THE RELATION BETWEEN RENAL DISEASE 
AND DISEASE OF THE CIRCU- 
LATORY SYSTEM. 
CLINICAL LECTURE DELIVERED AT THE HOSPITAL OF THE UNIVERSITY 
OF PENNSYLVANIA. 
BY JAMES TYSON, M.D., 
Professor of Clinical Medicine, University of Pennsylvania, Philadelphia. 
[Reprinted from International Clinics, Vol. IV., Second Series.] ill chi ct m\ 
THE RELATION BETWEEN RENAL DISEASE AND 
DISEASE OF THE CIRCULATORY SYSTEM. 
CLINICAL LECTURE DELIVERED AT THE HOSPITAL OF THE UNIVERSITY OF PENN- 
SYLVANIA? 
BY JAMES TYSON, M.D., 
Professor of Clinical Medicine, University of Panrtfylvania, Philadelphia. 
The patient I now show you is introduced more especially to 
illustrate the relation between kidney-disease and heart-disease, a 
relation not always easily made out. I desire first, however, to con- 
trast the form of disease presented with another variety of kidney-affec- 
tion, of which we have had some examples before us. I allude to 
parenchymatous or tubal nephritis, while this is a case of chronic in- 
terstitial nephritis, of which the final result is the chronically contracted 
kidney, the essential anatomical alteration in which is an overgrowth 
of interstitial tissue. In the parenchymatous disease, you will remem- 
ber, the lesion begins in the tubules. The cells swell, proliferate, dis- 
tend and enlarge the tubules, whence results enlargement of the whole 
organ. The man before you presents no evident symptoms. He has 
no general dropsy. There is, however, a little swelling below the eyes, 
to which I am glad to be able to call your attention, as it is a symp- 
tom the importance of which is often exaggerated. Such swellings 
occur quite independently of Bright’s disease, and some persons are 
particularly prone to them. Much more serious is a swelling of the 
upper eyelid, although this also occasionally occurs irrespective of 
disease. 
Notwithstanding the fact that there are no evident objective signs 
of illness in this case, one may still be led to suspect it by an examina- 
tion of the heart, even before examining the urine. No murmur is 
heard, but on placing the stethoscope on the aortic cartilage we note 
easily a sharp accentuation of the aortic second sound, whence at once 
hypertrophy of the left ventricle may be suspected. That such hyper- 
trophy is present is proven if an enlarged percussion-area of the heart 2 
INTERNATION A L CLIN ICS. 
downward and to the left can be demonstrated, or if there is displace- 
ment of the apex below and to the outside of its normal situation 
between the fifth and sixth ribs within the nipple-line. Such a state 
of affairs exists in this case. I will only add that it is not always 
discoverable, because a coexisting pulmonary emphysema may obscure 
it. Such a state of affairs always demands an examination of the urine, 
which one is almost sure to find albuminous, although the quantity of 
albumin will probably be small. Rarely also albumin will be found 
altogether absent. As in this case, too, you will most likely find a few 
small hyaline or slightly granular casts, or casts containing one or two 
small oil-drops; casts also may be wanting, but careful searching will 
seldom fail to find them. Finally, the twenty-four-hours’ urine will 
be found increased to fifty, to sixty, and even to seventy ounces, and 
the specific gravity will be lowered, 1005 to 1012. Such a combination 
of symptoms—hypertrophy of the left ventricle, no valvular disease, 
small albuminuria, a few hyaline or pale granular easts, no dropsy— 
admits of but one interpretation,—chronic interstitial nephritis. Such 
a state of affairs may continue for a long time and the patient may 
be but slightly ill. Or there may be headache, throbbing in the head, 
morning sickness, and symptoms of indigestion. 
I. 
We have, then, in this case an association of kidney-disease with 
heart-disease. The former is interstitial nephritis, the latter hypertro- 
phy of the left ventricle without valvular disease. Now, what is the 
order of these events? Without attempting to decide the question in 
the case before us, I may say that modern studies have made it pretty 
certain that this form of combined heart-disease and kidney-disease 
may occur in two ways: first, both conditions may result from one and 
the same cause; or, secondly, the heart-affection may be secondary 
to the kidney-disease and its direct consequence. 
Whichever may be the more common,—and I do not think this is 
certainly determined,—the first is the easier of explanation. For this 
combined kidney-affection and heart-disease, a thickened state of the 
blood-vessel wall, known as arterio-selerosis or arterio-capillary fibrosis, 
is held responsible. The thickening is more or less general, or diffused 
throughout the arterial system, but is more marked in the smaller ves- 
sels, and it is not confined to any one of the three coats. Usually it 
begins as an endarteritis, and the intima is therefore thickened, particu- 
larly as to its subendothelial connective tissue, but the muscular coat is 
also the seat of morbid changes not always the same. RENAL DISEASE AND DISEASE OF CIRCULATORY SYSTEM. 
3 
Gull and Sutton, in a paper which has become historic, announced 
in 18721 that the changes in the muscular coat were chiefly of an 
atrophic character, and, although the methods of these observers have 
been much criticised, the most recent studies on this subject by Coun- 
cilman and Arthur V. Meigs go to confirm their conclusions both as to 
the seat and the nature of the changes. Councilman2 finds atrophic 
changes in the muscular coat, including greater or less destruction of 
the muscular fibre-cells, and the formation of a homogeneous hyaline 
tissue invading both coats, but especially the intima, where it produces 
decided thickening, and encroachment to a varied extent upon the 
lumen, sometimes amounting to occlusion. The capillary walls are 
likewise thickened, and sometimes, especially in the glomerule of the 
kidney, obliterated. Meigs’s3 studies also find these changes for the 
most part confined to the intima, which is decidedly thickened. To a 
less extent the intima of the veins is similarly involved. The picture 
of the changes thus briefly described may be obtained from a small 
artery taken almost indifferently from any tissue or organ of the body, 
—for example, from the muscular substance of the heart, the kidney, 
or the liver. 
It is to be remembered, also, that there are at least two other forms 
of endarteritis, the first the nodular, where the changes are limited to 
small areas in the aorta and large arteries,—atheromatous patches, 
sometimes calcareous and sometimes fatty; the second the so called 
senile endarteritis, in typical instances of which the aorta and all its 
larger branches are converted into rigid inelastic tubes. It is doubtful 
whether the latter should be called endarteritis, it being rather an infil- 
tration of lime-salts as the result of impaired nutrition. It begins in 
the muscular coat, and the vessel-walls are thinned rather than thickened, 
their inner surfaces roughened, and their lumina irregularly dilated, 
while the vessels themselves are elongated, producing abnormal tortu- 
osities. Far from being enlarged in this form, the heart is often 
smaller, the seat of brown atrophy. Similar atrophic processes affect 
the liver as well as the kidney, and the result in the latter organ is 
often a typical contracted kidney. The rationale of the renal changes 
in senile endarteritis is similar to that in the diffuse form. The cardiac 
hypertrophy is, however, absent, because the nutrition of the heart is so 
seriously interfered with that it cannot exert its usual reactive influ- 
1 Arterio-Capillary Fibrosis, Medico-Chirurgical Transactions, London, 1872. 
2 On the Relations between Arterial Disease and Tissue Change, Trans. Assoc. 
Amer. Phys., vol. vi., 1891. 
3 New York Medical Record, July 7, 1888. 4 
INTERNATIONAL CLINICS. 
ence. Hence it undergoes atrophy at the same time with the liver and 
kidney. 
It cannot be said that these three varieties of endarteritis are 
always sharply separable one from the other, but it is the diffuse 
form which is the link between the hypertrophy of the left ventricle 
and the contracted kidney present in the ease before us. Of its conse- 
quent changes the hypertrophy of the ventricle is most easily explained. 
The resistance in the blood-vessels stimulates the ventricle to increased 
effort, and there result increased arterial tension and hypertrophy. 
The degree of cardiac hypertrophy is sometimes enormous, the organ 
weighing as much as eight hundred and fifty grams, or twenty-eight 
ounces, and the average in twenty-seven cases studied by Councilman 
being over four hundred grams, or thirteen ounces. 
The alterations in the kidney, which vary greatly in degree, being 
sometimes scarcely noticeable and sometimes extreme, are the direct 
result of an interference with its nutrition. The blood-supply to the 
renal elements being cut off, these gradually waste and ultimately 
disappear. The cells and tubules thus destroyed are gradually but 
irresistibly replaced by fibrous connective tissue, in obedience to the 
pathological law elaborated by Weigert, that parts destroyed are par- 
tially replaced by cicatricial connective tissue. This contracts and reduces 
the size of the kidney, and perhaps, also, in this contraction further 
destroys the proper kidney structure and thus augments the atrophy. 
It has been said that in this form of combined kidney- and heart- 
disease there is no cardiac murmur. Nor is there, as a rule. It is not 
impossible, however, for the endarteritis of which we are speaking to 
creep along the walls of the aorta until it reaches the aortic valves 
and so structurally changes them as to make them rough or incom- 
petent and give rise to murmurs. 
The causes of this form of Bright’s disease are, therefore, the 
causes of the endarteritis, and these are various. Among the most 
numerous are habitual excess in eating and drinking, the poison of 
gout, whether uric acid or something else, lead-poisoning, and syphilis. 
All of these conditions intr<xluce an irritant substance into the blood 
which in the course of its circulation excites an inflammation of the 
inner membrane of the vessel. To a less degree probably the specific 
causes of all the infectious diseases must be included in this category,— 
possibly, even, malaria. The subjects are usually middle-aged men, 
l)etween the ages of forty and fifty-five, but they may be younger. 
Councilman has found these changes more common in the negro than 
in the white race. RENAL DISEASE AND DISEASE OF CIRCULATORY SYSTEM. 
5 
I am, however, one of those who do not believe that every 
instance of renal disease associated with cardiac hypertrophy is the 
result of an intermediate endarteritis. Interstitial nephritis is not the 
only form of renal disease which is associated with cardiac hyper- 
trophy, although it is the variety most frequently thus associated. Any 
case of chronic nephritis is liable sooner or later to become associated 
with hypertrophy of the left ventricle, while pronounced contraction 
of the kidney may occur without general vascular change sufficient to 
explain the contraction. 
How is the cardiac hypertrophy to be accounted for in this second 
set of cases ? It must be admitted that the explanation is not so easy 
as in that where chronic endarteritis is present. I will first review 
the theories which have been from time to time given, for theories 
alone they must be acknowledged to be. The oldest, which may be 
termed the “chemical theory,” was advanced in its cruder form by 
Bright himself, whose acute observation had not failed to notice the 
association of cardiac hypertrophy with the disease so deservedly 
coupled with his name since 1827. According to this hypothesis, the 
retention of excrementitious substances in the blood is responsible for 
the increased arterial tension and the hypertrophy of the left ventricle. 
At the present day George Johnson in England and Senator in Ger- 
many still hold this view. At one time Johnson held that the hyper- 
trophied state of the muscular coat was the effect of its resistance to 
the onward movement of the noxious blood, while the coat thus thick- 
ened further reacted upon the effort of the heart to overcome it. 
More recently he ascribes this hypertrophy of the middle coat in the 
vessels of the kidney to an effort to cut down the supply of blood 
in accordance with the reduced demands of the small kidney. Recent 
studies by modern methods do not find the changes in the middle 
coat early described by Johnson, while experiments which have for 
their object charging the blood with urea and allied excrementitious 
substances have also failed to excite hypertrophy. It should be added, 
however, that it is not possible by experiment to produce precisely 
the conditions furnished by diseased kidneys, especially in the matter 
of duration. It is very generally conceded that uraemia is due to 
retained excrementitious substances which are in health eliminated by 
the kidney; while the experimental introduction of these same ma- 
terials has as yet failed to produce uraemia. Here, too, it is to be 
remembered that sound kidneys are encountered, which by copious 
diuresis promptly eliminate the substances introduced. 
The so-called “mechanical theory” of cardiac hypertrophy was 6 
INTERNATIONA!. CLINICS. 
advanced by Traube, whose researches in 1850 gave a decided impulse 
to clinical study of the subject. According to Traube, the increased 
arterial resistance was caused by two supposed states: the first being 
an over-fulness of the vessel because of the diminished withdrawal 
from the blood of water for the formation of the renal secretion ; and 
the second, that the movement of arterial blood into the kidney was 
hindered by the renal contraction itsdf. The first hypothesis was 
erroneous in the case of contracted kidney, where the urinary secre- 
tion is really increased, and the second is opposed by the fact that 
even ligature of the renal arteries fails to increase arterial pressure, be- 
cause of the ample space elsewhere to take up the blood thus diverted. 
Nor did Cohnheim’s further elaboration of the mechanical theory, which 
located the increased resistance more precisely behind the wasted 
glomerule, give any more permanent life to it. 
I incline to the belief that the difficulties are best met by supposing 
the primary changes in the heart to be compensatory in their nature, 
set up with a view to making up for the gradual loss of renal sub- 
stance. Such an action is paralleled everywhere in the physiological 
economy. Nowhere do we meet with loss of function which is not at 
once met by an attempt of nature to supplement it. The dependence 
of the urinary secretion upon cardiac pressure is well understood, and 
an increase of cardiac power is the most reliable means available for 
stimulating the action of the kidneys, when desired, in therapeutics. 
The diuresis which is so constant a symptom of the contracted kid- 
ney is certainly the direct result of a supplemental contraction of the 
left ventricle, which it is reasonable to suppose is induced for the pur- 
pose named, and rcsidts in hypertrophy. 
This view receives confirmation in the subsequent course of the 
disease. So long as the free secretion which is the result of the com- 
pensatory action of the heart is kept up, so long the patient remains 
tolerably comfortable, and perhaps even for a time unconscious of the 
presence of disease. But an organ thus overgrown is apt sooner or 
later to suffer in its nutrition, and especially is this the case if its arte- 
ries be the seat of an endarteritis which interferes with the free move- 
ment of the blood and produces also fibro-myoearditis. And what are 
the further consequences? The strong propulsive power of the heart 
declines, the pulse falls away in tension and power and becomes more 
frequent and sometimes irregular. The urine secreted diminishes in 
quantity and assumes a darker hue. Fortunate is the patient if the 
specific gravity of the urine rises pari passu with its reduced quantity, 
as it indicates that the normal quantity of solids is kept up. Too fre- 7 
RENAL DISEASE AND DISEASE OF CIRCULATORY SYSTEM. 
quently, however, this is not the ease, and excrementitious substances 
accumulate in the blood, laying the foundation for uraemia. Headache, 
nausea, a foul and even urinous breath, may be superadded, and uraemia 
set in, preceded by drowsiness, or it may be ushered in suddenly with 
convulsions. Or another set of symptoms may supervene. The patient 
becomes short of breath, first on slight exertion, and later this very 
distressing symptom occurs without such exciting cause. This sort of 
asthma is often spoken of as uraemic asthma, as if due to the same 
causes as uraemia, and this may sometimes be the case. More frequently 
the failing heart is responsible. The organ is no longer able to move 
the blood onward, the lungs become engorged, aeration becomes imper- 
fect, and hence the dyspnoea. For a time this symptom may be averted 
by whipping up the heart by cardiac stimulants, anti the right ventricle 
even comes to the rescue for a time, and hypertrophies in its effort to 
overcome the now disturbed compensation. Subsequently this as well 
as the left ventricle may become dilated, and oedema of the lungs set 
in, with annoying cough and serous frothy expectoration, sometimes 
blood-tinged. Nor does general dropsy continue absent, but ensues 
sooner or later with the growing heart-failure. Our resources are now 
almost at an end, but are not exhausted, as even these symptoms some- 
times subside. 
Finally, it must be stated that not every case of interstitial nephritis 
is attended with hypertrophy of the left ventricle. In addition to the 
cases of contracted kidney from senile endarteritis already referred to, 
cardiac hypertrophy is apt to be absent in the interstitial nephritis of 
the weak and cachectic. 
A pertinent question is one as to diagnosis,—as to whether it is 
possible to say of a given case that it is one of endarteritis with conse- 
quent renal cirrhosis and cardiac hypertrophy, or one in which the renal 
condition is primary. It is true that some symptoms may be referred 
to the vascular and others to the renal cause, and it is not unimportant 
to be able to recognize early the symptoms of arterial sclerosis before 
those of renal involvement make themselves apparent, since the latter 
indicate a more irremediable stage. Thus, the early head symptoms, 
such as headache and vertigo, are probably due to derangements in the 
circulation in the brain, while the apoplectic phenomena which often 
terminate the disease—when other symptoms would not lead us to ex- 
pect the end—are directly due to defects in the vessel walls associated 
with the extreme intravascular pressure. A throbbing sensation in the 
head is included in the symptoms ascribed to intravascular pressure, 
and it is reasonable to suppose that when this occurs associated with 8 
INTERNATIONA I, CLINICS. 
vertigo and without objective symptoms of Bright’s disease, such as 
albuminuria and casts, it is due to primary vascular change. Late in 
the disease, when the objective symptoms are well defined, it may be 
ascribed to secondary hypertrophy. When the arcus senilis attends 
these two symptoms, vertigo and throbbing, there is probably en- 
darteritis, although the arcus is more frequent with senile arteritis. 
There is no peculiarity in the vertigo by which it may be assigned to 
one or the other condition. It may be transitory, or may last long 
enough to force the patient to sit down, or even to cause him to fall, 
though even then the duration is apt to be for a few minutes only. A 
slow pulse is apt to be associated with these vertigoes, and sometimes 
an extremely hypochondriacal shite, all prior to the albuminuric stage. 
A tendency to a mild form of epileptic seizure is described by the 
French authors.1 
Epistaxis is another symptom which may be directly ascribed to 
the arterio-sclerosis, and it is often the first symptom to attract atten- 
tion by its profuseness and frequent recurrence. On the other hand, 
palpable stiffening of a blood-vessel wall attainable by the finger is 
more apt to indicate senile endarteritis. High arterial tension as de- 
tected by the sphygmograph before it is noticeable by the finger, and 
before any signs of cardiac or renal disease present themselves, points 
to endarteritis. 
There seems every reason to believe that the prognosis of arterio- 
sclerosis is more favorable before the renal and cardiac changes mani- 
fest themselves. It is desirable, therefore, that it should be discovered 
as early as possible; and attention to the facts named may lead to this. 
The treatment of the combined kidney- and heart-disease is not 
different from that of interstitial nephritis. Even greater rigidity is 
necessary in eliminating nitrogenous food, and all food should be re- 
duced to a minimum. A diet of milk diluted with water is the safest 
of all. Bread and butter may, however, be allowed, and even succu- 
lent vegetables easy of digestion, such as potatoes, peas, and string beans, 
while simple fruit-juices, as those of oranges and lemons, are allowable. 
Mental excitement and immoderate muscular exertion must be avoided, 
and the heart should not be overworked in any way. 
The medicinal treatment especially directed to the arterio-sclerosis 
mav be divided into that intended for the cure of the endarteritis and 
that directed to the relief of symptoms. The only drug from which 
results may tie expected for the former purpose is the iodide of potas- 
1 Grasset, Du Vertige Cardio-vasculaire, Paris, 1800. RENAL DISEASE AND DISEASE OF CIRCULATORY SYSTEM. 
9 
sium, which should be given a fair trial in doses as large as can be 
borne without deranging the stomach. For the relief of the symptoms 
more especially due to the sclerosis—viz., headache, throbbing, and 
vertigo—the nitrites are often useful, and this in my experience is their 
sole use in Bright’s disease. Nitro-glycerin should be given in doses 
of one-hundredth of a grain every four hours, rapidly increased to one- 
fiftieth, as the smaller dose is often without effect. The aim should be 
to produce the physiological effect, which is a sense of fulness or a 
flushing. The sodium nitrite may be substituted in three-grain doses. 
It has the advantage of being more permanent in its effect, although 
it is slower in its action. 
II. 
The second form of combined heart- and kidney-disease to which I 
wish to call your attention is that wherein the heart-disease is primary. 
It is commonly disease of the mitral valve. The kidney-disease does 
not occur in connection with aortic valvular disease until mitral dis- 
ease is superadded. It is well known that in mitral regurgitation, as 
soon as compensation ceases the blood accumulates first in the lungs, 
then in the right side of the heart, and finally in the venous system, 
engorging especially the liver, the stomach, and the kidneys. With 
the effects upon the first two I have nothing to do at present, although 
they are of a very positive character and generally manifest themselves 
sooner than the renal symptoms. 
Let us first study the condition of the kidney itself. As stated, it 
is engorged with blood from the venous side. The renal vein and its 
branches are filled with blood as far back perhaps as the Malpighian 
body. This backward pressure resists the onward flow of the arterial 
blood, and the congestion is thereby further augmented. The effect is 
to swell the kidney somewhat and to darken its hue, which on section 
will be found more intense in the pyramids. A slight hardness also 
results, and the combination of these two conditions, color and density, 
has suggested the term cyanotic induration for such kidneys. Further 
changes are not marked or constant. There is sometimes a slight 
overgrowth of the interstitial connective tissue, and a slight tendency 
to degeneration in the cells. 
Much more decided are the clinical phenomena resulting from such 
congestion. It is a well-recognized condition of copious secretion of 
urine that the blood should move freely through the kidney. A stasis is 
followed immediately by diminished filtration of water, the twenty- 
four-hours’ quantity being reduced to from thirty to twenty ounces, and 10 
INTERNATIONAL CLINICS. 
even to less. As the solids at first at least remain the same, the urine is 
dark-lined, the specific gravity is high, the reaction is markedly acid, 
and a copious sediment of urates and uric acid makes its appearance as 
soon as the urine cools off. There is almost always a small amount of* 
albumin found. Casts are sparsely, if at all, present, and are of the 
hyaline and faintly granular variety. Both red and white blood-cor- 
puscles are also sometimes detected, as might be expected. This con- 
dition of the kidney and the symptoms are the direct results of the 
cardiac valvular disease. They may also be produced by any cause 
producing venous stasis, as pulmonary emphysema, chronic pleurisy, 
and thrombosis of large veins. Their effect is further to augment the 
symptoms of the cardiac disease. The circulation, already everywhere 
obstructed, is further impeded, there is dyspnoea, dropsy increases, the 
appetite fails, there are nausea and constipation. Sleep, already dis- 
turbed by dreams, becomes more so, and a more distressing picture 
than is presented by such a case is rarely met. 
Yet these symptoms are often easily amenable to treatment so long 
as the heart-muscle remains capable of being influenced by digitalis. 
I have seen many a patient, apparently in extremis, gasping in orthop- 
noea and with legs heavy and almost bursting with dropsical effusion, 
completely relieved by a few large doses of this drug. But they must 
be large doses, not less than eight to ten minims or fifteen to twenty 
drops every three hours until an effect is produced. If digitalis fails, 
the tincture of strophanthus may be given in the same doses, or caffeine 
citrate in three-grain doses, each every four hours, or sparteine sul- 
phate in doses of one-quarter to one-half grain. Purgation should 
not be omitted, but should rather be pushed to the production of watery 
catharsis. The ingestion of fluids should be restricted, and the Hay’s 
treatment of dry diet with purgatives is sometimes useful. But I 
have found a restricted milk diet, limited to two ounces every two 
hours, associated with the drugs above named, more efficient.1 
Diuretin is a remedy from which good results may be expected in 
these cases. My own experience with it has not been large, but I shall 
use it more in the future. The dose is from seventy-five to one hun- 
dred grains daily in solution, about fifteen grains being administered at a 
time in a tablespoonful of water. The rapid increase of the twenty- 
four-hours’ urine from five hundred cubic centimetres to three thousand 
three hundred cubic centimetres is reported from its use. 
1 See some cases reported by the writer in a paper “ On the Management of Obsti- 
nate Dropsies,” Medical News, June 21, 1890. RENAL DISEASE AND DISEASE OF CIRCULATORY SYSTEM. 
11 
Such a kidney is of course liable to become the seat of an acute or 
a chronic nephritis. 
III. 
The next form of kidney-involvement to which I call your atten- 
tion as being secondary to disease of the vascular apparatus, commonly 
heart-disease, is more frequently seen on the post-mortem table than 
recognized in the living subject. It is embolic infarction, produced by 
the lodgement in some branch of the renal artery of an embolus de- 
rived from the heart or a blood-vessel. Its most frequent source is a 
fragment of vegetation or clot from a diseased heart-valve. An em- 
bolus may also arise from a thrombus in an artery, but more frequently 
it is caused by one in a vein. If from the latter, it must be carried 
first to the right heart and thence through the lungs into the left heart, 
and thence by the aorta to the kidney, and must of course be small. 
The effect of the lodgement of an embolus in the kidney is a wedge- 
shaped hemorrhagic infarct, which in time whitens, contracts, and is 
ultimately absorbed, leaving a mere cicatricial mark. 
Most frequently a renal infarct occurs without noticeable symptoms. 
Its occurrence, if looked for by reason of the presence of valvular 
heart-disease, might be ushered in by the sudden appearance of a small 
amount of blood in the urine. A sudden pain in the region of the 
kidney simultaneously occurring would go to confirm the diagnosis. 
No treatment is indicated, even if the event is recognized. 
IV. 
Finally, kidney-disease and disease of the vascular apparatus, and 
especially cardiac disease, may coincide accidentally, each the result of its 
own cause, and reacting the one upon the other in various degrees and 
variously aggravating the symptoms of each, so that it often becomes a 
very nice question to settle which is the preponderating disease. For- 
tunately, this difficulty does not always extend to therapeutics, the same 
remedies which are useful to one affection being commonly indicated 
for the other. A careful study of each case should, however, be made 
on its own merits, and due weight assigned to each factor of the disease.