Ultrafiltration Management in Peritoneal Dialysis
Peritoneal Dialysis International, Vol. 20, Suppl. 4
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Copyright © 2000 International Society for Peritoneal Dialysis
Evaluation and Management of Ultrafiltration
Problems in Peritoneal Dialysis
Salim Mujais, Karl Nolph, Ram Gokal, Peter Blake, John Burkart, Gerald Coles,
Yoshindo Kawaguchi, Hideki Kawanishi, Stephen Korbet, Raymond Krediet,
Bengt Lindholm, Dimitrios Oreopoulos, Bengt Rippe, and Rafael Selgas
For the International Society for Peritoneal Dialysis Ad Hoc Committee on
Ultrafiltration Management in Peritoneal Dialysis
Fluid balance management is one of the primary
functions of renal replacement therapy.
Peritoneal dialysis (PD), because of its continuous nature,
has been considered an optimal approach to this
therapeutic goal, avoiding fluctuant volume status and
affording better homeostatic stability (1). This
superior potential of PD has been illustrated in several
studies showing, in discreet patient groups, better blood
pressure control in PD compared to hemodialysis (HD)
(2). This therapeutic advantage, however, has not been
universally utilized and population surveys still show
as high a prevalence of hypertension and
cardiovascular mortality in PD as in HD populations (3_5). While
the latter may be ascribed in both populations to an
inherited disease burden from the pre end-stage
renal disease (ESRD) phase of renal disease, it is clear
that the full potential of PD for optimal volume
homeostasis has remained underutilized (6). Several factors
may be responsible for this underutilization and for the
assumption prevalent among physicians that HD
affords a more effective means of volume control. By its
very nature as a continuous therapy, PD lacks the
dramatic illustration of rapid volume removal observed with
HD. Similarly, by its very nature as a home therapy,
PD lacks the recurrent frequent examination by
physicians/nurses of volume status afforded by
three-times weekly HD, so the opportunities for triggered
interventions are more temporally spaced than in HD.
These two contrasting phenomena (dramatic volume
removal and frequent examination) may also explain why
the concept of "dry weight," a cornerstone clinical
operating indicator in HD, is not widely used in the
approach to volume management in PD. Patients on PD are
routinely instructed to measure their weight on a
daily basis. Guidelines on therapy modifications based on
changes in weight can be safely taught to
Goals of Fluid Management in Residual Renal Therapy
In HD, the replacement of the volume
homeostatic function of the native kidney is done by rapid
removal of accumulated fluid to a target weight ("dry
weight") that errs conceptually on the side of mild
intravascular hypovolemia (7,8). This is done under the
presumption that subsequent fluid accumulation is
unavoidable in the interdialytic interval, and
hence such mild intravascular hypovolemia
safeguards against dangerous hypervolemic deviations. The
usual homeostatic profile of a HD patient is to travel
from a state of mild intravascular hypovolemia
immediately after a dialysis session to mild/moderate
hypervolemia immediately before the next dialysis
session (7,8). The goal of attaining "dry weight" is to
position the patient in a homeostatic safety state where
the inevitable fluid accumulation is handled safely. In
HD, the correspondence between "dry weight" and
euvolemia is at best approximate, and in most clinical
situations "dry weight" is determined empirically
by clinical skill and trial and error. This absence of
rigor in the prevalent clinical approach has been
blamed for the persistence of volume-related
complications in HD patients; hence the proliferation of
experimental, clinical remedial approaches (7,8). A variety
of volume markers have been proposed for use,
varying from hormonal measurements (ANP, cGMP,
renin, etc.), to vena cava diameter by ultrasonographic
techniques, to bioimpedance measurements (7,8).
While initial descriptions are uniformly promising,
wider application frequently uncovers the proverbial
"initial description bias." Further, logistic burdens
have limited the wide and repetitive use of these
techniques in clinical practice. Another variant of this
approach is the proliferation of volume removal indicators for
use during dialysis. Despite initial enthusiasm
for their use (and imminent universal availability in
new hardware), these devices seem to be succumbing
to the inevitable life cycle of any new methodology
(7,8). In the majority of HD patients, "dry weight"
remains a goal defined by clinical criteria.
In PD patients attainment of target weight
has been based on clinical indicators. The continuous
nature of PD precludes the need for anticipatory,
relative intravascular hypovolemia; hence the need
to avoid the concept of "dry weight" and its
replacement in PD by "target weight" or "desired weight."
The avoidance of intermittent intravascular
hypovolemia and its attendant complications has been
considered to play an important role in the better
preservation of renal function in PD patients compared to HD
patients (9). Nevertheless, there is a need for a
more rigorous approach to the definition and the
evaluation of a target weight. For practical reasons, the
definition of target weight and its continuous
evaluation need to be addressed clinically. Further, it should
be stressed that the determination of a target
weight in a particular patient needs to be a dynamic
continuous process taking into account changes due
to nutritional status and cardiovascular profile
that may occur over time.
Attainment of an edema-free state is a readily
acceptable and definable target. It should be
recognized, however, that because of the limitations inherent
in clinical evaluations, an edema-free state is not
synonymous with euvolemia. Significant fluid
overload can be present in the absence of clinically
detectable signs. The desirable target weight in a PD
patient should ideally be that weight at which the patient
is euvolemic. However, as discussed above, clinical
determinations of euvolemia are at best
approximate. There is a need then to base the clinically
workable definition of target weight on exclusion clauses
explored in a dynamic clinical process. Hence, the
target weight that best approaches euvolemia is
that weight at which the patient is clinically
edema-free and below which undesirable clinical signs and
symptoms of hypovolemia occur (hypotension, cramp,
etc.). Reliance on clinical symptoms is less misleading
in PD than it would be in HD. In the latter, clinical
symptoms may appear when total extracellular fluid
volume is still abnormally high because of the
rapidity of fluid removal from the intravascular
compartment. In PD, however, the gradual nature of fluid
removal facilitates a concordance between intravascular
and total extracellular volume changes. This definition
implies that weight reduction needs to be pursued
beyond the edema-free state. It also implies that
the occurrence of undesirable clinical signs and
symptoms during the process of fluid removal before the
attainment of edema-free state is not sufficient.
To illustrate these two exclusion clauses, it is
useful to consider the hypertensive patient.
Attainment of clinically edema-free status does not guarantee
that the volume-dependent component of the
hypertensive state has been corrected. The edema-free state
can be considered the necessary but not sufficient
minimum bracket of desirable weight. Undesirable
clinical signs and symptoms can then be viewed as
the ceiling or upper bracket for fluid removal. The
weight range between these two brackets is highly
variable in individual patients. In a few clinical situations,
the relation between these two brackets is complex.
Patients with baseline hypotension, or patients
with underlying autonomic insufficiency may cross
the symptomatic threshold long before they are
edema free, hence the need for flexibility and deliberate
individualization of the approach to fluid removal.
In the absence of validated readily applicable
indicators of volume status, reliance on clinical judgement
remains the physician's best guide.
The changing nature of target weight needs to
be emphasized. Fluctuations in weight secondary to changes in lean body mass or fat do occur, and
re-evaluation of target weight at regular intervals
is necessary, guided by changes in nutrition and
- A systematic and thorough evaluation of fluid management should be considered a cornerstone of dialytic therapy. The routine monitoring and evaluation of volume status should be considered a necessary component of dialysis prescription and adequacy. Assessment, achievement, and maintenance of target weight are essential, with the aim of maintaining normotension with euvolemia. Regular assessment (annually, but more frequently if clinically indicated) of peritoneal function [modified peritoneal equilibration test (PET)], residual renal function, and solute clearance is essential.
- In the absence of validated readily applicable indicators of volume status, reliance on clinical judgment remains the physician's best guide.
Guidelines for Fluid Management in Peritoneal Dialysis
General guidelines on fluid management in
PD patients are summarized in Table 1. Routine
standardized monitoring and evaluation of volume
status should be considered a necessary component
of dialysis prescription and dialysis adequacy. The
appropriateness of a patient's body weight has to
be judged from two essential standpoints: the
nutritional and the cardiovascular. Control of the volume
component of hypertension, for example, needs to be titrated,
patiently taking into account the need to balance
volume removal with antihypertensive dosing. The
importance of dietary counseling cannot be overemphasized. The general assumption that
patients on PD tolerate greater dietary salt and
fluid indiscretion should not be construed as an
endorsement for such indiscretion (10). Tepid indifference
that allows patients to hover close to mild edema may
have pernicious long-term consequences (3). It is
recognized that dietary interventions are the hardest to
implement because they involve an elaborate process of
education and lifestyle modification.
- Routine standardized monitoring including awareness of peritoneal equilibration test status
- Dietary counseling concerning appropriate salt and water intake
- Protection of residual renal function
- Loop diuretics if residual renal function present
- Enhanced compliance via education
- Preservation of peritoneal membrane function
- Hyperglycemia control
Residual renal function (RRF) plays an
important role in both small solute adequacy and volume
control. The protective zeal that has become a
cornerstone of nephrologic management in the
pre-ESRD phase needs to be sustained after initiation of
dialysis. This is particularly important in the context
of the new directions in dialysis initiation where
patients are started on dialytic therapy at higher levels of
RRF than previously (11).
Attention to the nephrotoxic potential of
over-the-counter medications should become a component
of regular patient interviews. Further, the use of
aminoglycosides in the management of peritonitis
should be limited to cases where no safer effective
alternative is available. Protection from the nephrotoxic
potential of contrast agents is limited by the
obvious inability to use hydration methods. The promise
of adenosine antagonists (e.g., aminophylline) has
not been explored in this population and may be
considered by inference until tested. Urine volume can
be successfully increased even in advanced renal
failure by the use of large doses of loop diuretics,
alone or in combination with thiazides (12). While
these agents do not help preserve RRF, they do
increase urine output. Concern over potential ototoxicity
finds its origin in experience with large intravenous
doses. Oral administration seems not to carry the same
risk. As with all other aspects of therapy, success is
dependent on the patient's collaboration, which is
usually enhanced by continuing education and positive
re-enforcement. In cases of failure of a therapeutic
approach, it is always useful to ponder whether the
failure is due to the inappropriateness of the
regimen, the overwhelming effect of underlying pathology,
or the noncompliance of the patient.
Finally, because ultrafiltration (UF) is
dependent on the glucose gradient across the peritoneal
membrane, systemic hyperglycemia can interfere with
fluid removal by reducing the gradient. The effects of
hyperglycemia on thirst and excessive fluid intake
need to be considered as well.
Fluid removal in PD follows principles that
are detailed in the accompanying review by
Krediet, Lindholm, and Rippe. Table 2 summarizes a few
of the clinical guidelines useful in designing PD
prescriptions for optimal fluid removal. The most
frequently ignored principles are the need to avoid long
dwells in high transporters, and balancing glucose
concentration and dwell time (13).
Guidelines for Improved Fluid Removal in Peritoneal Dialysis (PD)
- Avoidance of long dwells with low glucose concentrations
- Use of nighttime exchange device
- Tailoring prescription to transport profile determined by peritoneal equilibration test
- Avoidance of long dwells with low glucose concentrations
- Use of short day dwells even when no additional exchange is needed for clearance
- Adherence to sound physiologic principles in the design and implementation of PD prescriptions is essential to prevent the emergence of fluid overload. The most frequently ignored principles in PD that lead to UF difficulties, are the need to avoid long dwells in high transporters, and balancing glucose concentration and dwell time. Prescription setting must take these into account.
Diagnostic Approach to Fluid Balance Problems
Definition of the Clinical Syndrome
Figure 1 Timeline of evaluation of fluid overload syndrome is depicted.
A structured diagnostic approach to the
evaluation of suspected UF problems is presented in
Figure 1. Patients presenting with the clinical
syndrome of inability to maintain target weight and
edema-free state need to be carefully evaluated according to
the diagnostic process described below, prior to being
labeled "ultrafiltration failure" (14_21). Indeed,
there is a need for circumspection in the utilization of
clinical labels in the absence of thorough delineation
of causation. The term "ultrafiltration failure" has
been liberally assigned in the past to cases where the
main fault may have been either with the prescription
or with the patient's nonadherence to clinical
directives. Deficiency in tailoring PD prescription to
transport type as determined by PET can readily lead to
failure in fluid removal that should not be blamed on
the therapy, but rather on its application. Low
dialysate glucose concentrations and long dwell times will
inevitably lead to inadequate fluid removal in
patients with high transport profile. The need for precision
in clinical labeling can be illustrated by the
following example: Low small solute clearance because of
inappropriately small fill volumes cannot be labeled
"clearance failure." Similarly, low clearance because of
a high residual peritoneal fluid volume from a
malfunctioning catheter is also not "clearance failure." A
parallel rigor in definition is required for fluid
removal and, in the same vein, the concept of adequacy
should be expanded to include fluid balance.
Initial Evaluation of Clinical Syndrome
In the workup of the syndrome of inability to
maintain target weight and edema-free state, it is
important to consider the multitude of factors that can
alter fluid balance (Figure 2) (20,21). The clinical
history may readily disclose the probable causation,
which can then be pursued with definitive diagnostic
testing. A history of noncompliance with either
dietary advice or PD prescription may direct the
evaluation to more interventional pathways and preclude
the need for expensive and tedious diagnostic
workup. Understandably, the detection and resolution of
patient noncompliance are not easy tasks. Parallel
evidence for noncompliance in other aspects of the therapy, or generalized evidence for nonadequacy
of the therapy may be helpful. Concomitant small
solute inadequacy and inadequate fluid removal are rarely due to true peritoneal membrane
pathology. The clinical profile of the syndrome is also
helpful when it is associated with a persistent reduction
in drain volume. Reductions in drain volume due to
mechanical problems have a more acute
presentation (22). A positional dialysate flow suggests a
malpositioned catheter, whereas sluggish outflow
(and/or inflow) may result from a partially obstructed or
entrapped catheter. Findings of edema localized to
the abdomen or inguinal area on clinical
examination can be important clues to the presence of a
Figure 2 Categories and possible etiologies of reversible causes of fluid overload are depicted.
At the time of the initial office evaluation, a
quick "fill and drain" with 2 L dialysate is beneficial in
order to directly observe the nature and rate of inflow
and outflow. The presence of fibrin clots may explain
abnormalities with flow that reduce the efficiency
of drainage and volume removal, and can often be
resolved with intraperitoneal heparin. If
incomplete drainage or positional drainage is observed, a
flat-plate radiograph of the abdomen will assess the
possibility of a malpositioned catheter. When an entrapped catheter or peritoneal leak is
suspected, peritoneography or peritoneal computerized
tomography (Tables 3 and 4) are valuable in their
diagnosis (23_26). It is extremely important to
communicate to the radiologist the purpose of any
radiographic procedure used in assessing problems with PD, as
well as personally reviewing the radiograph(s).
- Take flat-plate radiogram of the abdomen.
- Place 100 _ 200 mL of nonionic contrast in dialysate (2L bag).
- Infuse 1 _ 2 L dialysate into the supine patient.
- Have the patient change positions for mixing.
- Repeat flat-plate radiogram of the abdomen.
Dialysate Leaks: Dialysate leaks from the
abdominal cavity result in a decrease in drain volume
and net fluid removal. In the case of external leaks,
the impact is greater on drain volume. In leaks into
the abdominal wall or pleural space, net fluid removal
is diminished either because of reabsorption from
the interstitial spaces or sequestration in the
pleural space. Leaks into the interstitial space are
commonly accompanied by abdominal wall edema with or
without genital edema. Leaks can occur at anytime
but are often seen after being on PD for several
months (>4 _ 6 months) and usually occur at the catheter
insertion site, but can also be associated with an
abdominal wall hernia or a history of multiple abdominal
surgeries (23,24,27). Localized abdominal wall
edema or subcutaneous fluid collections are often
evident. Diagnosis is confirmed by utilizing radiographic
techniques that include intraperitoneal infusion of a
dialysis solution in which radiographic contrast
has been added (with computed tomography)
(Table 4), or through the intraperitoneal infusion of
radioisotope with peritoneal scintigraphy (23_26, 28_31).
Peritoneal Computerized Tomography (CT)
- Take plain CT of abdomen.
- Place 100 _ 200 mL nonionic contrast in dialysate (2L bag).
- Infuse 1 _ 2 L dialysate into the supine patient.
- Have the patient change positions for mixing.
- Ambulate the patient for 30 minutes.
- Repeat CT of abdomen at 1 and 4 hours post instillation. Cuts through the pelvic floor and genitalia need to be obtained.
Peritoneal membrane function is not
compromised and therefore peritoneal transport as evaluated
by the PET is not changed compared to baseline, but
the secondary increase in lymphatic absorption leads
to reduced fluid removal. Leaks associated with
hernias usually require surgical repair and a temporary
transfer to HD until adequate healing has occurred.
Leaks occurring in the absence of a hernia usually
represent a tear in the parietal peritoneum. In this
situation there is frequently a history of
multiple abdominal surgeries, pregnancies, recent
corticosteroid usage, or abdominal straining (coughing,
Valsalva maneuver). Small leaks may respond to
peritoneal rest with HD support or the use of intermittent
PD without the need for surgical repair. Recurrence
may require surgical repair (27).
Catheter Problems: Catheter-related problems
contributing to poor drain volumes include
obstruction, entrapment, or malposition. Catheter obstruction,
either partial or complete, often results from fibrin
plugs or buildup within the catheter lumen, but can be
due to omentum obstructing the catheter ports, or even
a kinked catheter. These lead to sluggish or
intermittent inflow/outflow of dialysate and thus alter
the efficiency of fluid removal. Fibrin strands seen in the
dialysate should raise suspicion of the problem,
but the diagnosis is otherwise one of exclusion
because radiographic evaluation is generally not helpful
except in identifying kinked catheters. Treatment
consists of aggressive "flushing" of the catheter with
a dialysate-filled syringe and, if this is
unsuccessful, the use of fibrinolytic agents when fibrin-related
occlusion is suspected.
The intra-abdominal portion of the catheter
may become "entrapped" in a compartment formed by
adhesions. This can lead to a reduction in
intraperitoneal capacity resulting in pain on inflow once
the compartment volume has been surpassed. With
the use of peritoneography (Table 3) the compartment
can be demonstrated. Treatment may be attained
with surgical lysis of the adhesions if they are not
Catheter malposition may occur because of
improper placement, but it often results from
migration of catheters originally in good position (32).
A malpositioned catheter has positional outflow
and does not drain the peritoneal cavity effectively,
leading to an increase in residual volume. A normal
residual volume (R) is approximately 200 _ 250 mL
(33) and can be measured from information obtained
during the PET using the following equation:
R = Vin(S3 _
S2)/(S1 _ S3)
where Vin = instillation volume,
S1 = solute concentration (urea or creatinine) in the pretest drain,
S2 = solute concentration of the instilled fluid (0 for
urea or creatinine), and S3 = solute concentration
immediately following instillation (33). An increase in
residual volume dilutes the glucose concentration
in freshly instilled dialysate. The effect is usually
less than 10%. This decreases the osmotic gradient
and thus reduces the rate of transcapillary UF
without any significant effect on solute transport. Net UF
is decreased while the dialysate-to-plasma (D/P)
creatinine ratio remains essentially unchanged. An
increase in the calculated residual volume should
raise the suspicion of a malpositioned catheter.
However, the presence of this problem is often clinically
apparent and the diagnosis is easily made with the aid
of simple radiographic techniques (flat-plate of the
abdomen) because PD catheters have radiopaque material imbedded within.
- In the evaluation of the causes of fluid overload, screening for reversible causes such as dietary indiscretion and noncompliance, problems in prescription design, and mechanical problems is imperative. These factors may account for a large proportion of causes of fluid overload.
Evaluation of Peritoneal Membrane Function
Figure 3 Components of the evaluation of peritoneal membrane function are depicted.
The exclusion of rapidly resolvable causes of
impaired fluid removal has diagnostic and
therapeutic advantages. The causes discussed above can be
frequently resolved with standard therapeutic approaches and the clinical syndrome hence
resolved. Streamlining of the diagnostic approach is also
aided by exclusion of mechanical causes. The next
diagnostic step is to evaluate the UF and transport
functions of the peritoneal membrane (Figure 3).
Traditionally, peritoneal membrane function
has been assessed by the PET. The PET has been
standardized both procedurally and interpretably to
classify membrane function (33). It is directed,
however, primarily at small solute clearance and, although
UF capacity is closely linked to the latter, the current
PET has not addressed the issue of quantifying
pathologic variations in UF. For the purposes of diagnosing
presence and causation of impaired fluid removal, the
required test is one which will (1) measure UF
under optimal conditions (to avoid false positive
results), (2) evaluate small solute transport to aid in
defining causation, and (3) have validated criteria that
correlate with clinical behavior (to avoid both false
negative and false positive results). Regrettably, a
fully validated test that satisfies all the above criteria
is not currently available and efforts to develop it
and standardize it are urgently required. The current
PET does provide a thorough evaluation of small
solute transport, but because of the modest osmotic
challenge of the 2.5%/2.27% dextrose concentration
utilized in the test, the osmotic drive for UF is
not optimal. Further, the normal ranges for UF
volume expected for each transport category have not
been fully defined nor have they been validated
against clinical behavior.
A modification of the standard PET introduced
by Krediet and his colleagues (34,35) offers a
reasonable alternative, albeit with remaining shortcomings.
The modification consists of replacing the 2.5%/2.27%
dextrose solution of the standard PET with a
4.25%/3.86% dextrose solution, thereby satisfying the criterion
of maximal osmotic drive defined above as required
for proper evaluation of UF capacity. A value of less
than 400 mL net UF in a 4-hour dwell correlates well
with clinical behavior and avoids any false positive results.
An additional advantage of this approach is that
it allows for determination of sodium sieving by
profiling the changes in dialysate Na+ concentration
induced by osmotically driven water flow. Because
water influx into the peritoneal cavity is mediated in
part by aquaporins, the enhanced osmotic drive will
draw water into the peritoneal cavity, thereby diluting
the Na+ concentration. The greater the influx of
water via aquaporins, the greater the decline in
dialysate Na+. Impaired aquaporin-mediated water
transport will lead to obliteration of the decline in dialysate
Na+. Hence, measurement of
Na+ sieving will allow better diagnostic discrimination of the causes of
impaired UF. The major limitation of this modification of
the standard PET is that its characterization of
small solute transport has not been fully examined and
related to the results of the standard PET with
2.5%/2.27%. A few studies have compared the
creatinine profile with 1.5%/1.36% and 4.25%/3.86% and
found no difference in D/P creatinine (36,37). Further,
preliminary results in 47 patients studied with both
2.5%/2.27% and 4.25%/3.86% reveals no major
discrepancies in patient allocation to different transport
groups on the basis of D/P creatinine (Burkhart
et al., unpublished observations). For the purpose of the
diagnostic endeavor at hand, the use of the modified
PET appears adequate.
Discrimination by UF
Response: Subsequent to initial exclusion of mechanical, compliance,
dietary, and other relevant clinical causes of impaired
fluid removal, and the limitations of the modified
PET (4.25%/3.86% dialysate dwell) notwithstanding,
the patient needs to undergo an evaluation of UF
response (Figure 4). The details of the test are
summarized in Table 5.
Modified Peritoneal Equilibration Test (4.25% Dextrose)
- On the evening prior to the test, the patient should perform a standard CAPD 8- to 12-hour overnight dwell.
- With the patient upright, drain the overnight dwell over 20 minutes and note volume drained. Save sample for creatinine and glucose to allow for determination of residual volume.
- With the patient supine, infuse 2.0 L 4.25% dialysis solution over 10 minutes. The patient should roll from side to side after each 400 mL of solution is infused.
- Note time the infusion is complete: this is the "zero hour" dwell time.
- At 0-hour, 1-hour, and 2-hour dwell times:
- Drain 200 mL effluent into bag.
- Mix bag by inverting 2 _ 3 times.
- Using aseptic technique, draw a 10 mL sample from medication port.
- Reinfuse the 190 mL of effluent into the patient.
- Transfer 10 mL sample to red-top tube and label appropriately.
- At 2-hour dwell time, draw blood sample for creatinine, sodium, and glucose measurements.
- At 4-hour dwell time:
- With patient upright, drain exchange over 20 minutes.
- Mix bag by inverting 2 _ 3 times.
- Using aseptic technique, draw a 10 mL sample from medication port.
- Measure and record volume drained.
- Transfer 10 mL sample to red-top tube and label appropriately.
- Send all effluent samples and one blood sample to laboratory for creatinine, sodium, and glucose measurements.
As can be gleaned from the detail of the test,
both fluid removal and small solute profiles are
obtained during the test. The former is the primary
discriminating measurement, and determination of
small solute profile becomes relevant only if fluid
removal is deemed abnormal. The rationale of sampling
for small solute profile in the test in parallel with
UF assessment, and prior to determination of fluid
removal adequacy, is to have at hand the means to
proceed with the diagnostic workup without the need
to subject the patient to further testing.
The primary intent of the test is to quantify
net UF in response to a 4.25%/3.86% dextrose
dialysis solution challenge. If net UF is greater than
400 mL/4 hours (drain volume greater than 2400 mL/4
hours), the subsequent diagnostic sequence needs to focus
on the following possible etiologies: (1) dietary
indiscretion or dialysis noncompliance, (2) inappropriate
prescription, and (3) recent loss of RRF for which
no adjustments were made in prescription. In effect,
a net UF greater than 400 mL/4 hours (a drain volume
greater than 2400 mL/4 hours) effectively rules
out any alterations in peritoneal functional
parameters as responsible for the inadequate fluid removal
and the ensuing clinical syndrome. If net UF is less
than 400 mL/4 hours (drain volume lower than
2400 mL/4 hours), the subsequent diagnostic sequence is
dependent on an examination of the results of small
solute profile measurement. Once it has been
determined that net UF is lower than the discriminatory
value, then the samples obtained during the test can be
assayed for small solute concentrations. When using
the values for net UF or drain volume indicated
above, the physician should keep in mind the possibility
of overfill of dialysis bags, which may be in the order
of 50 mL, and account for this volume in their
evaluation of the observed response.
A similar approach may be followed using a
standard PET with 2.5%/2.27% dialysate dextrose
with the following caveats: (1) since the osmotic
challenge is not maximal, there is a potential for false
positive results; (2) the discriminatory value is adjusted
downward to 100 mL/4 hours of net UF (2100 mL/4
hours drain volume). Further, if the standard PET is to
be used, no 4.25%/3.86% dextrose dialysate could
have been used immediately prior to the test. There is
no immediately obvious reason why a standard PET
is to be used in this diagnostic sequence, except the
remote possibilities of unavailable proper
concentration of dialysate test solutions or human error. In the
latter case, the results of the test can still be
interpreted based on the above caveats, and the patient is
not subjected to additional testing. Nevertheless, it is
the recommendation of the committee, based on the
argument of the need to maximize osmotic
challenge, that the 4.25%/3.86% dextrose PET be used in
Figure 4 Evaluation method of the ultrafiltration response is depicted.
Discrimination by Small-Solute Transport
Characteristics: The peritoneal conditions that would
result in a drain volume of less than 2400 mL/4
hours can be separated by examination of the small
solute characteristics (Figure 5). In the following
discussion, three categories based on D/P creatinine need to
be considered: high transporters, low transporters,
and high-average and low-average transporters. The
overall separation into these three categories is based
on creatinine and glucose handling and follows
standard values with which physicians are familiar. In a
few cases, however, the profile of Na+ handling
becomes crucial and this will be discussed where relevant.
Figure 5 Categories and possible etiologies for an impaired ultrafiltration response are depicted.
Several alternatives can be considered for
patient classification by small solute characteristics. In
patients who have had a recent standard PET
(within 3 months of current evaluation), there is no need
to repeat the profiling; the previously determined
profile would suffice if no intervening peritonitis has
occurred. In most other patients, a renewed
evaluation of small solute transport may be in order. As
discussed above, a small solute profile obtained during the
modified PET with 4.25%/3.86% dextrose can
substitute for a repeat standard PET. The conditions
discussed below may coexist in the same patient. While this
may be rare, it is important nevertheless to recognize the
possibility, particularly when diagnostic findings
are mixed. Adherence to a systematic diagnostic
approach will usually help resolve the issue. Finally, this
classification for purposes of clarity and precision
diverges from previous approaches that categorized
patients as having type I or type II or type III
"ultrafiltration failure." While the previous categories are
included in the following discourse, it is preferable to
abandon the old nomenclature and adopt the more
descriptive terms utilized herein.
- Evaluation of peritoneal membrane-related causes of fluid overload requires adherence to a structured diagnostic framework. The first step involves evaluation of the UF response to an effective osmotic challenge. The second step refines the diagnostic approach with an evaluation of small solute transport profile.
- Evaluation of peritoneal membrane function in this context is best performed with a modified PET utilizing 4.25%/3.86% glucose. In effect, a net UF greater than 400 mL/4 hours (a drain volume greater than 2400 mL/4 hours) effectively rules out any alterations in peritoneal functional parameters as responsible for the inadequate fluid removal and the ensuing clinical syndrome.
Low Drain Volume and High Transport:
Patients with a low drain volume (<2400 mL/4 hours with
a 4.25%/3.86% modified PET) and D/P creatinine greater than 0.81 likely represent the largest
group of patients with inadequate filtration due to
peritoneal membrane characteristics. These patients
fall into 3 groups: (1) patients with an inherent
high small-solute transport profile at initiation of
dialysis, (2) patients with peritonitis, and (3) patients
who develop a high transport profile in the course of
long-term PD. These patients tend to have good low
molecular weight solute transport, but have poor UF
during standard CAPD or continuous cycling PD
using glucose-containing dialysate, due to rapid
absorption of glucose and dissipation of the osmotic gradient.
If their dwell times are mismatched for their
membrane transport characteristics, they often appear to
have inadequate UF as they lose RRF and no longer
have urine flow to supplement net daily peritoneal
Inherent high transport: Ten percent of
patients starting PD display this transport profile. This
proportion appears to be constant in various
population groups (Table 6) and stable over medium periods
of observation (38). Patients in this group have very
efficient membranes for small solute clearance but
may have difficulty in UF, particularly in long dwell
cycles. These patients are at risk of high protein losses
in the peritoneum. A high level of technique failure
has been described on CAPD therapy, likely related to
fluid management. Retrospective analysis also
suggests higher mortality in this group (39_41). These
patients typically do well on CAPD until residual renal
volume decreases, at which time it may become
difficult to maintain euvolemia and blood pressure control
on standard CAPD with glucose-containing
solutions. Automated peritoneal dialysis (APD) and
icodextrin for the long dwell are recommended therapeutic
approaches in this group (see below).
Proportion of Peritoneal Equilibration Test Profiles in Different Populations
|High average (%)||53||44||36||46
|Low average (%)||31||28||35||33
Recent peritonitis: It is a common clinical
experience for PD patients to experience fluid retention
during episodes of peritonitis (42_45). These
patients often need a temporary change in their standard
dialysis prescription (shorter dwell times,
increased tonicity of fluids, or use of icodextrin) to achieve
net UF. When compared to baseline, PET data during peritonitis reveal an increase in the D/P
ratio for creatinine and a decrease in the
D/D0 ratio for glucose. There is also an increase in protein losses and a
significant decrease in net UF. These clinical and
physiological changes associated with peritonitis
are usually reversible and, after recovery from the
episode, membrane transport usually returns to
baseline. Several studies have indicated that UF during
an episode of peritonitis can be satisfactorily
achieved with the use of icodextrin (46).
High transport during long-term PD: An
increase in small solute transport during the course of
long-term therapy on PD is thought to be due to an
increase in peritoneal membrane functional surface area (47_52). This process is diagnosed in
patients whose D/P creatinine at 4 hours on PET changes
from baseline. Peritoneal equilibration testing confirms
an increase in D/P ratio for creatinine, a decrease in
the D/D0 ratio for glucose, and a smaller than usual
decrease in dialysate Na+ during the dwell. In
contrast to the situation seen with peritonitis, where
transport changes are usually transient and protein
losses are increased, the small solute transport changes
in this group tend to be permanent and protein
mass transport does not change. It is often easy to
maintain minimal total solute clearance goals in
these patients despite a tendency toward clinical
This was originally described with
acetate-containing dialysis solutions (14,53) but has also been
seen in patients who have only used
lactate-containing dialysis. A history of recurrent peritonitis and
extensive use of hypertonic exchanges has been
observed in some, but not all studies. The incidence seems
to increase with time on PD, implicating repeated
exposure of the peritoneum to dialysis solution as a
The natural history of peritoneal membrane
transport over time has been debated (38,52,54_58),
due mainly to noncomparability of the methods used.
A small number of studies used standardized 4hour dwell evaluations with examination of both UF
and solute transport, while a larger number utilized
clearance monitoring. The latter may mask opposing
directional changes in solute and fluid transport.
The potential increase in solute clearance due to an
increase in D/P creatinine may be masked by the potential decline due to lower UF. The emerging
picture, however, is that during long-term
observations (greater than 2 years) some degree of increase in
D/P creatinine does occur in patients on PD.
- For patients with net UF less than 400 mL/4 hours and a high transport profile of small solute clearance, APD and icodextrin for the long dwell are the recommended therapeutic approaches. This profile can also be seen during peritonitis and several studies have indicated that UF during an episode of peritonitis can be satisfactorily achieved with the use of icodextrin.
Low Drain Volume and Low Transport: This
combination of low drain volume in the face of
adequate osmotic challenge and low small-solute transport
is very rare and reflects a major disruption of the
peritoneal membrane and/or intraperitoneal fluid
distribution (59,60). It is usually due to adhesions,
and the functional consequences may be related to
fluid trapping in small spaces. Peritoneography may
be helpful in making the diagnosis by identifying
sequestered spaces. Poor UF in association with
low transport is reported to occur in advanced stages
of sclerosing peritonitis (60,61). It is important,
however, to realize that a high transport rate has
also been described prior to a diagnosis of sclerosing
peritonitis (60_62). Unfortunately, no large
prospective study of fluid problems in PD patients has been
performed, so it is not possible to state how often
UF failure, together with low transport, occurs.
Because this condition results in both inadequate volume
and inadequate solute removal, transfer to HD is
required for adequate patient management (19) unless patients have some degree of RRF.
Management of anuric patients in this category may be
difficult by PD.
A caveat on the diagnostic criteria is in order:
Patients with underlying low transport rate and
leaks or mechanical problems or high lymphatic/tissue
reabsorption may also present with the composite
picture of low drain volume and low small-solute transport. It is therefore important to exclude
these latter causes before accepting low transport as
the reason for the difficulty with peritoneal
- Patients who are functionally anephric and with net UF less than 400 mL/4 hours, and a low transport profile of small solute clearance have both inadequate volume and inadequate solute removal. Transfer to HD may be required for adequate patient management. Functionally anephric patients in this category often cannot be managed by PD. However, if some degree of RRF is present, maintenance on this dialytic modality may be feasible.
Low Drain Volume and High-Average or
Low-Average Transport: A low drain volume coupled
with high-average or low-average transport can result
from four possible etiologies: (1) mechanical
problems, (2) lymphatic reabsorption and/or (3) tissue
reabsorption, and (4) aquaporin deficiency.
Mechanical problems: The above profile of UF
and small solute transport results should invite a
reconsideration of mechanical problems as a cause of
the inadequate volume removal. This is particularly
true in patients in whom the workup for mechanical
problems was cursory or not entertained in the
initial evaluation. This possibility need not be considered
if the initial evaluation was rigorous and
mechanical problems were fully excluded.
Lymphatic reabsorption and/or tissue
reabsorption: Increased lymphatic absorption (or overall
peritoneal tissue reabsorption) can lead to a low drain
volume despite adequate response to an osmotic
challenge (63,64). Since enhanced lymphatic reabsorption
is ongoing, the response to the osmotic challenge is
obscured if one relies solely on final drain volume
or even on peritoneal volume. Lymphatic absorption
of peritoneal fluid negatively influences the overall
removal of water (decreases net UF) and solute
(partially negating the effect of diffusive and
convective solute transport). Since the absorption of
peritoneal fluid by lymphatics does not alter the
concentration of solutes in the dialysate, the D/P creatinine
ratio remains unchanged with increased lymphatic
flow, even though net UF can be significantly decreased.
The relative contribution by increased
lymphatic/tissue reabsorption to fluid removal problems has
not been definitively established. Proper assessment
of frequency of the condition will require further
work. Impaired net UF associated with the
disappearance of macromolecules administered intraperitoneally
was found in 2 of the 9 patients with UF failure
described by Heimbürger et al. (17). Krediet and his group
(35) found a dextran disappearance rate exceeding
2 mL/min in 7 of 19 patients with inadequate UF (net
UF < 400 mL/4 hours on 4.25%/3.86% glucose), often
in combination with the presence of a large
peritoneal surface area. Up to now, no evidence is present
suggesting that the prevalence of this cause of
impaired peritoneal fluid removal would increase with the
duration of PD.
Definitive proof of the condition requires
identification of high macromolecule clearance from the
peritoneal cavity (65,66). In the absence of such a
test, the diagnosis is made by exclusion of mechanical
catheter problems, aquaporin deficiency, and
increased hydraulic conductance. The rate of lymphatic
absorption is estimated by measuring the disappearance
of macromolecules, such as albumin or dextran 70,
from the peritoneal cavity (molecules too large for
transcapillary transfer by either diffusion or
convection). As described by Pannekeet et
al. (34), this can be done by adding 1 g dextran 70 per liter to a
2-L, 4hour, 4.25%/3.86% dextrose dwell. The
dialysate would be sampled at 0, 10, 20, 30, 60, 120, 180,
and 240 minutes and the lymphatic or tissue
resorption rate of dialysate would be calculated from the
dextran clearance from the peritoneal cavity.
Measurement of lymphatic flow is uncommon
in clinical practice due to the complexity of the
procedure. Since transcapillary UF is essentially
normal in this situation, osmotically-mediated water
transport into the intraperitoneal cavity results in the
normal dilution of the Na+ concentration of the
dialysate. (Because the sieving coefficient for
Na+ is < 1.0, the Na+ concentration in ultrafiltrate is less than that
of serum, leading to an increase in intraperitoneal
Na+-free water which dilutes the initial dialysis
solution Na+ concentration.) A 2 _ 4 mEq/L decrease in
the dialysate Na+ concentration will normally be
observed within 2 hours of a 2-L, 2.5%/2.27% dextrose
dialysate dwell (this decrease in Na+ concentration can
be augmented by the use of 4.25%/3.86% dialysate),
and has been used as indirect evidence of normal transcapillary UF. In patients with reduced net
UF secondary to increased lymphatic absorption, the
normal decline in Na+ concentration is maintained.
Aquaporin deficiency: This is a relatively rare
condition and only a small number of cases with
proven diagnosis have been reported (67).
Nevertheless, greater awareness and a more systematic
evaluation may allow a more precise determination of
its true prevalence. Further, this condition offers a
very interesting model for understanding
peritoneal transport and its alteration by pathologic states.
The peritoneal capillary membrane is not freely
permeable to solutes, but is a highly selective barrier
with the ability to impede diffusion and convection of
relatively small molecules while restricting large
macromolecules, but to a lesser degree than
standard HD membranes. This suggests that peritoneal
capillaries contain populations of various sized
"pores" that alter solute transport. This has led, through
computer simulations (68_74) and animal work
(75_77), to the "three-pore theory" of water and solute
transport across the peritoneal membrane (mainly
transcapillary movement of solute and fluid). This
theory proposed three populations of pores: a large
number of transcellular pores (radius 4 _ 5 Å), a large
number of small pores (40 _ 50 Å), and a small number
of large pores (200 _ 300 Å). This theory predicted
that 40% _ 50% of the total ultrafiltrate is
obtained through this transcellular path, and therefore
will be solute free when driven by an
osmotic-pressure differential. Animal work and indirect human
research has strongly pointed to aquaporins 1 and 3
being the water-channel transcellular pores
(ultrasmall pores). Aquaporin has been demonstrated
by in situ techniques to be present in the human
peritoneal capillary endothelium and mesothelium (78,79). The small pores are also involved in
water transport through colloid osmosis and
hydrostatic pressures that are in balance; these are also the
pores through which most of the small solute
transport occurs. Aquaporin deficiency is that situation
where there is damage to or a diminished number of
water-channel ultrasmall pores, which can lead to
deficient crystalloid-induced UF. There are few reports of
isolated aquaporin-mediated loss of UF, but it is
possible for this to occur (67,80).
Various indirect methods can be applied in
clinical practice to estimate the magnitude of
aquaporin-mediated water transport. The so-called sieving of
Na+ is the simplest one. The dialysate concentration of
Na+ decreases during the initial phase of a dialysis
dwell using a hypertonic glucose solution (4.25%/3.86%
glucose) (36,67,81_83). The minimum value is
usually reached after 30 _ 60 minutes. It is likely that
the dissociation between the transport of
Na+ and that of water is caused by aquaporin-mediated water
transport. Consequently, the magnitude of the dip
in D/P Na+ provides information on
channel-mediated water transport. However, in situations of a large
vascular surface area, the diffusion and/or convection
of Na+ from the circulation to dialysate through
small pores will also increase, thereby blunting the
decrease of D/P Na+.
Another simple way to assess
aquaporin-mediated transport is to calculate the difference in net UF
obtained after a 4-hour dwell with 1.5%/1.36%
glucose and with 4.25%/3.86% glucose dialysate. Using
1.5%/1.36% glucose induces only a small crystalloid
osmotic pressure gradient, and therefore limited
transport through water channels. On the other hand,
using 4.25%/3.86% glucose induces a very high
crystalloid osmotic pressure gradient and the net UF
obtained with it is therefore much more dependent on the
number and function of water channels.
Consequently, DUF 4.25%/3.86% _ 1.5%/1.36% will decrease in
situations with impaired aquaporin-mediated water transport. The
D/P Na+ ratio or DNa+ are
probably the simplest way for rough assessment of
channel-mediated water transport, but a correction for
diffusion should probably be applied when the
difference between the plasma and the initial dialysate
concentrations of Na+ exceeds, for example, 5 mmol/L.
- Patients with a net UF of less than 400 mL/4 hours and low-average, average, or high-average transport profiles, may have mechanical problems, high peritoneal absorption rates, or aquaporin deficiency.
Therapeutic Approach to Fluid Balance Problems
A summary of guidelines for the prevention of
fluid overload is presented in Table 1.
Monitoring: Routine standardized monitoring of desired weight, course of
RRF, and achieved UF with current dialysis
prescription should be emphasized in the care protocols of all
patients on PD. This approach will allow for early
detection of developing problems and early intervention
with corrective measures. The volume status of patients
on PD should be used as a core indicator of dialysis
adequacy. Constant re-evaluation, by physicians
and nurses, of the patient's target weight in the light
of blood pressure and other features suggestive of
fluid overload is required. Particular emphasis should
be placed on the desirability of normalizing blood
pressure by using fluid removal alone, without
antihypertensive drugs, until it is proven that this strategy
is not adequate. Routine performance of the PET, with
a view to identifying high and high average
transporters in whom monitoring of fluid status is
particularly critical, is highly encouraged. Use of icodextrin for
the long dwell, and utilization of APD may be the
preferred approaches in these patients.
Dietary Counseling: Dietary counseling
concerning appropriate salt and water intake is crucial.
Avoidance of dietary indiscretion can be enhanced by
detailed dietary counseling and regular
re-enforcement of taught guidelines. The tendency to be more
liberal in dietary restrictions with PD patients compared
to patients on HD should be tempered by the need
to maintain desired weight and reduction of
cardiovascular risk (10).
Diuretic Use: Routine use of high-dose loop
diuretics to maintain urine output in patients with RRF
is a viable consideration (12). Usually, large oral
doses are needed (furosemide range 250 _ 1000 mg)
with or without the addition of a thiazide-like
diuretic (metolazone 5 _ 10 mg given 30 minutes prior to
the loop diuretic). The concern over ototoxicity is
largely based on experience with large intravenous doses;
it has rarely been seen with oral administration.
Protection of RRF: Protection of RRF should
continue to be as high a priority in the ESRD phase as
it is in the pre-ESRD phase. Avoidance of
nephrotoxic agents (e.g., aminoglycosides, nonsteroidal
anti-inflammatory drugs, radio contrast dye) that
might cause accelerated loss of urine output should be
practiced rigorously. In patients with diffuse vascular
disease but not yet ESRD, angiotensin converting enzyme inhibitors may adversely affect renal
function. Recent analysis of the United States Renal Data
System data suggests that use of angiotensin
converting enzyme inhibitors was associated with better
preservation of RRF in patients on dialysis (84).
Enhanced Compliance and
Education: During the initial training period, emphasis should be placed
on the education of the patient in the diagnosis and
significance of fluid overload (e.g., awareness of
importance of hypertension, peripheral edema,
shortness of breath). Additionally, patients should be
provided appropriate education in what the indications are
to use more-hypertonic PD solutions. Routine
monitoring of patient compliance with PD exchanges,
and education of the patient in the importance of this
issue, are highly desirable. Better techniques to
determine and detect noncompliance need to be developed.
Hyperglycemia Control: In diabetic patients,
hyperglycemia can adversely affect the maintenance of
an osmotic gradient across the peritoneal
membrane. Control of hyperglycemia may allow improved
UF without the need to use hypertonic glucose
solutions unnecessarily. Because glucose control is, under
current practice conditions, mostly monitored and
modified by the patient independently, education of
the patient on the relevance of this activity to the
adequacy of dialysis is important.
Preservation of Peritoneal Membrane
Function: The acute (and possibly chronic) impact of peritonitis
on membrane function has been discussed above.
Minimization of damage to the peritoneal membrane
by implementation of strategies to decrease the
peritonitis rate should be universally applied. The use
of more-biocompatible solutions may also influence membrane preservation, partly via a reduction in
the peritonitis rate. Temporary cessation of PD has
been used in a few patients with high small-solute
transport characteristics with some success, and may be
a reasonable option to consider if other approaches
are unsuccessful (85_87). Alternatively, reduction in
exposure of the peritoneal membrane to glucose may lead to some improvement in transport
Therapeutic Guidelines for Specific Diagnostic Categories
Low Drain Volume and High
Transport: In addition to the universal guidelines discussed
above, therapeutic interventions in this constellation of
diagnostic findings need to address the basic
pathophysiologic mechanism of rapid dissipation of
the osmotic gradient. The latter phenomenon is
particularly prominent during the long overnight dwell
in CAPD and the daytime dwell in APD. The most appropriate intervention is the use of high
molecular-weight substitutes for glucose, such as
icodextrin. Dialysate solutions containing this polyglucose have
been shown to be superior to glucose-based
solutions in achieving net UF during long dwells in a
majority of patients, and particularly in high
transporters (89_95). Icodextrin has also been shown to be
effective during peritonitis (46). In areas of the
world where icodextrin dialysis solutions are not
available, shortening dwell time is the preferred approach.
In CAPD patients, this can be achieved with the use
of an automated nighttime exchange device. This approach will shorten dwell time and has the
additional benefit of improving small solute clearance with
little impact on patient lifestyle. Alternatively, patients
can be switched to APD where the use of short dwell
times in the night phase enhances UF (13). In patients
on APD, foregoing the daytime exchange and optimizing the nighttime regimen may be sufficient. If
small solute clearance suffers, then a short daytime
exchange with midday drainage will supplement
nighttime clearance without compromising UF. If
the preceding options are insufficient, then high
glucose concentrations may be required. In a few
patients, adjunctive, temporary, or permanent HD may
Preventive measures remain limited and
speculative because of a lack of thorough understanding
of the factors underlying high transport (96,97). In
patients with inherent high transport, there are no
clear associations with reversible conditions that can
be therapeutically addressed. The possible
association with higher indices of chronic systemic
inflammatory response remains unproven. The clearest category
for intervention is that of the transient, small-solute,
high transport rate associated with infection.
Approaches to reduce and/or prevent infections, using
improved connectology, patient training, and local
prophylaxis, have been successful but more remains to be
achieved. In patients who develop a high transport profile
in the course of chronic PD, the approach is more a
question of considered opinion rather than evidence
based. Reinforcing universal measures before relying
on chronic intensive use of 4.25%/3.86% glucose
dialysate is generally preferable. Further, where
available, use of icodextrin in lieu of any high glucose
dialysate for the long dwell is recommended.
Low Drain Volume and Low
Transport: The combination of reduced solute clearance and diminished
UF represents a state of significant shortcomings in
delivery of appropriate renal replacement by PD.
If therapeutic targets for both azotemia and
volume homeostasis cannot be met, then adjunctive HD
or permanent transfer to HD may be required in
anuric patients. In subjects with RRF, use of high-dose
loop diuretics may be beneficial.
Low Drain Volume and High-Average or
Low-Average Transport: Aquaporin Deficiency:
Adherence to the universal measures detailed above is
necessary in all conditions, whatever the underlying
etiology of the impaired UF. Patients with aquaporin
deficiency continue to have significant UF via nonaquaporin pathways. This can be enhanced by
the use of icodextrin in long dwells, allowing for
sustained fluid removal (92,95,98,99). For glucose-based
exchanges, short dwells are also preferable, as in
patients with high transport profile, with the
same provisions as far as optimizing maintained
solute clearance is concerned.
Lymphatic Reabsorption and/or Tissue
Reabsorption: When enhanced tissue reabsorption results
in reduced net UF, interventions to maximize overall
UF are required to reach a state favorable to fluid
removal. Ultrafiltration needs to exceed
reabsorption to allow proper volume homeostasis. All
interventions that maximize UF (short dwell time, high tonicity
of dialysate) need to be combined. Because tissue
resorption is a continuous process, and because UF tends
to decline with time, short-cycle therapy is required
to keep the balance of operation earlier than the
convergence of the two processes. Adjusting cycle
number and overall cycler time in APD, or cycle
number in CAPD, to the requirements of both UF and
solute clearance needs to be done meticulously (13).
Pharmacological reduction of lymphatic absorption
has been attempted (100). Intraperitoneal
administration of phosphatidylcholine has been found to increase
net UF, in both CAPD patients with UF failure and
patients with normal net UF (101_103).
Alternatively, a cholinergic effect could lead to a decrease of
lymphatic absorption, such as has been demonstrated
in rats for neostigmine. The parasympathomimetic
drug, bethanechol chloride, has been reported to
increase UF after oral administration (104). An effect on
lymphatic absorption was postulated, but not
investigated. More studies are required to confirm its
effect. Although there is a lot of promising investigative
evidence that tissue resorption can be reduced, no
pharmacological intervention can be recommended at
this time due to the lack of definitive clinical
- A systematic and thorough evaluation of fluid management should be considered a cornerstone of dialytic therapy. Routine monitoring and evaluation of volume status should be considered a necessary component of dialysis prescription and dialysis adequacy. Assessment, achievement, and maintenance of target weight are essential, with the aim of maintaining normotension with euvolemia. Regular assessment (annually, but more frequently if clinically indicated) of peritoneal function (PET modified), RRF, and solute clearance are essential.
- In the absence of validated readily applicable indicators of volume status, reliance on clinical judgment remains the physician's best guide.
- Adherence to sound physiologic principles in the design and implementation of PD prescriptions is essential to prevent the emergence of fluid overload. The most frequently ignored principles in PD that lead to UF difficulties are the need to avoid long dwells in high transporters and balancing glucose concentration and dwell time. Prescription setting must take them into account.
- In the evaluation of causes of fluid overload, screening for reversible causes, such as dietary indiscretion and noncompliance, problems in prescription design, and finally mechanical problems, is imperative. These factors may account for a large proportion of the causes of fluid overload.
- Evaluation of peritoneal membrane-related causes of fluid overload requires adherence to a structured diagnostic framework: The first step involves evaluation of UF response to an effective osmotic challenge. The second step refines the diagnostic approach with an evaluation of the small-solute transport profile.
- Evaluation of peritoneal membrane function in this context is best performed with a modified PET utilizing 4.25%/3.86% glucose. In effect, a net UF greater than 400 mL/4 hours (a drain volume greater than 2400 mL/4 hours) effectively rules out any alterations in peritoneal functional parameters being responsible for the inadequate fluid removal and the ensuing clinical syndrome.
- For patients with net UF less than 400 mL/4 hours and a high transport profile of small solute clearance, APD and icodextrin for the long dwell are the recommended therapeutic approaches. This profile can also be seen during peritonitis, and several studies have indicated that UF during an episode of peritonitis can be satisfactorily achieved with the use of icodextrin.
- Patients who are functionally anephric and have net UF less than 400 mL/4 hours and a low transport profile of small solute clearance have both inadequate volume and inadequate solute removal; transfer to HD may be required for adequate patient management. Functionally anephric patients in this category often cannot be managed by PD. However, if some degree of RRF is present, maintenance on this dialytic modality may be feasible.
- Patients with a net UF less than 400 mL/4 hours and low-average, average, or high-average transport profiles may have mechanical problems, high peritoneal absorption rates, or aquaporin deficiency.
Correspondence to: S. Mujais, Renal Division,
Baxter Healthcare Corporation, 1620 Waukegan Road, MPGR-D1
McGaw Park, IL 60085-9815 U.S.A.
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