Ascites Associated With End-Stage Renal Disease

Z. Gluck, MD, and K.D. Nolph, MD

• Patient characteristics, clinical outcomes, and proposed pathophysiologic mechanisms are reviewed in 138
patients reported in the literature to have had ascites associated with end-stage renal disease. Contributing mech-
anisms may include fluid overload, peritoneal membrane changes (not necessarily related to peritoneal dialysis),
hypoproteinemia, and lymphatic drainage disturbances. In 15% of cases, extensive evaluations may reveal an
underlying disease. The most effective therapy may be kidney transplantation.
© 1987 by the National Kidney Foundation, Inc.

INDEX WORDS: Ascites; end-stage renal disease; hemodialysis ascites; peritoneal dialysis and ascites; kidney
transplantation and ascites; idiopathic ascites in ESRD.

I N AN ANALYSIS of ascites published 75 years

ago, I renal disease was found to be responsible
for approximately 20% of clinically diagnosed as-
cites cases. With the introduction of specific thera-
peutic regimens for certain glomerulonephritis
forms , with the broad use of diuretics in addition
to salt and water restrictions , and with the intro-
duction of maintenance dialysis methods to control
uremia and fluid retention in advanced renal
failure, the incidence of ascites secondary to renal
disease was drastically reduced. 2
In 1970, ten years after the introduction of
chronic hemodialysis (HD) in the United States, a
new form of idiopathic ascites in patients on main-
tenance HD was first described ,3.4 although pre-
viously recognized. 5 Since then , 138 ascites cases
(of initially unknown origin) in patients with end-
stage renal disease (ESRD) have been reported in
36 publications or abstracts. 3.4.6-39 This review rep-
resents a summary of the reported cases, empha-
sizing the patient characteristics, their clinical
course and prognosis, the possible pathophysio-
logic mechanisms underlying this phenomena, and
possible treatments .
DEFINITION
Ascites of ESRD is defined as a clinically evi-
dent chronic ascites, occurring in patients with
ESRD without evidence for a directly causative
specific underlying disease .
INCIDENCE
At this time, no survey is available regarding the
overall incidence of ESRD-ascites. Based on the
reviewed papers, the incidence ranges from 0.7 to
20 %. 4.7.13.14,16,18,21.22,39 These reported incidence
rates are biased, however, since the available data
are based on reports from selected groups dealing
more frequently with this problem, whereas in
some other centers this problem is nonexistent, as
mentioned by Feingold et al. 18 Furthermore, it
seems that the incidence of this complication, with
most of the cases reported 10 to 15 years ago, de-
creased over time as a result of technical advance-
ments and the introduction of new treatment con-
cepts for patients with ESRD , eg, the development
and use of more effective dialyzers, better control
of uremia and fluid balance with three instead of
two weekly HD treatments, more frequent use of
isolated ultrafiltration, and a better approach to
nutritional as well as psychologic aspects of
ESRD. This trend was implicitly suggested by
Singh et al l4 and Gotloib and Servadio.22
PATIENT CHARACTERISTICS
AND CLINICAL COURSE
Thirty-eight cases from a survey conducted by
Cinque and Letteri 8 are listed separately in Table
1. In order to prevent data duplication, these were
not added to the other cases, since we assume that
some of the survey cases were also published in
individual case reports.
Of the 138 cases described or mentioned in the
reviewed literature, 20 were found to have an un-
derlying disease directly associated with ascites
formation and are listed in Table 2 and excluded
From the Department of Medicine . University of Missouri.
Health Sciences Center. 1/,4 Hospital. and Dalton Research
Center. Columbia.
Presented in part at the Annual Scientific Meeting of the Na-
tional Kidney Foundation. New Orleans. December 14. 1985.
Address reprint requests to K.D. Nolph . MD. Director. Divi-
sion of Nephrology. Department of Medicine. University of
Missouri. MA436 Health Sciences Center, Columbia. MO
65212.
© 1987 by the National Kidney Foundation. Inc.
0272-6386/8711001-0002$3.00/0

American Journal of Kidney Diseases, Vol X, No 1 (July), 1987: pp 9-18 9

10 GLUCK AND NOLPH

from Table 1. These patients are not included in

further analyses except when discussing results of
diagnostic tests and procedures.
The mean age of the 118 patients in Table 1
(ij >-
_UJ Q)
CJ::c:O_
Cl
ranges from 11 to 71 years (mean 42 ± SD 13
.~~.~~~
a. Q).-
years) with a male:female ratio of 2: 1 and a black:
a.J:
white distribution of 1: 1. The primary renal dis-
ease was reported in 64 of the total 118 cases in
Table 1: 39 % had glomerulonephritis, 31 % hyper-
tension, 8 % chronic pyelonephritis (PN) or ob-
structive uropathy, 8 % unknown etiology, 5 %
polycystic kidney disease, 5 % diabetes mellitus,
and the remainder had systemic diseases. Perito-
neal dialysis (PD) treatment preceded HD in 69 %
of the cases. Ascites occurred at any time between
18 months prior to initiation of HD and up to 69
months thereafter. In six cases, ascites occurred
prior to any dialysis treatment, in ten cases during
PD treatment, and during HD for the remainder.
Duration of ascites ranged from 2 weeks to 30
months (mean 11 ± 9 months).
From the incidence of accompanying clinical
features listed in Table 1, the most striking find-
ings are a high incidence of fluid overload at the
time of ascites formation, an incidence of pericar-
ditis (historical or at time of observation) nearly
!! twice as high as reported for an unselected ESRD
c:
.!!! population,40.4\ as well as a relatively high per-
'lG
a. centage of patients with frank hypoalbuminemia
'0 ranging from 19% in the reviewed series to 37%
in that desctribed by Cinque and Letteri. 8 Hyper-
tension was listed in the analysis only if described
at time of ascites formation or during its course;
this was present at a high incidence of 74 % in pa-
tients where BPs were cited. This result, however,
should be interpreted with caution since BP values
at this stage of the disease were reported in only 39
cases and might not be representative for the rest
,.... (/)
E·g
~

-s.
~

of the cases.
Q) .!!1 a. -
jj m c: 0
a. 0 J: Transaminase alkaline phosphatase, lactic dehy-
fl. drogenase (LDH), and amylase values were nor-
mal in almost all cases. Mean creatinine and BUN
values were 13.5 ± 3 (n = 42) and 77 ± 29 (n
= 21) mg/dL, respectively, mean serum total pro-
tein and albumin 6.1 ± 0.9 (n = 42) and 2.9 ±
0.6 (n = 68) g/dL, respectively. Hemoglobin and
hematocrit values were comparable to those of
nonselected dialysis patients, and hepatitis-serol-
ogy results were reported in only a few cases. No
parathyroid hormone (PTH) values were reported.
 ASCITES IN ESRD 11

Table 2. List of Established Etiologies for Ascites, Diagnosed From 138 Cases of Ascites in Patients With ESRD
No. of Cases
Ref. No. Diagnosis Diagnosed Diagnostic Melhods

13, 15, 22,39 Liver cirrhosis 5 Laparoscopy (1), liver

biopsy (2), autopsy (1), ? (1)
7 Pancreatitis with pancreatic pseudocysts 4 ?
33, 39 Congestive heart failure 3 Cardiac catheterization (2),
autopsy (1)
13, 39 Tuberculous peritonitis 2 Autopsy (1), ? (1)
20, 39 Chronic active hepatitis 2 Autopsy (1), serology and
clinical course (2)
36 Constrictive pericarditis Cardiac catheterization
21 Budd-Chiari syndrome Cavography
Inferior vena cava compression (Hodgkin's disease) Cavography
38 Hypothyroidism Hormonal constellation,
clinical presentation
Total Pathologic findings 20

The ascitic fluid was typically straw-yellow in
appearance and rarely bloody (two cases) . It
showed exudate characteristics with total protein
concentration >2 .5 g/dL in most of the cases
(mean 3.8 ± 1.2 g/dL; n = 65). Leukocyte
counts in ascitic fluid ranged from 25 to 1,600
(mean 475 ± 391; n = 34), and the differential
reported in only a few cases found neutrophils
ranging from 6% to 70%, lymphocytes from 5%
to 96 %, and in some reports , up to 90 % mesothe-
lial cells. Determinations of LDH and amylase in
the ascitic fluid were nondiagnostic . Searches for
acid-fast bacilli were positive in one case 39 ;
searches for malignant cells were negative in all
cases. Positive bacteriologic cultures were en-
countered in only two cases (Streptococcus viri-
dans and Candida albicans) and interpreted as as-
cites superinfection.
Peritoneal histology was available in 47 cases.
Pathologic findings were noted in 21 patients
(Table 3) .
Liver biopsy was performed in 29 of the total
138 cases: ten biopsies showed centrilobular con-
gestion, two liver cirrhosis (Table 2), and five he-
mosiderosis of various degrees , while five other
biopsies revealed nonspecific mild alterations.
Cardiac catheterization performed in eight cases
revealed congestive heart failure in two and con-
strictive pericarditis in one (Table 2) . From six
cavography examinations, two revealed obstruc-
tion of the inferior vena cava, and from six lap-
aroscopies performed, a possible hepatic cirrhosis
was diagnosed in one case; these three cases with
diagnostic findings are all listed in Table 2.
The clinical course was not uniform, with pa-
tients differing in their clinical presentations, re-

Table 3. Pathologic Results of Peritoneal Histology (Obtained by Biopsy or Autopsy)

Ref. No. Pathologic Histologyl* Pathologic Results

8 (survey) 4/8 3 Nonspecific chronic inflammation

1 Severe fibrinous peritonitis
7 2/2 2 Chronic peritonitis with
proteinaceous deposits
11 1/1 Mild chronic fibrosing peritonitis
12 8/8 8 Mild chronic fibrinous reaction
14 2/6 1 Organizing peritonitis
1 Necrotizing peritonitis (Candida)
16 3/3 3 Chronic inflammation and fibrosis
18 ?17 ? Slight fibrosis
21 1/2 Serofibrinous peritonitis
27 4/5 4 Mild chronic inflammation with low
degree of mesothelial proliferation
Total 21/34

'Number of patients biopsied in the given publication .

12
sponse to treatments, and prognosis. A selected
group of patients with common clinical features of
uncontrolled hypertension, wasting, ascites for-
mation, and high mortality was described by
Feingold et a1 18 ; nephrectomy to control hyperten-
sion was undertaken in some. Many other patients
represented a picture of fluid overload, with or
without concomitant hypertension, and large inter-
dialytic fluctuations of body weight. 22 Some of
them responded with the disappearance of ascites
to salt and fluid restrictions alone 22 or combined
with intensive ultrafiltration. 28 In many other
cases, however, ascites persisted after disappear-
ance of all other peripheral signs of fluid overload.
These patients may have done well even with per-
sistent ascites or suffered progressive deterioration
with wasting symptoms. Some patients developed
ascites without any obvious concomitant predis-
posing factors.
Approximately one third of the patients devel-
oped cachexia, which appeared either prior to as-
cites l8 or, in most of the cases, during its course;
in the latter it was believed to be a direct result of
increased abdominal pressure, loss of appetite,
and vomiting.
Appearance of ascites in dialysis patients was
initially believed to be an ominous finding, indi-
cating extremely poor prognosis. 6.12 In the present
review, one third of the 118 patients in Table 1
died 10.7 ± 7.0 months after onset of ascites,
with a mean dialysis duration of 23.5 ± 14.0
months (patients who died after resolution of the
ascites are not included). The mean ascites dura-
tion until resolution, death, or date of report was
Table 4. Summary of Treatment Modalities for Ascites of ESRD and Their Results
ReI. No. Method of Treatment
8 (survey) Nonsurgical general measures
Successful transplantation
8,13,16,17,22,24 Fluid restriction and intensifying
HD
10, 28 Isolated ultrafiltration
6, 19,20,25,27,29 Local steroids
4,12,20,23,26,34 Peritoneovenous shunt
4, 12, 18,20,37 Reinfusion of ultrafiltered ascites
16, 18,21,31 Bilateral nephrectomy
16 Laparotomy
13-15,17,22,30,31,39 Transplantation
30, 33 Maintenance PD or CAPD
'Exact number of patients treated this way not known since not always individually reported.
tSignificant decrease of ascites, disappearance of associated symptoms, and a better hemodynamic response to HD.
GLUCK AND NOLPH
11 ± 9 months. Mean dialysis duration in these
patients until death or end of report was 24 ± 16
months.
In more than 50% of the cases, ascites totally
disappeared or could be obviously reduced using
different treatment modalities (Table 4).
Based on these results, it seems that patients
with ESRD-ascites represent a higher risk group
with a relatively high mortality rate. Ascites, how-
ever, seems to be more a consequence than the
cause of the increased risk. Furthermore, it seems
that the prognosis of such patients is not as bad as
initially presented.
PATHOGENESIS
Peritoneal fluid formation is a dynamic process.
Oncotic and hydrostatic forces control the net flux
of fluid between the peritoneal capillary bed and
the peritoneal cavity. Movement of protein be-
tween the compartments is modified by the perito-
neal membrane and is influenced by the lymphatic
drainage system. Perturbation of these forces by
increased capillary hydrostatic pressure (liver cir-
rhosis, heart failure, constrictive pericarditis, ve-
nous obstruction, or fluid overload) and/or de-
creased oncotic pressure (hypoalbuminemia),
peritoneal membrane changes (inflammation), or
congested hepatic sinusoids (heart failure) might
favor movement of fluid into the peritoneal cavity
to form ascites. Additionally, a disturbed lym-
phatic drainage from the peritoneal cavity might
contribute to the formation of ascites.
Analyses of potential pathophysiologic proc-
esses predisposing to ascites formation in patients
No. of Patients No. of
Treated Successful Results
38 14
4 4
? All reviewed cases' 10
4 4t
14 4t
12 11 t
7 5t
7 4
2 2
12 12
6 6
ASCITES IN ESRD
with ESRD suggest that patients with ESRD are at
much higher risk for developing ascites as com-
pared to normals.
Fluid Overload
According to the "overflow" theory of Lieber-
man et al,42 ascites formation may be a conse-
quence of plasma volume expansion resulting from
renal sodium retention in patients with cirrhosis.
Most patients with ESRD are prone to salt and wa-
ter retention. Consequently, excessive intakes of
salt and water result in volume expansion, leading
to potential fluid overflow and formation of edema
and ascites. 9 Once formed, ascites is more diffi-
cult to remove than edema because of the compart-
mentalization phenomena, which is a result of a
rate limited fluid absorption from the peritoneum
with a maximum of about 900 mLl24 h 43 com-
pared to a much higher mobilization rate of
edema. Such mechanisms of overflow and fluid
compartmentalization, with formation of slowly
removable ascites as compared to other fluid com-
partments, were demonstrated in patients with
dialysis ascites by Eknoyan et al.9
Fluid retention appears to be a common denomi-
nator in approximately two thirds of the cases pre-
sented and appears to play a predominant role in
the formation of ascites in many of the reported
cases, as clearly demonstrated by Gotloib and Ser-
vadio. 22 The high protein content of the ascites
fluid suggests a similarity to the pattern found in
humans with congestive heart failure 44 and can be
attributed to the presence of intact hepatic sinu-
soids. Normal sinusoidal endothelium is thin and
highly porous to albumin. An increase in hepatic
vein outflow pressure thus may result in a leak of
protein-rich fluid.
Peritoneal Membrane Changes
Functional and/or anatomical changes of the
peritoneal membrane may play a role in ascites
formation.
Uremic toxins may induce increases in vascular
permeability similar to those observed in the
lungs 45 .46 and, as postulated by some
authors, 12.14.15 may be contributing factors in asci-
tes formation. It is, however, difficult to accept
such causative mechanisms in patients with good
control of uremia and when ascites occurs months
or years after initiation of HD. An angiotensin-
13
induced increased vascular permeability47-49 may
lead to ascites formation in dialysis patients with
dialysis hypertension as postulated by Feingold et
al.1 8 Many patients with ascites have high renin
levels. 50 In this context, other hypothetical renally
produced substances with similar vascular effects
have been postulated. 8 .1 8 Such theories are, how-
ever, difficult to accept, since in some se-
ries, 20.2 U I bilateral nephrectomy neither pre-
vented nor was able to reverse a preexisting ascites
in HD patients with uncontrolled hypertension.
Based on previous reports demonstrating altered
permeability of the peritoneal membrane by hy-
pertonic PD,51 a PD-induced sodium transport de-
fect was postulatedl 6 as an underlying mechanism
for ascites formation. There is, however, evidence
that functional changes associated with chronic PD
or with peritonitis are reversible after interruption
of this treatment modality.52.53 This, together with
the fact that in most cases reported, ascites oc-
curred months to years after cessation of PD,
makes this theory less likely.
In the present review, 45 % of the available his-
tologic specimens of the peritoneum demonstrated
pathologic changes. The predominant findings
were chronic inflammatory changes in most, and
peritoneal fibrosis in some, other cases.
Histologic change in the peritoneum may be sec-
ondary to contact with dialysis solution containing
a low pH, high osmolality, nonbicarbonate
buffers, and possible contamination with trace
amounts of foreign substances and in association
with repeated episodes of bacterial peritonitis.
Peritoneal membranes from patients exposed
chronically to PD solutions show mesothelial-cell
as well as connective-tissue alterations. 54 It is,
however, unknown if such alterations are persist-
ent after interruption of PD. The possibility that
introduction of talcum powder or other particulate
material into the peritoneal cavity with peritoneal
dialysis caused chronic peritoneal inflammation in
some cases cannot be excluded. II However,
chronic inflammatory peritoneal changes were
found in three patients that had never had PD. 12
Inflammatory involvement of serous mem-
branes occurs commonly in patients with renal
failure 4o .41.55.56 and it seems likely that at least
some of the observed cases with unexplained
chronic peritoneal inflammation in this series rep-
resent renal failure-associated serositis. Such peri-
14
toneal changes may contribute to exudative ascites
formation, a process similar to that seen in uremic
pericarditis. 19 Calculation of serum-ascites al-
bumin differences seems to be helpful in separa-
tion of transudative and exudative ascites forms. 57
Differences of serum-ascites albumin concentra-
tions >0 .9 g/dL suggest transudation , while those
<0.9 g/dL are suggestive of true exudation. We
performed such calculations in some cases in
which adequate data were available.9.12.15.30 In 11
of 22 cases, serum-ascites albumin differences
were 0.9 g/dL or lower. This finding strongly sug-
gests that, in at least some dialysis ascites cases,
the high ascitic fluid protein content may represent
a true exudative process, possibly secondary to
chronic peritoneal inflammation.
Lymphatic Drainage
Impairment oflymphatic drainage from the peri-
toneum of patients with ESRD-ascites was demon-
strated by Morgan and Terry.32 This factor might
contribute to the propensity of fluid-overloaded
patients with ESRD to develop ascites.
Cardiac Failure
Some conditions that are commonly associated
with ESRD may increase the likelihood of these
patients developing ascites. Patients with ESRD
demonstrate a high incidence of cardiac failure, 58
arterial hypertension playing a major role in its
pathogenesis. 59.60 It is of interest that the incidence
of hypertension, as a primary renal disease, is ap-
proximately 50% higher in the reviewed series
compared with unselected HD patients. It is,
therefore, possible that the incidence of cardiovas-
cular complications in this group of patients is
higher than that of unselected HD patients . This
issue, however, was not analyzed in the present
review because of inadequate information.
Constrictive Pericarditis
The incidence of pericarditis in cross-sectional
studies of dialysis patients between 1966 and 1975
ranges from 15% to 18%.40.41 Approximately 1%
to 4 % of acute pericarditis may lead to chronic
pericardial constriction. 40.61 Although relatively
uncommon, the incidence ofthis complication that
might lead to ascites formation is much higher in
dialysis patients as compared to normals.
GLUCK AND NOLPH
Hypoproteinemia
Inadequate nutrition in total calories and high
quality proteins, resulting in wasting and hypopro-
teinemia, can be observed in patients treated by
dialysis. In the present series, 19 % of the patients
had significant hypoalbuminemia. This can repre-
sent a vicious cycle in patients with ESRD-ascites.
Hypoalbuminemia may predispose to ascites for-
mation and then worsen because of poor appetite
and vomiting. Ascites can cause increases in in-
traabdominal pressure, which can explain the loss
of appetite and vomiting.
Hyperparathyroidism
An association between uremic pericarditis and
severe secondary hyperparathyroidism was pre-
viously suggested. 4o.62 If true, the same mecha-
nism might also affect the peritoneum. From the
papers reviewed, no adequate information about
accompanying hyperparathyroidism is available.
Interestingly enough, however, three of eight pa-
tients with ascites described by Gutch et aP2 were
found to have extensive metastatic soft-tissue
calcification, and severe hyperparathyroidism was
recognized in three of seven patients presented by
Zerefos et al. 7 Ascites in some of these cases
could, however, be a direct consequence of pan-
creatitis, which might have been perpetuated by
the severe hyperparathyroidism. 7
Pancreatitis
An increased incidence of pancreatic disease in
chronic renal failure was previously recog-
nized 63 .64 and might cause ascites in patients with
ESRD.7
Hepatitis
Dialysis-associated hepatitis, mostly caused by
hepatitis B virus, may result in some cases in
chronic active hepatitis, with the potential devel-
opment of liver cirrhosis. 65
TREATMENT
Ascites of ESRD was considered, at first, un-
treatable. 46 According to these initial reports,
general measures, eg, intensive HD, rigid fluid
control, high protein diet, albumin infusion, and
paracentesis, or more specific approaches, eg, ste-
ASCITES IN ESRD
roid therapy, reinfusion of concentrated ascItIc
fluid, or implantation of a peritoneoatrial pump,
were all found to be ineffective.
Treatment results, however, seem to be more en-
couraging in the survey analysis of Cinque and
Letteri S wherein improvements secondary to non-
surgical measures were observed in 14 of 38
cases (Table 4). Four other patients who survived
transplantation experienced the complete disap-
pearance of ascites. An exact definition of "treat-
ment success" in this review is difficult, since it
was not exactly defined in most of the papers, and
treatments are reported here as successful not only
when ascites completely disappears, but also when
significantly reduced. These patients often develop
arterial hypotension during HD with consequent
low flow and underdialysis. Palliative measures,
such as ascites reinfusion or implantation of a peri-
toneovenous shunt, may lead to better tolerance of
dialysis and the improvement of patients' general
condition. In such cases, treatment is considered
successful.
General Measures
Fluid restriction and HD with dialytic ultrafIltra-
tion were performed in almost all cases and were
found to be successful in ten. Six of these patients
responded to increased HD up to five or six ses-
sions per week for a limited period. s. )3,22.24 The
remainder responded to adequate fluid restriction.
The usefulness of intensive psychotherapy to in-
crease dietary compliance was demonstrated by
Gotloib and Servadio. 22
Isolated Ultrafiltration
The use of aggressive dialytic ultrafiltration in
patients with ascites was largely limited because of
their propensity to develop hypotension during
such procedures. The use of isolated ultrafiltra-
tion,66,67 which is associated with fewer hypoten-
sive side effects, was reported to resolve or signif-
icantly decrease ascites in some cases. 10.2S
Local Steroid Treatment
The rationale of this therapeutic approach is
based on the fact that uremic ascites may be simi-
lar in its origin to uremic pericarditis, and that lo-
cal steroid application was reportedly successful in
the treatment of some cases of intractable uremic
15
pericardial effusion. 6s Some authors found this
treatment modality to be effective in patients with
ESRD-ascitesI9.25.29; others, however, could not
confirm its efficacy.6,20,27 This controversy is not
surprising, since ESRD ascites may have different
etiologies.
Peritoneojugular Shunt
A continuous reinfusion of ascites fluid directly
into the venous system, using mostly the Le Veen
shunt,26 was shown to effectively reduce ascites
volume 20,23,26.34 and to prevent dialysis induced
hypotension 20 in the majority of the cases of
ESRD-ascites (where it was used). Complications
known to accompany this treatment 26 were not re-
ported in the patients reviewed here.
Reinfusion of Ultrafiltered Ascites Fluid
This seemed to be successful in reducing asci-
tes 69 ,70 and improving hemodynamic responses to
HD in some cases. IS ,37 This treatment was fre-
quently associated with pyrexia. Other complica-
tions were not reported.
Bilateral Nephrectomy
This was suggested by Feingold et aps as the
treatment of choice in HD patients with continuous
wasting and persistent hypertension after initiation
of regular dialysis. The effect of nephrectomy in
reversing or preventing ascites formation is con-
troversial, as noted before. Furthermore, there are
now far better possibilities for BP control with po-
tent antihypertensive drugs. Moreover, the poten-
tial of using angiotensin converting enzyme inhibi-
tors to control the effects of high angiotensin-II
levels might replace the questionable need for bi-
lateral nephrectomy in any case.
Peritoneal Dialysis
Maintenance PD30 and continuous ambulatory
peritoneal dialysis (CAPD)33 were effective in as-
cites treatment in six of six cases tried. An ex-
pected initial accelerated protein loss with ag-
gravation of hypoproteinemia seems to be self-lim-
ited in these cases. 30
Laparotomy
Laparotomy performed for reasons unrelated to
ascites resulted occasionally in definitive reversal
16
of ascites. 16 The mechanisms for this phenomenon
are unclear, and it was postulated that in some
cases, total emptying of the abdomen may inter-
rupt a vicious cycle that had previously been
created. 16
Transplantation
Renal transplantation seems to be the most ef-
fective treatment for ascites in ESRD. All twelve
cases reported to have successful kidney transplan-
tation 13-15,17,22,30,31.39 showed resolution of ascites.
In two cases, ascites recurred after loss of kidney
function. 30 ,31 It is of interest that in a patient who
was free of ascites during maintenance HD, tran-
sient ascites developed 3 weeks after successful re-
nal transplantation,71 in association with a moder-
ate reversible impairment of renal function.
DISCUSSION
Chronic ascites without evidence for directly
causative underlying disease is an established
complication of ESRD. Its etiology is not fully un-
derstood. The state of ESRD is associated with dif-
ferent factors that may increase the propensity of
the patients to develop ascites; fluid-overload and
peritoneal membrane changes not necessarily re-
lated to previous PD may be present in patients
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3 _Cinque TJ, Letteri J: Idiopathic ascites-Complication of
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1970
4_ Mahoney JF, Gutch CF, Holmes JH: Intractable ascites in
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GLOCK AND NOLPH
with ascites and play a role in its etiology. Other
factors, such as hypoproteinemia and lymphatic
drainage disturbances, may contribute to its for-
mation. Extensive investigation of ascites occur-
ring in patients with ESRD may provide the
diagnosis of a causative underlying disease in at
least 15% of the cases. It seems, therefore, that an
intensive investigation is necessary before de-
claring that patients have idiopathic ascites. The
presentation of ascites is variable, there being no
truly characteristic clinical or laboratory findings.
Patients with ESRD-ascites represent a higher risk
group with a high mortality rate. Using different
therapeutic modalities, a total reversal or a signifi-
cant reduction of ascites and its associated symp-
toms can be achieved in more than 50 % of the
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