Kidney International, Vol. 28 (1985), pp.
991 05
Acquired cystic disease: Replacing one kidney disease with
another
Medical students often are taught that most renal diseases
end with kidney fibrosis and atrophy, and what could be more
boring than the study of end-stage kidneys that are removed
from chronic dialysis patients? Fortunately, Dunnill, Millard,
and Oliver [1] were not deterred, performed such a study, and
were the first to describe rigorously the development of a
unique type of bilateral diffuse renal cystic disease in patients
maintained for long periods on intermittent hemodialysis. De-
spite considerable initial skepticism about this seminal 1977
report, the observation has been confirmed repeatedly through-
out the world [227]. Acquired cystic kidney disease (ACKD)
now is thought to be a natural consequence of the progression
of a variety of noncystic primary kidney diseases in patients
whose lives are prolonged by dialysis. In effect, we treat
end-stage renal disease by a method that promotes development
of a secondary disorder. Unfortunately, the acquired disease
sometimes leads to serious complications.
Frequency of acquired cystic kidney disease and renal tumors
in dialysis patients
Dunnill, Millard, and Oliver [1] evaluated necropsy kidney
specimens in 30 long-term dialysis patients and found acquired
cystic disease in 14 (46.6%). These patients did not have any
evidence of renal cystic diseases when they were accepted into
the hemodialysis programs. Subsequently, ACKD has been
reported in 262 of 601 dialysis patients surveyed by autopsy,
sonography, or computed tomography (CT), an overall inci-
dence of 43.6% (Table 1). Renal tumors, which are often
multiple, are less common and have been found in 43 of 601
(7.1%) chronic dialysis patients, generally in those with cystic
kidneys (Table 1). Forty-three of 262 patients (16.4%) with
ACKD have had renal tumors (Table 1). Although most of the
tumors were small and considered to be adenomas, others were
malignant and showed renal vein extension or systemic metas-
tases [1, 10, 15, 16, 251. Among the patients surveyed in Table
1, two of 43 patients (4.7%) with renal tumors had metastatic
disease. The overall frequency of metastatic renal cancer in
dialysis patients is 0.33% (Table 1), a frequency approximately
equal to that in the general population [281.
Since the autopsy rates in medical centers are low, it is likely
that the data in Table 1 underestimate the frequency of overt
renal cell carcinoma in dialysis patients. Three new cases of no invasion of the cyst walls. The tumor cells may have a foamy
metastatic renal carcinoma have been reported recently in cytoplasm because of lipid deposition, or show an eosinophilic
dialysis patients from one of our affiliated hospitals [29], and we granular appearance. 2) Some tumors are composed of tubular
Received for publication December 26, 1984
1985 by the International Society of Nephrology
99
EDITORIAL REVIEW
know of several additional unreported patients in other dialysis
centers in the United States. Clearly, the propensity of dialysis
patients to develop renal cancer must be evaluated quickly by
careful surveys of large numbers of such patients.
Pathologic findings
On gross pathological examination, acquired cystic disease is
characterized by multiple, bilateral small cysts that predomi-
nate in the renal cortex, but usually involve the renal medulla
also. The cysts may attain sizes of 2.5 to 3.0 cm, but most are
less than 0.5 cm in maximal dimension (Fig. 1). The cysts may
contain clear fluid or hemorrhagic material. Analyses of cyst
fluid have not been reported, but, in a few instances, we have
found the fluid pH to be less than that of plasma. The affected
kidneys often retain the markedly shrunken appearance char-
acteristic of end-stage renal disease. However, sometimes the
cysts result in progressive renal enlargement so that the appear-
ances resemble those of autosomal dominant polycystic kidney
disease.
Microdissection studies in ACKD have shown continuity
between the cysts and renal tubules, suggesting that the cysts
begin as fusiform tubular dilatations or as saccular tubular
outpouchings [16]. At histologic examination, most cysts are
lined by a low cuboidal or columnar epithelium, with the cells
having large vesicular nuclei and granular eosinophilic cyto-
plasms. However, most patients also have atypical cysts lined
by hyperplastic multilayered epithelium with papillary projec-
tions. Mitoses are observed in the epithelial cells often. Smooth
muscle proliferation within the kidney blood vessels and
hyperplasia of Bowman's capsule occur often also, and focal
and interstitial calcification and calcium oxalate precipitates
within cyst walls and lumens are common findings.
Scanning electron micrographs of cyst lining cells (Fig. 2)
show that some have an apical brush border configuration,
suggesting that such cysts derive from proximal tubules. The
linings of other cysts show a typical cobblestone appearance,
punctuated by sessile polyps (Fig. 3). These cysts may be
derived from more distal segments of the nephron and collect-
ing system.
Dunnill (personal communication) points out that renal tu-
mors in ACKD fall into at least three histologic categories: 1)
Papillary tumors project into the cyst cavities and usually show
structures. The tubules are lined by a simple cuboidal epithe-
hum with the cells showing oncocytic change or a foamy
appearance because of lipid material. These tumors appear to
arise between the cysts. 3) Solid tumors contain sheets of cells
100 Grantham and Levine

Table 1. Surveys of acquired cystic kidney disease in dialysis patients

Metastatic
Patients ACKD Tumors disease
Year of surveyed
report Authors N N % N N %
1977 Dunnill et a! [1] 30 14 47 6 20 1 3
1977 Elliott et al [3] 18 5 28 0 0 0 0
1980 Bansal et a! [6] 52 5 10 1 2 0 0
1980 Hughson et al [81 66 20 30 9 14 0 0
1980 Mirahmadi et a! [13] 32 15 47 0 0 0 0
1980 Fayemietal[10] 80 24 30 9 11 1 1
1980 Krempien et a! [11] 22 21 95 4 18 0 0
1980 Ishikawa et a! [9] 97 41 42 3 3 0 0
1980 Bommer et a! [12] 14 5 36 0 0 0 0
1981 Feiner et a! [16] 15 8 53 2 13 0 0
1983 Turani et al [251 15 10 67 3 20 0 0
1984 Levine et a! [20] 30 13 43 4 13 0 0
1984 Mickisch et a! [261 108 70 65 1 1 0 0
1984 Vaziri eta! [27] 22 11 50 1 5 0 0
Totals 601 262 43.6 43 7.1 2 0,33
Abbreviation: N, number of patients.

I'
I, -,

t.
Fig. 2. Scanning electron micrographic appearance of cyst brush
border lumen surface in acquired cystic kidney disease. )< 1600 (Cour-
tesy of Walter Richardson, M.D.)

Clinical and radiologic diagnosis

Although ACKD may be superimposed on most types of

chronic renal disease, most often the underlying renal disease is
glomerulonephritis, tubulointerstitial nephritis, nephrosc!ero-
sis, or diabetes mellitus. Among dialysis patients, various
studies including our own have shown duration of dialysis to be
the major factor that correlates consistently with the presence
Fig. 1. Surgical specimen of left kidney in long-term dialysis patient of absence of ACKD [9, 201. The disorder is seen rarely in
who developed massive perirenal hemorrhage. Kidney is studded with patients who have been dialyzed for less than three years. In
multiple small cysts consistent with acquired cystic disease. Hemor- our series of 30 patients, we found no relation between efficacy
rhage originated in a cyst located laterally (arrow). of dialysis, reflected in such blood chemistry values as urea
nitrogen, creatinine, uric acid, parathyroid hormone, and alka-
line phosphatase, and the development of ACKD [201.
with no obvious tubular differentiation and may show central Most patients with ACKD are asymptomatic. However,
hemorrhage and necrosis. Distinction between adenoma and hemorrhage into the cysts is common, apparently because
carcinoma is often difficult. unsupported sclerotic vessels in cyst walls rupture with minor
 Acquired cystic disease 101

It is reasonable to suppose that as surviving nephrons de-

crease in number in patients with chronic renal disease,
renotropin production will increase, leading to nephron and
collecting duct hyperplasia. Prolonged renotropic stimulation
leads to cyst formation and, in extreme cases, to renal tumors.
This hypothesis recognizes that hemodialysis and peritoneal
dialysis are relatively imperfect substitutes for normally func-
tioning kidneys, and although they maintain an internal envi-
ronment that prolongs the patient's life, certain insufficiently
eliminated substances accumulate and promote the production
of renotropic factors. This hypothesis is supported by the
finding that successful renal transplantation in dialysis patients
leads to regression of established ACKD and reduction in size
of the affected native kidneys [35], presumably by removing the
stimulus to renotropin production. In this regard, it is interest-
ing to note that renal cysts produced experimentally in rats by
diphenyithiazole disappear after drug withdrawal [36]. The
Fig. 3. Scanning electron micrographic appearance of cyst lumen renotropic stimulus in dialysis patients must be specific for the
surface in acquired cystic kidney disease. Two adenomatous polyps
(arrows) project from the cyst wall into the lumen. x400 (Courtesy of kidneys, since hyperplasia and cyst formation have not been
Walter Richardson, M.D.) observed in other organs.
It has been suggested also that ACKD may be caused by
chemicals leached from hemodialysis equipment [37]. Certain
trauma. Bleeding may remain confined to the cysts, but often chemicals such as diplenylamine [38], diphenylthiazole [36, 39],
extends into the renal collecting system, resulting in painful nordihydroguairetic acid [40], and cisplatin [41] cause acquired
macroscopic hematuria [15]. Alternatively, hemorrhage may cystic disease in animals that are otherwise normal. However,
extend from the cysts to involve the subcapsular or perirenal none of these substances is known to be present in dialysis
spaces (Fig. 4), leading to severe flank pain and fall in hemato- equipment. Furthermore, patients treated by peritoneal dialysis
crit [17, 20, 30]. Metastatic carcinoma sometimes may be the develop ACKD also and, more important, fully developed
first clinical manifestation of renal tumors occurring in ACKD ACKD has been detected in patients with longstanding renal
[29]. insufficiency who have never been dialyzed [12, 42]. Thus,
The diagnosis of ACKD can be established by CT (Figs. 5 and chemicals leached from dialysis equipment conceivably could
6) and sonography [9, 1922, 311. We prefer CT because, in our affect the progression of ACKD, but they do not appear to be
experience, frequently shrunken end-stage kidneys are difficult essential to the initiation of cyst development.
to visualize sonographically, and CT is more sensitive than Although diphenylthiazole causes reversible renal cystic dis-
sonography in detecting small renal tumors (Fig. 5). ease in rats [361, cisplatin produces a nonreversible type of
Retroperitoneal hemorrhage is diagnosed and localized most renal cystic disease [41]. The possibility exists, therefore, that
accurately by CT also (Fig. 4). Selective renal arteriography certain exogenous or endogenous chemicals may affect renal
may be helpful in further evaluation of renal tumors detected by cells to the point of causing them to grow autonomously. In
CT or sonography [221, but the accuracy of this technique has such instances, cancer may be the consequence.
not been established firmly. Several mechanisms may lead to cyst formation from renal
tubules in dialysis patients (Table 2). Studies of drug-induced
renal cystic disease in animals suggest that altered compliance
Etiology and pathogenesis of acquired cystic kidney disease of the tubular basement membrane is the basis for cystic tubular
and renal tumors dilatation [43]. It is possible that cystogenic chemicals accumu-
lating in dialysis patients may have a similar effect on the renal
The factors that lead to renal cyst and tumor formation in tubules. It has been postulated also that cystic dilatation of
dialysis patients are not known. However, clinical and experi- renal tubules in dialysis patients may result from tubular
mental evidence leads us to propose a pathogenetic scheme obstruction caused by surrounding interstitial fibrosis, focal
outlined in Table 2. In this view, the loss of a critical number of hyperplasia of tubular epithelium, or intraluminal oxalate crys-
functioning nephrons is the cause of the disorder. Because of tals, which are abundant in end-stage kidneys [10, 11].
the loss of functioning renal mass, there is increased production
of so-called renotropic factors, unique chemicals that are in- Mechanism of fluid accumulation in the cysts
strumental in causing hyperplasia of surviving glomeruli, neph- Microdissection studies have shown continuity between the
rons, and collecting tubules [3234]. Evan (personal communi- cysts and the tubular segments from which they arose [161. It is
cation) found in a recent study that rats subjected to 5/6 not certain, however, that these segments are connected with
nephrectomy and high protein intake developed profound cystic functioning glomeruli. The glomeruli in these kidneys are
changes in the residual renal tubules. This observation supports markedly atrophic, and structurally intact glomeruli have been
the concept that loss of functioning renal mass, whether by found in only a few cases. This raises the intriguing possibility
ablation, cell necrosis, or fibrosis secondary to diffuse paren- that the renal cysts are filled by transepithelial fluid secretion
chymal diseases, promotes the development of ACKD. rather than by the sequestration of glomerular filtrate, as has
102 Grantham and Levine

Fig. 4. Postcontrast CT scan shows a relatively lowdensity perinephric hemorrhage (arrows) surrounding the right kidney. Multiple small cysts
are present in both kidneys. (Reprinted with permission from Levine et a! [20].)

V
I t

Fig. 5. Postcontrast CT scan shows multiple, small bilateral renal cysts. In addition, there is a homogenous, sharply marginated solid mass located
anteriorly in the midregion of the left kidney (arrow). The lesion, believed to be a small renal tumor, had an attenuation value of 38 H, which is
less than that of noncystic renal parenchyma. (Reprinted with permission from Levine et al [20].)

been proposed for autosomal dominant polycystic kidney dis- Management and follow-up of acquired cystic kidney disease
ease 144]. Clearly, measurements of cyst fluid composition in
ACKD need to be made if we are to understand the mechanism The management of patients who develop symptomatic
of fluid accumulation in these structures. ACKD during dialysis depends on individual clinical circum-
 Acquired cystic disease 103

Fig. 6. Postcontrast CT scan shows multiple lesions of varying sizes scattered throughout both kidneys. The larger lesions had fluid attenuation
values consistent with cysts. Although most smaller lesions are probably cysts also, partial-volume averaging precludes definite characterization.
There is atherosclerotic calcification of the left renal artery (arrow). The mean renal volume was 205 cm3, which is large for end-stage kidneys in
a long-term dialysis patient. (Reprinted with permission from Levine et al [20].)

Table 2. Potential factors in the pathogenesis of acquired cystic [201 and those of other surveys, we suggest that it is prudent to
kidney disease and renal tumors in long-term dialysis patients screen routinely patients dialyzed for longer than three years
1. Loss of functioning nephrons for ACKD. Although some workers recommend sonography for
2. Epithelial and vascular hyperplasia this purpose, we prefer CT since small kidneys are difficult to
Unique renotropic growth factors image by sonography and since CT is more accurate for
Retained renotropic growth factors detecting small renal tumors. The first CT scan gives a baseline
3. Accumulation of cystogenic chemicals
Endogenous
against which future tumor formation can be judged. Small
Exogenous (dialysis tubing) renal tumors diagnosed by CT in the end-stage kidneys of
4. Tubular obstruction by polyps, oxalate crystals, or surrounding dialysis patients pose a serious management problem. Typi-
fibrosis cally, renal cell carcinomas grow slowly, and their metastatic
5. Ischemia of tubular segments potential is difficult to predict even on pathologic examination
6. Altered epithelial growth secondary to tubular basement mem-
brane abnormalities [45, 46]. Most reported dialysis-related renal tumors have been
Altered basement membrane synthesis diagnosed as adenomas confined to the kidneys, and their
Altered basement membrane turnover natural history is unknown.
Although even small renal tumors may cause metastases [47],
it is known that those less than 3.0 cm in diameter rarely
stances. In patients with retroperitoneal hemorrhage that can be metastasize [481. Although some workers recommend routine
identified by sonography or CT, it may be prudent to take a resection of such small lesions, we think that the available
conservative approach over the short term. In autosomal dom- evidence does not justify this approach. In patients who are not
inant polycystic kidney disease, the cysts sometimes rupture, candidates for renal transplantation, the loss of renal mass
causing retroperitoneal or parenchymal hemorrhage, but bleed- resulting from bilateral nephrectomy may increase the transfu-
ing usually subsides and does not require nephrectomy. This sion requirements and thereby jeopardize the comfort and
may hold true for ACKD also. If bleeding persists or becomes lifestyles of such patients. We think, therefore, that if CT
difficult to control, selective renal arterial embolization may reveals renal tumors of less than 3.0cm in dialysis patients, an
stop the bleeding and obviate the need for nephrectomy. annual CT should be followed [29] or implemented more
From the results of our prospective study of dialysis patients frequently if symptoms such as flank pain and hematuria
104 Grantham and Levine
develop. Time will tell whether this non-operative approach is
appropriate. On the other hand, renal tumors larger than 3.0cm
within the cystic kidneys should be resected. Also, bilateral
nephrectomy would seem advisable in prospective renal trans-
plant recipients with renal tumors, regardless of their size.
Conclusion
This high prevalence of acquired cystic kidney disease in
dialysis patients suggests that it is the natural consequence of
most scierosing renal disease in patients who survive unnatu-
rally. Flank pain and hematuria are the principal symptoms,
but, fortunately, these occur in only a small percentage of
dialysis patients. Thus, ACKD does not appear to be a major
cause of dialysis morbidity. On the other hand, 16.4% of
patients with ACKD have renal tumors, the malignant potential
of which is illustrated by metastases in several patients. Al-
though relatively small, the number of cases reviewed here
raises concerns about the long-term consequences of leaving
end-stage kidneys undisturbed in dialysis patients. A controlled
survey of the morbidity of ACKD and of the frequency of renal
carcinoma in dialysis patients is needed urgently.
JARED J. GRANTHAM
ERROL LEVINE
Kansas City, Kansas, USA
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