder the on- 
ward flow. The essence of the blood circulation is that the 
large majority of the corpuscles never touch the wall of the 
vessel, but glide in the central stream. Were the colored cor- 
puscles to rub against the wall of the vessel, the friction would 
be so enormous over the whole capillary system that the heart, 
as at present constituted, would be wholly inadequate to drive 
the blood onwards. Indeed, my own impression is that if the 
blood corpuscles all differed materially from the specific 
gravity of the plasma, the circulation could not be carried 
on even with a much more powerful heart.” 
Now, what is the actual condition of the blood in cases of gran- 
ular degeneration of the kidneys? From the various sources 
from which I have been able to get statistics, I have estima- 
ted, roughly, that the blood is about ten per cent, more hy- 
dremic in cases of renal cirrhosis, than in the normal con- 
dition. It must not be forgotten, that other circumstances in- 26 
Purdy—Bright's Disease. 
[May, 
fluence the deviation from the normal, in this disease, but all 
observers agree that it is somewhat lighter than in health. 
My own calculation from the few tables I have been able to 
find, places the average specific gravity of the blood serum 
in renal cirrhosis at 1025.5. These estimates, in the light of 
Professor Hamilton’s researches, teach us, to say the least, 
a very probable explanation of that interesting and import- 
ant series of cardio-vascular changes, which so uniformly ac- 
company the granular kidney. 
Not only may the loss of balance between the plasma and 
corpuscles call for more muscular development in the fibres 
of the heart, resulting in hypertrophy of the ventricle, but if also, 
as Professor Hamilton points out, even a part of the red cor- 
puscles of the blood are forced into the peripheral stream, 
they may by their friction against the vessel walls be the 
source of an irritation, which gives rise to the degenerative 
changes therein. 
It has occurred to me that Professor Hamilton’s laws may 
explain a phenomenon which is often present in renal cirrho- 
sis, and which, heretofore, I have never been able to explain 
satisfactorily to myself. I refer to the singular circumstance 
that in such cases the patients often pass much larger quanti- 
ties of urine at night than in the day time. It now seems plain 
enough to me, that if the blood plasma is reduced in density, 
when the patient assumes the recumbent position more of the 
red corpuscles gravitate into the peripheral stream, and the extra 
friction induced thereby, calls for more force of the heart, and 
thus the intra-vascular pressure becomes high, and this latter 
we know always increases the quantity of urine. 
We may not as yet be able to comprehend all the causa- 
tive relations of these vascular changes, but we are very certain 
of one fact, namely, that increased intra-vascular pressure and 1885.] 
Purdy—Bright's Disease. 
27 
high tension of the vessel walls are the most constant of all the 
early symptoms of this disease. As indications of these con- 
ditions, I would call attention to the character of the pulse, 
which is hard, unyielding, and rolls under the finger like a 
cord. The pulse is notably prominent under the finger in 
chronic Bright’s disease. But high pressure of the vessels is 
estimated much more accurately by means of the sphygmo- 
graph, and hence this instrument has proven of the greatest 
value in pointing out the true condition of the circulatory 
apparatus in chronic Bright’s disease. 
Fig. 5 is the pulse tracing of a healthy man, under three 
ounce pressure, and may be fairly said to represent the usual 
pulse tracing by the sphygmograph, in perfectly healthy con- 
ditions of the heart and vessels. 
Fig- 5- 
Fig. 6. 
Dr. Mahomed estimated high tension as follows : First. “A 
line must be drawn from the apex of the up stroke, i, Fig. 6, to 
the bottom of the aortic notch, 2. No part of the tracing 
should rise above this line ; if it does, then the pulse is one of 
high pressure.” Second. “ The height of this notch is another 
good gauge of pressure, the higher it is from the respiratory 
line AA, the higher is the pressure; the nearer it approaches 
the respiratory line AA, the lower is the pressure.” The 28 
Purdy—Bright's Disease. 
[May, 
length of the systole of the heart, 5 to 6, Fig. 6, compared with 
that of the diastole, 6 to 7, is also considered a gauge of high 
pressure. In normal tracing the length of the systole, as marked 
on the respiratory line, AA, Fig. 6, should be about half as long 
as that of the diastole. In conditions of high pressure, the 
systole is lengthened, in some cases exceeding the length of 
the diastole. 
I think it is unfortunate that the terms high tension and 
high pressure have been so much confounded with each other 
by nearly all authors. 
I consider a pulse of high tension one in which the vascu- 
lar walls are rigid and inelastic from organic change. It may 
or may not include high vascular pressure. The term high 
pressure I define as increased intra-vascular force, coming 
from increased power of the heart, or resistance in the capil- 
laries. 
Dr. Byrom Bramwell* says: “ I am in the habit of consid- 
ering a pulse of high tension as synonymous with a strong pulse 
and vice versa, a pulse of low tension, with a weak pulse.” 
Now, the above does not by any means follow, as I will 
illustrate. Fig. 7 shows the pulse-tracing of a patient of mine, 
taken March 8th, whose case I had diagnosticated eight months 
previously as cirrhosis of the kidneys. 
Fig. 7. 4 oz. pressure. 
It will be observed that this tracing shows in a marked man- 
ner the characteristics of high tension. The tidal wave is sus- 
tained above an imaginary line from apex of percussion stroke to 
* “ Students’ Guide to the Examination of the Pulse and use of the 
Sphygmograph, 1883.” ! 8S5.] 
Purdy—Bright's Disease. 
29 
the bottom of the aortic notch. About two days after this trac- 
ing was taken, March 11, the patient was suddenly seized with 
gastric hemorrhage, losing a large amount of blood (over a 
pint) the first twenty-four hours. The hemorrhage continued 
interruptedly, sometimes ceasing for a day or so, till March 26, 
when he died, at 3 a. m., from direct loss of blood. 
The autopsy revealed granular kidneys, though not advanced 
to contraction, atheromatous arteries everywhere, including 
that of the aorta. No appreciable hypertrophy of heart. Be- 
hind pylorus of stomach a scirrhous mass, which latter doubt- 
less was the cause of the hemorrhage. 
Now, no one will pretend to claim that high intra-vascular 
pressure could be present after the first great loss of blood, 
much less as the hemorrhage progressed day after day, till the 
patient died from anaemic exhaustion, yet it will be noted 
throughout that the tracing maintained the usual characters of 
high tension, even when the characteristics of high pressure 
were abolished and the pulse became somewhat dicrotic. Nor 
Fig. 8. 
Fig. 9. 
Fig. xo. 30 
Purdy—Bright's Disease. 
[May, 
Fig. 11. 
were the indications of tension lost till the pulse became even 
hypodicrotic, as shown by the tracing of Fig. 11, taken a few 
hours before death. 
This case has shown me that we may have tension or rigid- 
ity of the vessel walls, with very ordinary, or indeed low intra- 
vascular pressure. High tension, then, is due to rigidity of the 
vessel walls, from atheroma, or allied conditions, and it is pre- 
sumptive evidence of chronic Bright’s disease. I may state 
that I have never failed to find the characters of high tension 
in the tracing of a patient’s pulse in renal cirrhosis, no matter 
how early the form. It is not positive evidence of chronic 
Bright’s disease, because we have atheroma aside from Bright’s 
disease sometimes, and if we can separate the causes, it will 
give us pretty positive evidence. 
High pressure includes high tension, and is due to powerful 
and prolonged contraction of left ventricle of the heart, fre- 
quently with hypertrophy of the latter, and as such is almost 
pathognomonic of chronic Bright’s disease. 
Fig. 12. 
Fig. 12 shows the characters of the tracing of high pressure. 
The prolonged systole, i to 2, and 3 to 4, as compared with 
the diastole 2, 3, and 4, 5. It shows also the high and sustained 
tidal wave c. c., and the aortic notch e. e., high and well away 1885.] 
Purdy—Bright's Disease. 
from the respiratory or base line A. A. For comparison with 
characters of tracing in simple high tension, see fig. 6. 
The late Dr. F. A. Mahomed collected the records of sixty- 
one patients, treated in Guy’s Hospital during the years 1879 
and 1880, for chronic Bright’s disease. They possessed the 
following characters : “ They all had the signs of high arterial 
pressure. They all had very considerable hypertrophy of the 
heart. In all cases the urine was free from albumen at some 
time while under observation. In eleven cases albumen was 
present on one or two rare occasions during a long period of 
observation. In three cases, though absent during long periods 
of observation, it occurred just previous to death; in three other 
typical cases of Bright’s disease, the patients were admitted 
with albuminuria, which disappeared under treatment, and they 
left without it. Three cases had urine very variable in its 
character, sometimes albuminous, sometimes not. In the 
remaining forty-one cases, albumen was never discovered in the 
urine I It may be added that in all these cases daily observa- 
tions were made. The quantity, specific gravity, solids, and 
albumen present in the urine, were appended. 
It is the rule, then, that high arterial pressure invariably ac- 
companies chronic Bright’s disease, and that it precedes the 
albuminuria. 
Dr. Mahomed found high pressure to precede the disease so 
invariably, and in some cases so long, that he was led to be- 
lieve that it was the cause of chronic Bright’s disease, at least 
in some cases. I cannot believe that this view is in keeping 
with the clinical history or pathology of the disease, and 
moreover, if it were correct, bleeding and purgatives should 
arrest the disease. 
Epistaxis of an obstinate character is another symptom of 
chronic Bright’s disease to be ranged under those pertaining to 32 
Purdy—Bright's Disease. 
[May, 
\ 
the vascular system. It also is due to degenerated vessels, 
and high arterial pressure, which accounts for its obstinacy. 
In some of my cases, inquiry into their history has revealed 
the occurrence of an obstinate attack of bleeding from the nose 
very early, and I attach considerable importance to such oc- 
currences. Epistaxis, due to renal causes, may sometimes 
occur, as far back as two or three years, or more, before any 
appreciable symptoms of the disease are manifest. Vertigo is 
also one of the early symptoms which is well to note the im- 
port of. It may be so pronounced that the patient may fall in 
walking, as was the case with one of my patients more than 
once before its cause was made out. Tortuous arteries, as the 
radial and temporal, quite uniformly accompany renal cirrhosis 
and are manifest quite early. I have noted small aneurisms of 
superficial arteries, particularly in the wrist and neck, as some- 
times present. I have not seen this noted in the literature of 
this disease, but it has occurred in my cases often enough to 
call my attention to it as a sign. The superjicialis voice, in 
the wrist, and small branches of the external carotid are the 
most usual seat of these small aneurismal sacs, according to my 
observations. 
THE NERVOUS SYSTEM. 
Valuable as are the symptoms referable to the vascular sys- 
tem in an early diagnostic point of view, those of the nervous 
system are scarcely less so. Among the most important of 
these are retinal changes and visual disturbances. 
Retinal changes are often the first symptom leading to dis- 
covery of the disease. Bartels says : “ Very often some dis- 
order of vision, provoked by the specific structural change that 
has taken place in the retina, forms the first event that attracts 
the patients own attention. No small number of my patients 
first went, on account of their eyes, to my colleague Voelckers, 
and were first induced by him to place themselves under med- 1885.] 
Pur dy—Bright's Disease. 
33 
ical treatment, which they were not aware they needed.” The 
frequency of these retinal changes in the course of renal cirr- 
hosis are such as to constitute them important occurrences to 
note. Kale’s* statistics, founded on observations of the fundus 
in one hundred cases of granular kidneys, show the presence 
of retinal change in twenty-eight, or one in three and a half. 
Gowers says : “ The retinal disease presents certain elements 
which are variously combined in different cases. These are 
(1), diffuse slight opacity and swelling of the retina, due to 
oedema of its substance ; (2) white spots and patches of various 
sizes and distribution (fan shaped), due for the most part to 
degenerate processes ; (3) hemorrhages ; (4) inflammation of the 
intra-ocular end of the optic nerve; (5) the subsidence of in- 
flammatory changes may be attended with signs of atrophy of 
the retina and nerve.” 
The degenerative is the most frequent form, beginning in 
small white spots, which spread out in fan shape near the 
macula lute a. This leads to impairment, not complete loss, ol 
vision, and comes on slowly, and is rarely, if ever, completely 
recovered from, though improvement is common. The hem- 
orrhagic form comes on very suddenly, as a rule, and often 
results in total blindness. It may be recovered from com- 
pletely, or induce inflammatory changes. 
Gowers has made the important observationt that in many 
cases of chronic Bright’s disease, there is to be seen a notable 
diminution in the size of the retinal arteries, independently of 
the existence of any special retinal disease. He says : “ The 
veins are in such cases not larger than the normal, but the 
arteries are not more than one-half, or even one-third, the diam- 
eter of the veins, instead of being two-thirds, or three-quarters 
♦Birmingham Med. Review, January, 1880. 
t British Medical Journal, Dec. 9th, 1876. 34 
Purdy—Bright's Disease. 
[May, 
the diameter. The comparison must be made between arteries 
and veins which run side by side, and correspond in distribu- 
tion.” I regard the above discovery as only second in import- 
ance to the indications afforded by the sphygmograph in cases 
of chronic Bright’s disease. 
Other symptoms of nervous disorder are more or less fre- 
quently present in early cirrhosis. Neuralgia is perhaps the most 
common. It is most often occipital, but may be temporal or 
vertical. In patients, without previous history of neuralgia or 
assignable cause, it is important to note such symptoms. In- 
somnia is frequent, and marked in a large number of cases. 
THE URINARY SYSTEM. 
Often the first symptom that the patients notice is that they 
get up at night to urinate. This, as I have previously noted, 
is because more urine is secreted at night than during the day- 
time. Usually before the urine contains albumen, if observed 
it will be found of high specific gravity, say from 1.020 to 1.035. 
And here I would insist, that the specific gravity of any single 
specimen of urine, unless it be a part of the whole twenty-four 
hours’ quantity, is entirely valueless from a diagnostic point of 
view. The urine must be saved during the whole twenty-four 
hours', and the specific gravity compared with both the normal 
gravity and quantity. If found constantly much over 1.020, 
the fact becomes important. The urine throws down, as a rule, 
numerous envelope-shaped crystals of calcium oxalate, and 
also uric acid crystals; in fact, the urine is often loaded with 
urates in these cases. Lastly, the urine may give the blue color 
reaction with peroxide of hydrogen solution and tincture of 
guaicum, showing the presence of blood crystalloids. This 
latter is important when present, but it is not so constant as 
the others. Such, in the main, are the symptoms most likely 
to be met with in the pre-albuminuric stage of chronic Bright’s 1885.] 
Purdy—Bright's Disease. 
35 
disease. Our diagnosis is rather to be sought through their 
collective than individual study, for it is only upon a thor- 
ough comprehension of all the phenomena surrounding the 
morbific changes of this disease, that it becomes possible to 
penetrate its varied symptomatology during its incipiency. 
All life, and growth is influenced, not only by the soil or 
pabulum which sustains and nourishes it, but also, by the in- 
herent qualities of the seed or germ from which it sprang; so 
with disease and decay, not only are they maintained by the 
lesion of the individual organ, but also influenced by inherent 
inherited qualities; they follow no stereotyped laws of symp- 
tomatology in all cases, but the first manifestations become 
apparent in this location in one case, and in the next location in 
another, as one or the other part of the organism is inherently 
weak, or has been unduly taxed. Chronic Bright’s disease is 
no exception. In one class of patients, the results of im- 
paired renal function will first fall upon the circulatory system, 
while in another, it may be on the nervous, the respiratory, 
the digestive, or the urinary system itself. Our diagnostic con- 
clusions should hence be drawn, not alone from the local symp- 
toms, as perhaps has been too much the custom, for if we wait 
for marked evidences of impairment here, the disease will often 
escape detection till the anatomical changes become so far 
advanced that the disease will be practically beyond the reach 
of medication. The textural changes, from their very nature, 
are such, that when once thoroughly engrafted upon the organ, 
their removal is not within the compass of the present state of 
medical science, and hence our only hope of arresting this dis- 
ease, must rest on its discovery during the functional stage. 
If, fortunately, I shall have contributed in any way to the eluci- 
dation of the latter question, the object of this paper will have 
been accomplished. 
163 State Street.