From Dropsy to Bright's Disease to End-Stage Renal Disease

Author(s): Steven J. Peitzman

Source: The Milbank Quarterly, Vol. 67, Supplement 1. Framing Disease: The Creation and
Negotiation of Explanatory Schemes (1989), pp. 16-32
Published by: Wiley on behalf of Milbank Memorial Fund
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From Dropsy to Bright's Disease to
End-stage Renal Disease

STEVEN J. PEITZMAN
The Medical Collegeof Pennsylvania

"B
< - RIGHT S DISEASE'WAS THE
term applied to diffuse noninfectious bilateral renal dis-
ONCE FAMILIAR

ease, usually marked by albuminuria and sometimes by

the symptom complex of uremia. "ESRD" stands for "end-stage renal
disease" and this acronym entered widespread use as a result of Section
2991 of Public Law 92-603 passed by Congress on 30 October 1972.
This unprecedented legislation provided federal financial support to
essentially all Americans with a particular chronic disease-kidney
failure-so that they could receive treatments to prolong their lives.
The treatments were, of course, dialysis and transplantation. Neither
Bright's disease nor ESRD referredor refersto any single disease entity
as defined by pathologic examination or by cause.
Knud Faber (1930, 211) in his book Nosography,still honored with
rereadings sixty years after its publication, said about morbid cate-
gories that the clinician "cannot live, cannot speak, cannot act without
them." This remains true, and in this article I will return to these
names, Bright's disease, ESRD, and others, these labels placed on
categories of sickness, and look at them more closely. I hope to show
how the changing use of names in renal medicine reflected how
physicians and others thought about kidney disease. Certainly one
theme must be ways in which individual physicians initially, then
the community of scientific medicine, and finally government or so-
ciety, fashioned both conceptions of disease and the names which label

The MilbankQuarterly,Vol. 67, Suppl. 1, 1989

? 1989 MilbankMemorialFund

i6

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FromDropsyto Bright's Disease to ESRD 17

the conceptions. I also will attempt to suggest how some patients

have thought about their kidney disease, or at least how they expe-
rienced it. The patients' contribution to the idea of a disease remains
far more elusive, less readily traced, than that of the physician. Yet,
it warrantsinclusion, even if fragmentary, and assumes perhaps greater
importance near the end of my narrative, when renal patients become
dialysis patients. My article will not provide a comprehensive account
of the evolution of pathological categories, etiology, and management
of renal disease, though such would be a worthy and so far undone
task. I will be instead episodic and selective, as I seek to reconstruct
the way in which successive generations have construed the experience
of kidney disorder, and constructed its nomenclature.

Dropsy

The prehistory of Bright's disease was dropsy. From a universe of

dropsical patients, Richard Bright of Guy's Hospital beginning in
the 1820s would recognize a special subset, the forbears of all renal
patients.
For hundreds, perhaps thousands, of years two forms of serious
chronic disease dominated medical practice. They induced in their
victims equally grotesque but oddly antipodal transformations. The
one was consumption, which thinned and shrank the body; the other
dropsy, which bloated it. Physician and nosologist William Cullen
discussed the species of disease called dropsy in the 1787 edition of
his popular First Lines of the Practiceof Physic. Dropsies were "distin-
guished from each other according to the parts they occupy, as well
as by other circumstances attending them; yet all of them seem to
depend upon some general causes, very much in common to the
whole." Dropsies are often associated with a scarcity of urine. "This
scarcity of urine may sometimes be owing to an obstruction of the
kidneys, but probably is generally occasioned by the watery parts of
the blood running off into the cellular texture, and being thereby
prevented from passing in the usual quantity." Cullen did not see
dropsy as a "cardiac"or "renal disease." His analysis remained more
general and symptomatic than local and pathological.
Let us focus on one man's dropsy. In the last year of his celebrated
life, writer and lexicographer Samuel Johnson suffered with asthma

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i8 StevenJ. Peitzman

and dropsy, and told of the experience to Boswell, to his doctors,

and to other friends (Johnson 1952). On 11 February 1784 he wrote
to Boswell: "The asthma, however, is not the worst. A dropsy gains
ground upon me; my legs and thighs are very much swollen with
water, which I should be content if I could keep it there, but I am
afraid it will soon be higher."
Then in late February of 1784 a remarkable event relieved Dr.
Johnson's pulmonary and peripheral edemas: "Last week I emitted in
about twenty hours, full twenty pints of urine, and the tumour of
my body is very much lessened, but whether the water will not gather
again, He only knows by whom we live and move." Boswell included
this mighty postdevotional discharge of fluid in the Life, making it
unquestionably the most famous diuresis in the history of the English-
speaking people. But Johnson's suffering was not over. On July 21
he wrote to one of his physicians: "The water has in these summer
months made two invasions, but has run off again with no very
formidable tumefaction." Into late summer and early fall, armed with
archaic diuretic remedies squill and cantharides, Johnson battled the
floods, which would rise and fall. On November 4 he reported (to
John Ryland) that the "water grows fast upon me." Two days later
(to Dr. Brocklesby): "The water encreasesalmost visibly and the squills
which I get here [Lichfield] are utterly inefficacious. My spirits are
extremely low."
Johnson eventually succumbed on 13 December 1784, and the
autopsy revealed both cardiac and renal disease (the right kidney
atrophic, the left cystic). But in life Johnson, like many similar
patients had dropsy, not Bright's disease or congestive heart failure.
The experience of his disease was dreadful: a constant struggle against
the drowning of his body by floodwaters from within, a struggle
waged with drugs he knew to be inadequate, unpredictable, and
noxious.

Bright's Disease

Widespread in private and hospital practice, hideous and lethal when

advanced, dropsy captured the attention of some early nineteenth-
century physicians who were remapping diseases based on morbid
anatomy and physical examination. In 1827 Richard Bright of Guy's

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From Dropsyto Bright's Disease to ESRD I9

Hospital (1789-1858) published the first volume of his magisterial

Reportsof Medical Cases. Almost one-half of this volume deals with
dropsical patients, and the first 24 cases reveal Bright's discovery.
Certain patients with dropsy have albumin in their urine (detected
by the spoon and candle-heat coagulation), and-previously unrec-
ognized-many of these show striking morbid changes of the kidneys
at autopsy. Furthermore, many such dropsical patients experience
characteristic symptoms, including vomiting, headaches, pericarditis,
seizures, amounting to what later would be recognized as uremia.
Bright's discovery has been hailed as one of the gleaming achievements
of clinical/pathological correlation. Dropsy was ubiquitous, heat-coag-
ulable urine little explored, the uremic symptoms variable, the pa-
tients hectically sick, the autopsies undoubtedly odorous and oozing;
yet, Bright made sense out of all this, and established the basis of
renal disease.
Not only was the detection of albuminuria, as Bright used it,
arguably the first practical laboratory aid to diagnosis, but Bright
went farther. He encouraged several physician-chemists to perform
analyses of the urine and blood of some of the renal patients (Peitzman
1981). William Prout, John Bostock, and George Owen Rees showed
that sometimes urea was detectable in the blood but deficient in the
urine, while the albumin was decreased in the serum. In 1842 Bright
received permission from the managers of Guy's Hospital to assign
during the summer a number of beds to receive only renal cases, for
careful prospective clinical and laboratory study. This hinted at the
"metabolic ward" or clinical study unit of the next century.
Bright's way of understanding the new disease was, however, solidly
of the early nineteenth century. Although he recognized that albu-
minuric renal dropsy could follow scarlet fever, Bright stressed in all
his writings exposureto cold as the most important source. Cold could
"suppressthe insensible perspiration," leading to "sympathy" between
the "checked" skin and the kidneys. This sort of language and way
of thinking go back at least to Galen, and the physician of 1989
simply no longer shares them with Bright and his day. Yet, for Bright
the association of cold with renal disease was not a "theory" or spec-
ulation, but indeed a repeated clinical observation: the patients he
cared for and reported almost all did recount some recent exposure
to cold and wet as part of their story. Cold gave way to microbial

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20 StevenJ. Peitzman

explanations, then these to immunologic models, as accepted causes

of diffuse kidney disease.
We ought to be on firmer grounds with Bright's morphological
descriptions, enhanced by the magnificent hand-colored mezzotint
engravings appended to his Reports.Dr. Bright in the initial 1827
publication, based on 24 cases, suggested three forms of that deranged
kidney structure which accompanies albuminuric dropsy. The first is
a kind of softening with yellow mottling. The second form is one in
which "the whole cortical part is converted into a granulated texture,
and where there appears to be a copious morbid interstitial deposit
of an opake white substance." The third form of disease "is where
the kidney is quite rough and scabrous to the touch externally, and
is seen to rise in numerous projections not much exceeding a large
pin's head, yellow, red, and purplish... The form of the kidney
is often inclined to be lobulated [and there is a] contraction of every
part of the organ" (Bright 1827, 67-69). These three categories and
the descriptions hold little meaning for the nephrologist of the 1980s,
who sees other striking differences-mainly ignored by Bright-when
viewing the colored plates. There are two bases for the difficulty.
First, Bright relied on a sort of macroscopic tissue pathology of the
1820s derived from Xavier Bichat and (more directly) from Bright's
colleague at Guy's Hospital, Thomas Hodgkin. Second, the renal
physician today rarely sees or touches a fresh diseased kidney, and
does not replicate the visual and tactile examinations at autopsy which
for Bright repeatedly assured in his mind the reality and reproduci-
bility of albuminuric renal disease.
Importantly, Bright allowed that the three forms he distinguished
might be only stages of one process. But he seemed to favor three
categories. So from the first publication on the disorder, Bright's
disease was not held to be one specific entity, not even by Bright.
Although Richard Bright surely did not propose the name, the
disease or diseases he described became known almost immediately
as "morbus Brightii," "Bright's kidney," "Bright's disease," or "ma-
ladie de Bright." In fact, I believe that Bright's disease may be the
earliest regularly used eponymous name for a disease in English. It
is the only such disease name in the index to the 1844 edition of
Thomas Watson's popular Lectureson the Principlesand Practiceof Physic
(unless one counts "St. Vitus's Dance"). Watson did not, however,

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From Dropsyto Bright's Disease to ESRD 21I

like the term. "For this disease," he wrote, "we have no appropriate
name. I wish we had. Some call it granular degeneration of the kidney,
but the epithet granular is not always applicable. It is most familiarly
known, both here and abroad, as Bright's kidney, or Bright's disease;
after the eminent physician who in 1837 [sic; should be 18271 first
described it, and showed its great pathological importance. These are
odd-sounding and awkward terms; but in the lack of better, I must
employ them."
Why did the naming of this new disease pose a problem, and lead
to a new way of naming diseases? One obvious answer is the rec-
ognition, already noted, that no one morbid appearance defined
Bright's disease. But I would argue there was more to it than this.
Bright's disease required a new sort of naming because it represented
a new, nineteenth-century, way of thinking about and defining disease.
A patient had Bright's disease if he had at least some of the following:
certain symptoms, such as dropsy; certain physical findings, such as
a hard pulse, or a pericardial rub; certain morbid changes in the
kidney, if he came to autopsy; and-perhaps most novel in the 1820s
and 1830s-a primordial laboratory abnormality, albuminous urine.
The last two of these elements-albuminuria, morbid changes of the
kidney-could only be detected by the physician. So this sickness is
no longer mainly the patient's disease: it's also the physician's disease,
Dr. Bright's disease. Bright recognized that not all these elements
were present in every such patient. For example, case 4 of his 1836
"Cases and observations illustrative of renal disease accompanied with
the secretion of albuminous urine" provides "a strong example of the
disease of the kidney passing to its most fatal period, without the
slightest symptom of dropsical effusion-a state of things, which,
above all, is apt to throw us off our guard" (Bright 1836). Gradually
it would become clear as well that some patients might progress to
renal failure without ever showing important albuminuria. Others
might display profound anasarcaand albuminuria although their kid-
neys show no defect to the naked eye or even to the light microscope.
Bright's disease then may be said to have been understood as a way
of getting sick through your kidneys. It was a term presumably useful,
even indispensable, to most physicians. It was a term which I suppose
(without strong evidence) gradually became in some way comprehen-
sible and useful to patients.
By 1950 the term Bright's disease evidently lost much of this

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22 StevenJ. Peitzman

usefulness; doctors found it old-fashioned. The last two monographs

in English that I can verify with "Bright's disease" as part of the title
both appeared in 1948, one by Henry Christian, the other by Stanley
Bradley. Thomas Addis, a leading student of renal disease from 1915
to 1949, wrote two books. His first appeared in 1931 titled The Renal
Lesion in Bright's Disease; the second in 1948 he called Glomerular
Nephritis, though its content extended well beyond that particular
form of renal disease (Addis and Oliver 1931; Addis 1948).
Not until writing this article did I perceive the vacancy left with
the demise of "Bright's disease." Currently, no term mutually ratified
by patients and physicians adequately expresses "getting sick through
your kidneys." Without such a joint frame of reference, I often find
it difficult to discuss a new diagnosis of chronic renal failure with a
patient.
Before we leave Richard Bright and Guy's Hospital, let me try to
evoke the patient's experience of Bright's disease in the nineteenth
century, so that I can later draw a contrast with the present day.
Here is Bright's (1827, 29-31) description of case 13 of the Reports,
Thomas Drudget, a carman hospitalized on 7 December 1826:

About a fortnight before his admission he was attacked with

sickness at the stomach, and shortness of breath; purging then came
on, and vomiting: about nine days before admission his face and
legs began to swell. The urine had been deficient in quantity the
whole time. He complained much of tenderness in the pit of his
stomach.

His urine coagulated to heat. Drudget was treated with cupping

over the chest, mercurials, magnesium sulphate, tincture of camphor,
potassium supertartrate, jalap, and capsicum, some of which brought
temporary improvement. But on the 17th he mentioned to some of
his ward mates of a headache. "About eight o'clock it was observed
that he lay in bed making a very singular noise, and on going to
him he was in a state of profound apoplectic stertor. Mr. Stocker was
immediately called; took away twenty ounces of blood from the tem-
poral artery, gave him ten grains of calomel, and a colocynth injection.
He had one or two fresh attacks, accompanied with so much convulsion
that he could scarcely be held in bed." Bright orders more blood-
letting, an enema, and a cantharidis plaster to the neck, but to no
avail: another case enters the Reports. The sectio cadaverisshows an

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FromDropsyto Bright's Disease to ESRD 23

intracranial bleed as the terminal cause of death; the kidneys are pale
and soft with a "motley granulation."
Edematous and convulsive, poor Drudget may stand in for all the
victims of advanced Bright's disease before the invention of dialysis.
I might have chosen a patient that Robert Tyson, an American au-
thority on Bright's disease, presented to students on 20 October 1892
at University of Pennsylvania Hospital. She was a 55-year-old woman
whose massive "collection of fluid ruptured the skin." She had al-
buminuria and granular casts in the urine, and was treated with milk
and caffeine (Swan 1890-1893). Tyson sometimes used pilocarpine,
often his beloved "hot-air bath," and even venesection in refractory
cases of Bright's disease (Tyson 1881, 120-23, 137-47). Or I might
have described Thomas Addis's (1948) patient from the 1930s, the
young physicist whose case (possibly a composite) is poignantly and
instructively narrated in GlomerularNephritis. Over many years Addis
helped prolong this patient's useful life with diet, simple medications,
small Southey's tubes to drain tissues, and encouragement. Eventually,
edema and nausea announce that the disease has entered a conclusive
stage, confirmed by changes in urinary sediment, albuminuria, and
measures of azotemia. Finally, Addis offers paraldehyde to ease the
death of the young man, edematous, nauseated, and exhausted with
terminal uremia. Any of these cases and countless others recorded
reveal the patient's experience of renal disease in earlier times, and
the physician's struggle to cure or palliate it.

Nephritis in Threes

The names that came to compete with Bright's disease, or designate

its subcategories, indicate the way that nineteenth-century authorities
wished to think about the disease. That way remained increasingly
anatomic. The term "nephritis" existed well before the writings of
Bright and his contemporaries, and appears for example in Cullen's
(1800) Nosology. The suffix "itis" even by then conveyed the idea of
inflammation-that is heat, redness, pain, swelling, loss of function.
Bright strongly suggested that his disease might be a state of conges-
tion or inflammation seated in the kidney, and elsewhere (e.g., per-
icardium). Though not all subsequent physicians and pathologists
would agree on the essentially inflammatory nature of Bright's disease,

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24 StevenJ. Peitzman

the term "nephritis" entered use by 1840 and the task of classifiers
reduced to adding the appropriate modifiers.
The story of the superceding and competing classifications is far
too tedious to explore except in the broadest of strokes. Oddly,
nephrologists and pathologists looking at altered kidneys have always
favored as much as possible a tripartite organization, either seeking
simplicity or emulating Dr. Bright. Virchow in 1858 suggested "par-
enchymatous nephritis," "interstitial nephritis," and "amyloid de-
generation" (Bartels 1877; Tyson 1881, 79-84). George Johnson in
1873 proposed the separation of an acute form (acute nephritis); and
three chronic varieties: "red granular kidney," "large white kidney"
and "lardaceouskidney" (which is the same as amyloid kidney). Osler
in his influential text favored "acute Bright's disease," "chronic par-
enchymatous nephritis," "chronic interstitial nephritis" with amyloid
dispatched to its own pathological category (Osler 1909, 686-703).
In the twentieth century, the extremely influential monograph by
Volhard and Fahr in 1914 provided a fresh-but still trinitarian-
organization: degenerative diseases, "the nephroses";inflammatorydis-
eases, "the nephritides"; and arteriosclerotic diseases, "the nephro-
scleroses." Thomas Addis (1928) of Stanford University offered a
modification of this last framework which gained some popularity:
"hemorrhagic Bright's disease," "degenerative Bright's disease," and
"arterioscleroticBright's disease." (Even today nephrologists seek first
to place a new case of renal parencyhmal disease into one of three
broad categories: glomerular disease, tubulo-interstitial disease, or
vascular disease.)
The point is that nineteenth-century physicians interested in
Bright's disease relied on gross and microscopic pathology to organize
their thinking and teaching about the disorders. Increasingly, ex-
amination of the urinary sediment aided clinicians, for the sick kidney
accommodatingly sheds bits of itself into the urine. Thus, all later
nineteenth-century texts on Bright's disease contain extensive discus-
sion of casts,often carefully illustrated. Sediment examination extended
histologic diagnosis to the living patient, as would renal biopsy be-
ginning in the late 1940s. Chemical examination, such as blood urea
measurement, though precociously commenced by Bright's collabo-
rators, lay nearly dormant until the invention of simpler assays in the
early twentieth century.

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From Dropsyto Bright's Disease to ESRD 25

Functional Diagnosis and Bright's Disease

Although pathology remained the underpinning of organized knowl-

edge and diagnosis in Bright's disease, clinicians of course continued
to struggle at the bedside with its obvious functional derangements-
dropsy and uremia. In the last decade of the nineteenth century and
the early part of the twentieth, some investigators subjected Bright's
disease to a more subtle and formal sort of "functional diagnosis,"
using the laboratory. Methods and thinking analogous to those applied
to the stomach and heart were applied to the kidney. In the late
1890s Alexander von Koranyi used cryoscopy to measure the "power"
of renal concentrating ability in health and in renal disease (Faber
1930). As other workers added tests of dye excretion, test meals, and
urea loads, the term "renal insufficiency" entered the language of
Bright's disease (Faber 1930, 112-171; Fishberg 1930, 39-54). The
"insufficient" kidney lacked normal power and reserve; further weak-
ening later became known as "renal failure," which meant frank
retention of urea and other substances usually discharged by the renal
filters.
Thomas Addis, mentioned earlier, represents one of several figures
transitional between the dominantly anatomic and dominantly func-
tional ways of envisioning renal disease. An appealing and enigmatic
figure, Addis (1881-1949) was a Scots physician with sound chemical
training hired as a young man by the new Stanford University medical
school in 1911. There he took up in the clinic and in the laboratory
a lifelong study of Bright's disease. He titled both his Harvey Lecture
of 1928 and his monumental book of 1931 (with pathologist Jean
Oliver) The Renal Lesionin Bright's Disease (Addis and Oliver 1931).
By "renal lesion" he meant both the type of disordered structure and
the amount of functional loss. His scheme for pathologic classification
gained validity from his method of standardizing and quantifying the
urine sediment examination; that is, the classification and the "Addis
count" were inseparable in his mind, and the clinical usefulness of
the one depended upon the other. "Renal lesion" as loss of working
renal mass Addis estimated by a timed measurement of urea content
of blood and urine expressed as the "urea ratio" (urine urea per unit
time/plasma urea concentration, or UV/P). Now this ratio can claim
physiologic meaning as the urea clearance. But Addis thought of this
number as the amount of "still functioning renal tissue." In a letter

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26 StevenJ. Peitzman

to Alfred Cohn of 15 May 1934 about a patient, Addis reports "her

old 'ratio' figures which show that she then had 69% of the amount
of renal tissue proper for her size" (Cohn papers 1934). He did not
state that her urea clearance was 69% of normal. Indeed, Addis
occasionally decried the introduction of too much physiology into
medicine, and in 1931 urged a return to the "straight and narrow
road of morphology" (Addis and Oliver 1931, 4-5).
But physiologists such as Homer W. Smith and A. Newton Rich-
ards in the 1930s and 1940s would build a language of clinical renal
physiology based largely on the mathematical idea of clearance and
the measurement with it of glomerular filtration rate. Physiological
analysis increasingly displaced structural thinking as a medical sub-
specialty called "nephrology" matured (Peitzman 1986). Eventually,
measurement of creatinine succeeded urea in importance, and the
nephrologist of the 1980s uses mainly the serum creatinine as the
cardinal indicator of renal health. An elevated creatinine value in a
patient is "renal failure," and translates-if thought about more-
into a decreased glomerular filtration rate. It does not call to mind
an anatomic image of shrunken renal tissue, as did the urea ratio for
Addis, who frequently saw such kidneys at autopsies. For the ne-
phrologist of the late twentieth century, the serum creatinine does,
however, have associations, is more than an abstract number. To the
renal fellow called to see a new consult in the emergency room, a
creatinine of "ten" (milligrams per deciliter) conveys far more than
twice the urgency of a creatinine of "five." It means "decide about
dialysis now," instead of "call me back when the work-up is un-
derway." As with the tone of a clarinet, qualitative changes occur as
one goes up the scale of serum creatinines.

ESRD-Disease of Entitlement?

The introduction of dialysis and renal fellows into this discussion leads
to the last term to be investigated: "ESRD"-end-stage renal disease.
It is, perhaps, the strangest of all labels applied to those with diffuse
renal disease.
In 1948 Henry Christian published a small book on renal disease
which he could still title Bright's Disease. In the same year appeared
Thomas Addis's GlomerularNephritis, which movingly recounts one

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From Dropsyto Bright's Disease to ESRD 27

patient's decline and death from terminal uremia. One wonders if

either author had noted the appearancein 1947 of a slim and somewhat
obscure paperbound monograph called New Ways of Treating Uremia
by Willem Kolff. Kolff in the 1940s was the most successful of several
workers who devised practicable artificial kidneys (hemodialysis). In
its first decade or so of regular use, hemodialysis mainly aided patients
with acute and reversible renal failure. Then, in the early 1960s
engineer Wayne Quinton and physician Belding Scribner perfected
the arterial-venous shunt, which allowed repeated dialysis treatments
and the indefinite life support of persons with advanced irreversible
renal failure and uremia (McBride 1984). (Scribner first became fas-
cinated with renal disease during an elective course for senior medical
students with Thomas Addis at Stanford.)
In 1972 Congress included within Public Law 92-603 a provision
by which "chronic renal disease [is] considered to constitute disability"
(Sec. 2991). This law provided federal financial support for almost
all Americans requiring chronic dialytic treatment. Within a few years
the "end-stage renal disease program" under Social Security was formed
to implement and regulate this support. "End-stage renal disease"
was defined in 1974 as "that stage of renal impairment that cannot
be favorably influenced by conservative management alone, and re-
quires dialysis and/or kidney tranplantation to maintain life or health"
(FederalRegister1974). Although clinicians may have used the phrase
"end-stage renal failure" or the like before the passage of P.L. 92-
603, with the initiation of the federal program ESRD became a disease
definedby eligibility to receivefunding for a particulartreatment,a disease
of entitlement.
The typical patient with ESRD today is a 55-year-old person with
diabetes complicated by retinopathy and nephropathy. When the pa-
tient's creatinine reaches the range of 5 to 7 (milligrams per deciliter),
surgical preparations are made for chronic hemodialysis or peritoneal
dialysis. The patient then has ESRD. Dialytic treatments may begin
when the person reports morning nausea or occasional vomiting, per-
haps skin itching or some other early uremic symptom. There are
exceptions, of course, and some patients do present with advanced
uremia and edema. But ESRD is not the same as "uremia," since
most patients will usually begin the dialytic treatments soon enough
to avoid all but the early and subtle symptoms. Nor is ESRD equal

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28 StevenJ. Peitzman

to "chronic renal failure" (CRF), since many patients with creatinines

of 4 or 5 are said to have "CRF" but still not ESRD.
ESRD, a legislative phrase, can lay claim to being a disease. It has
become something patients can have, although relatively few use the
term. One who did, a dialysis patient in Georgia, wrote: "Possibly
the name is most frightening, end-stage renal disease. It sounds like
the end of the world. That's the way I felt [upon first learning of
it]. I cried and cried" (Jones 1984). ESRD is a disease nephrologists
can write books about, such as End-stageRenal Disease, An Integrated
Approach(Stone and Rabin 1983).
Moreover, ESRD like other diseases encompasses a set of charac-
teristic signs and symptoms. These are a mixture of late consequences
of renal failure rarely seen until dialysis lengthened the lives of renal
patients and complications of the treatment itself. Examples include
chronic anemia, renal bone disease, aluminum toxicity, dialysis-in-
duced hypotension, and especially clotting and infections of catheters
and shunts for dialysis. These last complications harry the days of
dialysis patients. Today, since ESRD treatment is started before most
patients suffer from engulfing edema or florid uremia the experience of
ESRD is mainly the illness of dialysis. The treatmentbecomes the sickness.
When renal patients write about their experiences-and a fair number
do-they write mostly about beinga dialysispatient, about the hours
on the machine, about their remarkable ability to cope and prevail.
Here are some examples:

Next I spent almost five years on home hemodialysis with my

mother as "nurse," two years on CAPD, then back to the machine,
in-center. I had a parathyroidectomy in 1976 and had my "closest
call" that year with a case of pulmonary edema (Jones 1984).
I personally am convinced that the physical aspects are very
uncomfortable, and I could gladly do without nausea, cramps, and
hypotension so bad I have to crawl into bed after a sudden drop
in pressure-because if I stood up I would pass out (Sand 1986).
Home dialysis, like many things in life, had its high and low
moments. There were times of sharing friendship and thankfulness
for extended life and its meaning and pleasures. There were also
times of despair, crisis, pain and weariness (Campbell and Camp-
bell 1978).
I suppose the longer an individual is on dialysis, the more he

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FromDropsyto Bright's Disease to ESRD 29

incorporates the process into his life. When I am at dialysis I am

more willing to take an active role, and when I am away from the
unit, the thought of dialysis has an easier time escaping my thoughts
(Levi 1984).
The first time I saw the kidney machine I thought it looked
like a big washing machine. I said "I hope you all aren't going to
put me in that machine!" (Rosenberg 1980)

The physician's experience of renal disease has changed as well.

Relying on sequential laboratory measurements, early dialysis, and
potent diuretics, the nephrologist today only rarely encounters ful-
minant uremia, or dropsy bursting through the skin. Indeed, the
renal fellow only a few times in a year enjoys the palpable fulfillment
of seeing his dialysis machine staunch seizures, penetrate the coma,
defeat severe uremia. The chronic dialysis patient has been called a
"marginal man," suspended between the worlds of the sick and the
well, beneficiary and victim of a half-perfected technology. The renal
physician, oddly, shares with his ESRD patient an incomplete, un-
resolving medical encounter, as he struggles more with the woes of
chronic dialysis than with the woes of uremia. The nephrologist has
even lost touch, literally, with the diseased kidney itself, the old
granular kidney of Dr. Bright. Autopsies of ESRD patients seldom
occur, and the renal doctor now sees kidneys only microscopically, a
biopsied bit at a time, or views shadowy reniform images on an
ultrasound screen.
Be assured that I am notcalling for more uremic seizures and deaths,
or a return to Southey tubes. Clearly, the dialysis machine is life-
saving. It is the routinization and scale of that lifesaving, with its
daily imperceptibility, that are both extraordinary and numbing.
This article has dealt mainly with names. The naming of diseases,
I argue with Knud Faber and many others, remains essential to the
modern physician who must select a diagnosis and recommend treat-
ment. To most patients, the name of the illness matters less than
does getting well, but sometimes contains meaning. Samuel Johnson
in 1784 wrote: "My diseases are an Asthma and a Dropsy, and, what
is less curable, seventy five." "End-stage renal disease," wrote the
dialysis patient in Georgia two hundred years later, "it sounds like
the end of the world." "Dropsy," "Bright's disease," "nephritis,"
"ESRD": each of these names is to some extent elusive, ambiguous.

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30 StevenJ. Peitzman

None refers to a well-defined etiologic or pathologic entity. These

terms suggest to me an increasing complexity in the encounter of
renal patient and of physician. Evident and clear to both, "dropsy"
was disease as symptom. "Bright'sdisease"was more the physician's
abstraction, with two of its key elements-albuminuria and renal
structural change-invisible to the patient. Yet, I believe "Bright's
disease" could nonetheless make sense to patient and doctor talking
together. The still evolving histologic nomenclature of "nephritis"and
"glomerulonephritis" represents a language of the renal specialist, too
esoteric for patient or general doctor. Finally, "ESRD" is a diagnosis
often uncovered by autoanalyzer, defined by need for dialysis, and
formally bestowed by government.
Each term has had its use, its particular reality, and its message.
Each reflects in some way the experience of the sickness felt and
questioned by the patient. Each reflects as well an experience of the
disease observed, contemplated, classified, and treated by the phy-
sician-treated with good intent, and with the imperfect medicines
and machines of the day.

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Acknowledgments: This study was supported in part by grants from the Amer-
ican Philosophical Society. The author is grateful for specific suggestions
from Richard J. Baron, Russell C. Maulitz, and Charles E. Rosenberg. The
influence of the last named on the intent of this paper will be evident to
readers of Professor Rosenberg's works.
Addresscorrespondenceto: Steven J. Peitzman, M.D., Departments of Medicine
and Community Medicine, Division of Nephrology and Hypertension, The
Medical College of Pennsylvania, 3300 Henry Avenue, Philadelphia, PA
19129.

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