Received: 25 October 2021 Revised: 4 January 2022 Accepted: 13 January 2022

DOI: 10.1111/sdi.13063

REVIEW ARTICLE

Peritoneal dialysis fluids

Sanmay Low1 | Adrian Liew2

1
Division of Renal Medicine, Department of
Medicine, Ng Teng Fong General Hospital,
National University Health System, Singapore
2
The Kidney and Transplant Practice, Mount
Elizabeth Novena Hospital, Singapore
Correspondence
Sanmay Low, Division of Renal Medicine,
Department of Medicine, Ng Teng Fong
General Hospital, National University Health
System, Tower B level 2, 1 Jurong East Street
21, Singapore 609606.
Email: sanmay_low@nuhs.edu.sg
Abstract
There have been significant advances in the understanding of peritoneal dialysis
(PD) in the last 40 years, and uptake of PD as a modality of kidney replacement ther-
apy is increasing worldwide. PD fluids, therefore, remains the lifeline for patients on
this treatment. Developing these fluids to be efficacious in solute clearance and ultra-
filtration, with minimal adverse consequences to peritoneal membrane health and
systemic effects is a key requirement. Since the first PD fluid produced in 1959, mod-
ifications to PD fluids have been made. Nonetheless, the search for that ideal PD
fluid remains elusive. Understanding the components of PD fluids is a key aspect of
optimizing the successful delivery of PD, allowing for individualized PD prescription.
Glucose remains an integral component of PD fluids; however, its deleterious effects
continue to be the impetus for the search of an alternative osmotic agent, and
icodextrin remains the main alternative. More biocompatible PD fluids have been
developed and have shown benefits in preserving residual kidney function. However,
high cost and reduced accessibility remain deterrents to its widespread clinical use in
many countries. Large-scale clinical trials are necessary and very much awaited to
improve the narrow spectrum of PD fluids available for clinical use.

1 | I N T RO DU CT I O N (UF). Nonetheless, the search for the ideal PD fluid remains

In 1923, Georg Ganter, a German physician utilized physiological
saline as possibly the first peritoneal dialysis (PD) fluid when he
demonstrated that single or repeated instillation and drainage into the
peritoneal cavity improved both uremic symptoms and blood urea
nitrogen levels in guinea pigs and rabbits.1 He subsequently demon-
strated the feasibility of this treatment in sporadic patients with
variable results, but it was only in 1959 that the first commercially
available PD fluid allowed for clinical use emerged as an alternative
therapeutic option for patients with kidney failure.2
It has been more than 50 years since the first introduction of
PD as a form of kidney replacement therapy (KRT). The PD
solutions of early days have been rather rudimentary, with proper-
ties a long way from what would have been considered an ideal
PD fluid (see Table 1). Since the first PD fluid produced by Dan
Baxter Company in 1959, modifications have been made, aiming to
enhance the biocompatibility of the solution and to improve its
efficiency in maintaining acid–base balance, removal of uremic
toxins, and achieving euvolemia through adequate ultrafiltration
elusive.
This review will provide an overview of the physiological rationale
for the key components of the PD fluid, a summary of the important
technological advances impacting on clinical outcomes, and a consid-
eration for future developments.
2 | C O M P O S I T I O N OF E L E C T R O L Y T E S I N
PD FLUID
The optimum electrolyte composition in a PD fluid is that which best
serves the homeostatic needs of the patient with kidney failure and
considers the peritoneal removal of electrolytes and effects on perito-
neal health. PD fluids contain sodium, magnesium, calcium, and, in
some cases, potassium while electrical neutrality is maintained by the
addition of chloride and lactate and/or bicarbonate. While the electro-
lyte composition of PD fluids by various manufacturers may vary
slightly (Table 2), specific fluids with defined electrolyte concentra-
tions are available for different clinical situations.

10 © 2022 Wiley Periodicals LLC. wileyonlinelibrary.com/journal/sdi Semin Dial. 2024;37:10–23.


LOW AND LIEW
TABLE 1 Key properties of the ideal PD fluid
Possess a physiological electrolyte and buffer composition
Maintain a predictable and sustained solute clearance with minimal
absorption
Achieve adequate ultrafiltration
Correct acid-balance
Free of and inhibit the growth of pyrogens and micro-organisms
Free of toxic metals
Be inert to the peritoneum with minimal risk of hypersensitivity
reactions
Freedom from instillation pain
Does not induce hyperglycemia and its associated local and systemic
adverse effects
2.1 | Sodium
With the loss of residual kidney function (RKF), patients on PD may
develop hypervolemia and hypertension.3 Maintaining sodium balance
is a key strategy in managing fluid overload. Lowering the dialysate
sodium concentration could enhance sodium removal during PD,
achieved by increasing diffusion from the blood. Current PD fluids
have a sodium concentration of 132–135 mmol/L, which is slightly
lower than plasma sodium concentration and could typically achieve a
daily peritoneal sodium removal of 100 mmol/L of UF in CAPD and
4
80 mmol/L of UF in APD.
Clinical studies on the use of low sodium PD fluids began in the
1990s, using sodium concentrations of 120 mmol/L in either 1.36% or
2.27% glucose fluids.5 Some of the authors have even gone on to
evaluate the effects of ultralow sodium dialysis fluids with concentra-
tion of 98 mmol/L during CAPD.6 Across these earlier descriptive
studies, patients were observed to have a significant increase in the
sodium removal from the peritoneal fluid and a drop in their body
weight and mean arterial blood pressure. Subsequent controlled trials
evaluating the management of hypervolemia with low sodium dialy-
sate concentrations (102–126 mmol/L) also showed similar benefits.
Davies et al. showed in a controlled trial of using peritoneal dialysate
sodium concentrations of 102 and 115 mmol/L that patients using
the lower sodium dialysate achieved improvement in nocturnal blood
pressure and a reduction in sensation of thirst7, while a double-
blinded, randomized controlled trial (RCT) of 125 and 134 mmol/L
sodium dialysate demonstrated that a low sodium dialysate resulted in
higher sodium removal and reduced anti-hypertensive use but were
8
unable to prove its non-inferiority effect for total Kt/Vurea.
However, there are issues with the use of low sodium peritoneal
dialysate. A more recent study evaluated the possible benefits of
substituting one of the daily standard PD exchange with a low sodium
dialysate (112 mmol/L) in a RCT. Notwithstanding that there was no
demonstrated superiority of this treatment regimen, patients in the
9
low sodium group also had more hypotensive episodes. There was
also a higher drop-out rate due to hyponatremia in at least one of the
studies,5 and the effect on the RKF with such excessive UF has not
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11
been systematically evaluated. Despite this, some investigators had
even gone on to demonstrate the ability of a zero-sodium peritoneal
dialysate to remove substantially greater amount of sodium in porcine
and early human studies,10 though the clinical effects of this strategy
remain untested.
The use of low sodium PD fluids, however, has not affected clini-
cal practice, and currently, low sodium PD fluids are not readily avail-
able commercially. Nonetheless, there may be a case in the future for
patient-tailored PD prescriptions, and low sodium dialysate may be
considered in PD patients having difficult issues with fluid
management.
2.2 | Calcium
Commercially available PD fluids have a calcium range of 1.0–
1.75 mmol/L (2.0–3.5 mEq/L) (Table 2). In the 1970s, 1.75 mmol/L
was the most commonly used calcium concentration, but the
increased use of calcium-containing phosphate binders had resulted in
a higher prevalence of hypercalcemia and adynamic bone disease.11
This led to the preferred use of lower calcium containing PD fluids
(1.25 mmol/L), where approximately 1–1.5 mmol of calcium is
removed daily during PD.4 The use of lower calcium PD fluids has
resulted in fewer episodes of hypercalcemia with patients able to tol-
erate higher doses of calcium-containing phosphate binders12–14 and
the potential to reverse adynamic bone disease.11 However, these
purported benefits of lower calcium PD fluids have to take into
account the risk of progression of hyperparathyrodisim,15,16 which
may be prevented by the administration of Vitamin D.17 Therefore, it
is not likely that additional clinical benefits can be gained by reducing
the dialysate calcium concentration any lower, and while the default
calcium concentration is mainly 1.25 mmol/L, a higher concentration
of 1.75 mmol/L is still available for patients with parathyroidectomy
or with refractory hypocalcemia.
2.3 | Magnesium
Magnesium concentration in PD fluids ranges from 0.25 to
0.75 mmol/L (0.5–1.5 mEq/L). The serum magnesium concentration
in PD patients is determined mainly by nutritional intake and diffusive
PD removal. Originally, PD fluids had magnesium concentrations of
0.75 mmol/L; however, this resulted in frequent occurrence of
hypermagnesemia,18 due to the imbalance between gut absorption
and dialytic removal. High serum magnesium levels may possibly be
associated with adynamic bone disease19; thus, the use of lower mag-
nesium concentration PD fluids (0.25 mmol/L) became more wide-
spread. This appeared to normalize serum magnesium levels in
patients with previous hypermagnesemia13,14 but at the expense of a
higher frequency of hypomagnesemia in the general PD population,20
with an associated higher risk for hospitalizations21 and mortality.22
Accumulating evidence in recent years also suggest that higher serum
magnesium levels may be protective against vascular and coronary
 Composition of frequently used pd fluids
12

TABLE 2

Sodium,
mmol/L Calcium, Magnesium, Low
Solution/manufacturer Chambers Osmotic agent Concentration (mEq/L) mmol/L (mEq/L) mmol/L (mEq/L) Buffer, mmol/L pH GDPs
Conventional PD fluids
Dianeal™/Baxter 1 Dextrose 0.5% (5 g/L) 132 (132) 1.00 (2.0) or 0.25 (0.5) Lactate, 40 5.2 No
1.5% (15 g/L) 1.25 (2.5) or
2.5% (25 g/L) 1.75 (3.5)
4.25% (42.5 g/L)
Dianeal PD-101™/Baxter 1 Dextrose 0.5% (5 g/L) 132 (132) 1.62 (3.25) 0.75 (1.5) Lactate, 35 5.2 No
1.5% (15 g/L)
2.5% (25 g/L)
4.25% (42.5 g/L)
CAPD/DPCA stay.safe™/ 1 Glucose 1.5% (15 g/L) 134 (134) 1.25 (2.5) or 0.5 (1.0) Lactate/ 5.5 No
Fresenius Monohydrate 2.3% (22.7 g/L) 1.75 (3.5) Bicarbonate,
4.25% (42.5 g/L) 35/2
DEFLEX™ Standard/ 1 Dextrose 1.5% (15 g/L) 132 (132) 1.75 (3.5) 0.75 (1.5) Lactate, 35 5.5 No
Fresenius 2.5% (25 g/L)
4.25% (42.5 g/L)
DEFLEX™ Low Mg, Low 1 Dextrose 1.5% (15 g/L) 132 (132) 1.25 (2.5) 0.25 (0.5) Lactate, 40 5.5 No
Cal/Fresenius 2.5% (25 g/L)
4.25% (42.5 g/L)
Glucose-sparing PD fluids
Extraneal™/Baxter 1 Icodextrin 7.5% (75 g/L) 133 (133) 1.75 (3.5) 0.25 (0.5) Lactate, 40 5–6 Yes
Nutrineal™/Baxter 1 Amino Acids 1.1% (87 mmol/L) 132 (132) 1.25 (2.5) 0.25 (0.5) Lactate, 40 6.6 NA
Biocompatible PD fluids
Physioneal™/Baxter 2 Glucose 1.36% (15 g/L) 132 (132) 1.25 (2.5) 0.25 (0.5) Lactate 15 + Bicarbonate 25 7.4 Yes
Monohydrate 2.27% (25 g/L) (Physioneal 40)
3.86% (42.5 g/L) Lactate 10 + Bicarbonate 25
(Physioneal 35)
Balance™/Fresenius 2 Glucose 1.5% (15 g/L) 134 (134) 1.25 (2.5) or 1.75 0.5 (1.0) Lactate 35 7.0 Yes
Monohydrate 2.3% (22.7 g/L) (3.5)
4.25% (42.5 g/L)
BicaVera™/Fresenius 2 Glucose 1.5% (15 g/L) 134 (134) 1.75 (3.5) 0.5 (1.0) Bicarbonate 34 7.4 Yes
Monohydrate 2.3% (22.7 g/L)
4.25% (42.5 g/L)
DEFLEX™ Neutral 2 Dextrose 1.5% (15 g/L) 132 (132) 1.25 (2.5) or 1.75 0.25 (0.5) or 0.75 Lactate 35 + Bicarbonate <3.5 7.0 Yes
pH/Fresenius 2.5% (25 g/L) (3.5) (1.5)
4.25% (43 g/L)

Abbreviation: GDPs, glucose degradation products.

LOW AND LIEW

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LOW AND LIEW
calcification.23,24 The optimal PD fluid magnesium concentration is
unclear, and newer PD fluids (Balance™, Bicavera™) contain an inter-
mediate level of 0.5 mmol/L magnesium concentration (Table 2). It
may be prudent to monitor the serum magnesium levels in PD
patients, with oral supplementation as required to maintain a high nor-
mal serum magnesium level, while awaiting further studies on the
optimal concentration of magnesium for PD fluids.
2.4 | Potassium
Potassium removal by peritoneal dialysis is lower compared with
25
hemodialysis (30–40 mmol/day versus 70–150 mmol/day), and as
such, commercially available PD fluids generally do not contain potas-
sium. However, hypokalemia is a frequent occurrence in PD patients26
possibly due to the intracellular movement of potassium mediated by
the release of insulin as a result of glucose absorption from the PD
fluids.25 While low serum potassium level in PD patients is easily miti-
gated with oral potassium supplementation, the use of intraperitoneal
potassium treatment has been successfully considered in patients
with refractory and life-threatening hypokalemia,27 though intuitively
it may increase the risk of contamination when injecting the potas-
sium replacement into the PD bags.
3 | BUFFER
Conventional PD fluids are rendered acidic to prevent the car-
amelization of glucose during the heat sterilization process and the
chemical transformation of glucose to 5-hydroxymethylfurfural and its
28
acidic metabolites. Buffers to the PD fluids minimize the unwanted
effects of an overly acidic solution used for PD exchanges and are also
needed for the correction of metabolic acidosis seen in patients with
kidney failure. Three different buffers have been considered in PD
fluids—acetate, lactate, and bicarbonate, with the latter two currently
used in clinical practice.
3.1 | Acetate
Acetate was used as a buffer in earlier PD fluids; however, this has
been limited by infusion pain, alkalemia, peritoneal membrane dam-
age, and an association with encapsulating sclerosing peritonitis
(EPS).29,30 Acetate-based dialysate is no longer in clinical use.
3.2 | Lactate
Currently, lactate is the standard buffer in conventional PD fluids due
to its clear and well-defined metabolic pathway, stability in parenteral
solutions, and long history of safety in intravenous and intraperitoneal
solutions.31 Commercially available PD fluids use lactate
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13
(predominantly L-lactate) as a buffer in concentrations of 35–
40 mmol/L, giving rise to an overall acidic pH of 5.2–5.5 in the fluids.
Lactate diffuses from dialysate to blood, and this diffusion is rapid
during the first hour of the dwell, with the majority absorbed within
2 h32 and is rapidly metabolized to pyruvate by lactic dehydrogenase.
Pure lactate-based buffers do not contain bicarbonate; thus, bicarbon-
ate will diffuse from the blood to the dialysate. However, as the over-
all lactate gain exceeds bicarbonate loss, the net effect is alkali gain,
and thus correction of metabolic acidosis.33,34 Stable chronic PD
patients have normal lactate levels, but lactate levels may be elevated
during intercurrent illnesses even in the absence of hypoxemia and
gut ischemia.35
The main issue with the use of lactate-based PD fluids is its
reduced biocompatibility due to the unphysiological acidic pH and glu-
cose breakdown products, which had been shown in many studies to
result in detrimental effects on the health of the peritoneal
membrane,36–38 a greater incidence of infusion pain,39 and unwanted
consequences to peritoneal immunity.40,41 This led to the consider-
ation of bicarbonate as an alternative and more physiological buffer in
PD fluids.
3.3 | Bicarbonate
The use of bicarbonate was initially limited by its precipitation with
calcium and magnesium, and several investigators had taken on to
inject sodium bicarbonate into conventional PD fluids immediately
prior to infusion as a treatment option for inflow pain. However, the
need to do such injections had led to increased therapy burden, higher
overall treatment cost, and higher rates of peritonitis.39 The creation
of a dual-chamber dialysate bag was designed to circumvent these
problems, allowing the bicarbonate solution at a high pH to be stored
separately from the solution with glucose and electrolytes. Just before
instillation into the abdomen, the chambers are mixed, creating a PD
fluid with a neutral pH.
Bicarbonate-only PD fluids are available at concentrations of
34 mmol/L, achieving similar levels of serum bicarbonate correction
as standard 35 mmol/L of lactate PD fluids.42 Mixed buffer PD fluids
containing both bicarbonate and lactate are available, with some
reports suggesting that these mixed buffer PD fluids are more physio-
logical and cause less infusion pain than a pure bicarbonate PD
fluids.43 As buffer concentrations in currently available PD fluids var-
ies from 35 to 40 mmol/L, investigators have proposed individualiza-
tion of the PD prescription based on an individual's acid base
status.44,45 Patients with a tendency for acidosis may have better cor-
rection of acidosis with 40 mmol/L solutions, while patients with a
tendency for alkalosis may be prescribed 35 mmol/L solutions. Indi-
vidualized approach to buffer prescription may allow a larger percent-
age of PD patients to achieve normal acid–base status, with potential
nutritional benefits. However, such a strategy has not been widely
adopted in clinical practice in many countries due to PD fluid availabil-
ity, cost and logistics consideration.

14
4 | OSMOTIC AGENT
An osmotic agent is needed for effective UF and maintenance of fluid
balance in patients on PD, where an ideal osmotic agent should be
biologically inert with the least amount of absorption causing mini-
mum metabolic effects. The reflection coefficient of an osmotic agent
for a particular peritoneal membrane pore was first defined by
Staverman46 as a ratio of the effective and theoretical osmotic pres-
sure of the molecule, and provides an indication of the efficiency of
its UF profile. Simplistically, the closer the reflection coefficient of an
osmotic substance approaches a value of 1.0 (the value of an ideal
osmotic agent), the less likely that it will be absorbed and the longer
the osmotic gradient could be maintained with a consequent desirable
efficiency in the UF. Glucose, for example, has a net reflection coeffi-
cient of 0.03, indicating a fairly rapid movement across the peritoneal
membrane and hence, systemic absorption.47 Despite the aspirational
properties for an osmotic agent, glucose is still the main osmotic agent
used in clinical practice as it is accepted that it has more advantages
than drawbacks, while the search for an improved molecule
continues.
4.1 | Glucose
Glucose has the main advantages of being cheap, safe, and easily
available. PD fluids contain 1.5%, 2.5%, and 4.25% of dextrose mono-
hydrate (which corresponds to 1.36%, 2.27%, and 3.86% of dextrose
anhydrous respectively). Unfortunately, while glucose is an effective
osmotic agent, it is not ideal as it is short-lived and rapidly absorbed,
resulting in various local and systemic adverse effects.
Local adverse effects of glucose to the peritoneal membrane
include direct cytotoxic consequences on peritoneal mesothelial cells,
and diabetiform changes in the postcapillary venules.48 In addition,
heat sterilization of glucose accelerates the production of glucose
degradation products (GDPs), which binds to proteins and lipids to
produce advanced glycation end products (AGEs) contributing to peri-
toneal fibrosis and subsequent impairment of UF.49 These negative
effects on the peritoneal membrane may lead to an increase in perito-
neal solute transport rate over time and the need for hypertonic glu-
cose solutions to maintain UF volume, with a trend towards worse PD
technique survival.50,51 Furthermore, a large contemporary analysis of
a US cohort showed a linear association between peritoneal solute
52
transport rate and mortality.
Systemically, the rapid and cumulative absorption of glucose con-
tributes to obesity, hyperglycemia, dyslipidemia, and other metabolic
complications in PD patients.53–56 Some authors have shown that the
development of the metabolic syndrome in PD patients and the use
of hypertonic glucose solutions are associated with adverse cardiovas-
cular outcomes and all-cause mortality.57,58 Nonetheless, in the
absence of a more cost-effective agent, glucose continues to be used
rampantly for PD treatment and glucose sparing strategies are contin-
ually being developed to improve clinical outcomes in the PD popula-
tion (see section on Glucose Sparing Strategies).
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LOW AND LIEW
4.2 | Icodextrin
Icodextrin was first introduced in the 1990s and is a glucose polymer
with a molecular weight of 16,800 Da. The average reflection coeffi-
cient of icodextrin had been estimated to be 0.7659 and can sustain a
colloid osmotic gradient, with a slower and reduced rate of absorption
compared with glucose, allowing for increased UF. It is slowly
absorbed via the lymph vessels and metabolized into oligosaccharides
and maltose by circulating α-amylase, and subsequently, tissue malt-
ase converts the metabolites to glucose within the cells, without pro-
ducing hyperglycemia seen in conventional glucose-containing
solutions.60 Therefore, the interference by maltose with conventional
glucometers using the glucose dehydrogenase pyrroloquinoline qui-
none (GDH PQQ) method, may lead to falsely elevated glucose levels
in patients on icodextrin.
4.2.1 | Effect of icodextrin on ultrafiltration, volume
control, blood pressure, and sodium removal
Clinical evidence over the years have shown efficacy of icodextrin in
increasing UF in PD patients when compared with standard glucose-
based PD fluid.61–64 Mistry et al. showed in a multi-center RCT of
209 patients that the mean peritoneal UF at 12 h was five times
greater with icodextrin compared with 1.35% glucose PD fluid.62 This
beneficial effect of icodextrin on UF was substantiated with subse-
quent RCTs,61,63,64 and all meta-analyses done to date have shown
significantly better daily peritoneal UF with icodextrin compared with
standard glucose solutions.65–67 In addition, some meta-analyses
showed the use of icodextrin led to a significant reduction in reported
episodes of uncontrolled fluid overload.66,68
Improved UF with icodextrin consequently results in improved
fluid balance and volume control in PD patients. Woodrow et al.
showed that use of icodextrin resulted in improved fluid balance, bet-
ter estimates of total body water, extracellular water, and extra/
intracellular water ratio by bioimpedance spectroscopy, when com-
pared with 2.27% glucose PD fluid.69 Paniagua et al. performed a
multi-center, open-label RCT and observed a more pronounced reduc-
tion in total body water with the icodextrin group compared with
standard glucose PD fluid. At 1 year follow up, icodextrin-treated
patients had a significant and stable reduction in extracellular water as
compared with baseline, whereas extracellular water remained
unchanged in the standard glucose group.70 Evidence has also shown
that icodextrin may result in improved blood pressure control. A
crossover study of 14 patients on APD showed that patients treated
with icodextrin had a reduced office blood pressure, and six patients
had a reduction in anti-hypertensive mediations.69 These effects were
reproduced in RCTs, all consistently showing that icodextrin-treated
patients with hypertension had better blood pressure control with
fewer anti-hypertensive medications.61,71 In addition, with improved
UF, more sodium is also removed by convection compared with stan-
dard glucose-containing PD solutions72 which may be important in
maintaining optimal volume status, and this was demonstrated

LOW AND LIEW
clinically in several studies.73–75 A multi-center RCT by Plum et al. in
APD patients found that patients randomized to icodextrin showed a
significant decrease in sodium and chloride concentrations, and an
enhanced dialysate sodium excretion which remained stable through-
out the treatment phase.75 Moreover, while sodium removal has been
shown to be more efficient in CAPD compared with APD, Fourtounas
et al. showed that the use of icodextrin as an adjuvant treatment was
effective in increasing peritoneal sodium removal for
modalities.74
4.2.2 | Preservation of peritoneal transport status
with icodextrin
Various systematic reviews have shown variable results on the impact
of icodextrin on peritoneal transport status or peritoneal creatinine
clearance. Earlier meta-analyses by Qi et al.65 and He et al.76
suggested that icodextrin improved small solute clearance; however,
more recent meta-analyses did not show any effect of icodextrin on
peritoneal solute transport rate or peritoneal small
clearance.66,67
4.2.3 | Effects on residual kidney function and
metabolic profile
Meta-analyses have not shown any benefits to RKF with icodextrin
use66,67 though RKF was not evaluated as a primary outcome in these
studies. In a multi-center RCT from Korea examining changes in resid-
ual glomerular filtration rate and urine volume as the primary out-
comes, the study suggested that icodextrin may be associated with
slower residual urine volume loss compared with standard glucose PD
fluids.77
Use of icodextrin as a glucose-sparing strategy minimizes glucose
exposure and therefore may improve metabolic profile. Possible bene-
fits include improved lipid profiles,78 reduced insulin requirements
70
and improved glycemic control (see section on glucose sparing
strategies).
4.2.4 | Effect on technique and patient survival
Despite benefits to metabolic and fluid control, effects of icodextrin
on patient and technique survival remains uncertain. Earlier studies by
Wilkie et al.79 and Johnson et al.80 suggested that substitution of
icodextrin for a long-dwell glucose exchange may result in extension
of technique survival by 22 months and 11.6 months, respectively. In
another multi-center retrospective study of 2163 patients in Korea,
icodextrin use was associated with a significantly lower risk of tech-
nique failure (HR 0.60, p = 0.018).81 However, this possible benefit in
66–68
technique survival has not been replicated in meta-analyses.
recent meta-analysis showed probable decreased mortality risk com-
pared with glucose only PD solutions (19 trials; 1685 patients; odds
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15
ratio: 0.49; 95% CI: 0.24–1.00), but no difference in technique sur-
vival (18 trials; 1401 patients; odds ratio 0.77; 95% CI: 0.39–1.50).68
Nonetheless, there had not been any safety signals or worse out-
comes with the use of icodextrin, and given its desirable UF profile,
icodextrin has become an indispensable therapeutic option in manag-
ing volume overload in PD patients.
both
4.2.5 | Novel use of icodextrin
Several new applications for icodextrin have been postulated. Some
authors have studied the use of twice daily icodextrin exchanges to
reduce peritoneal glucose exposure and systemic glucose absorption.
Benefits with this 2-bag-a-day approach have been observed in
patients with UF failure, including increase in UF volume, decrease in
body weight and serum brain natriuretic peptide, increased left ven-
tricular mass, and improvement in several parameters of cardiac func-
tion.82 A separate study reported decrease in body weight, blood
pressure and enhanced UF.83 Although there have been no reports of
solute overt toxicity with prolonged use of icodextrin solutions beyond the
approved label of 1 bag a day, there is a paucity of data to recommend
this for mainstream clinical use. A large multicenter trial is in progress
to test the efficacy and safety of icodextrin twice daily dwells in
elderly incident PD patients (DIDo).
The use of “bimodal” solutions has also been investigated, where
icodextrin and dextrose are combined in various concentrations in a
single bag. The authors report an increase in UF in the long-dwell of
bimodal solution in comparison with that obtained by icodextrin
solution.84
4.2.6 | Potential adverse effects of icodextrin
Icodextrin has generally been shown to have good long-term safety
data, although there have been some adverse effects reported.
These include cutaneous reactions,85 association with culture nega-
tive peritonitis,86 and interference by maltose with conventional
glucometers leading to falsely elevated glucose. Hyponatremia has
been reported to be associated with the use of icodextrin. The
possible mechanisms behind icodextrin-associated hyponatremia
include a rise in the osmotic pressure of the extracellular fluid
because of the presence of glucose polymers or their degradation
products,87 and possibly due to a negative sodium balance related
to increased convective sodium removal with the use of
icodextrin.73 Previous studies have observed that over the course
of an icodextrin exchange, sodium levels acutely decline with initia-
tion, stabilize over time, then return to baseline levels following
completion of the exchange.75,87 Recent meta-analyses performed
have not found any significant differences in adverse events
between icodextrin and glucose PD fluids.67,68
A Based on available evidence, ISPD recommends that once-daily
icodextrin should be considered as an alternative to hypertonic glu-
cose solutions for long dwells in PD patients who are experiencing

16
difficulties maintaining euvolemia due to insufficient peritoneal UF,
taking into account the individual's peritoneal transport (Grade
88
1B). Similarly, the European Best Practice Working Group (EBPG)
recommend that icodextrin be used for the longer dwell in high
transporters with net UF of less than 400 mL during a 4-h
exchange with a 4.25% glucose solution.89 The main drawback to
the use of icodextrin is that it remains expensive and is currently
not available nor reimbursed in many low income countries, includ-
ing countries that practice a “PD first” approach. Hence, icodextrin
remains predominantly used as a salvage therapy rather as an early
glucose sparing modality, and thus its potential may not be fully
realized.
4.3 | Amino acids
Protein losses in patients on stable CAPD averages about 5 g per day,
80% of which is albumin.90 Persistent negative protein balance may
result in malnutrition, which is increasingly being recognized as a neg-
ative predictor of outcome in patients with ESRD.91,92 The addition of
amino acids into PD fluids offers an attractive option to supplement
these losses. The only commercially available amino acid PD fluid,
Nutrineal™, was launched in the 1990s, containing 1.1% (87 mmol/L)
of amino acids which exerts a similar osmotic force to 1.5% dextrose
PD fluid93 (Table 2).
The nutritional benefits of amino acid PD fluids have been exten-
sively studied but have returned with conflicting results.94–98 Recent
studies found increased muscle amino acid uptake in patients using a
1.1% amino acid PD fluid,99 and Tjiong et al. reported improved nitro-
gen balance in a randomized crossover trial.96 While a single daily
exchange of amino acid dialysate may improve nutritional parameters,
the available clinical evidence has been weak. Metabolic acidosis and
elevated serum urea levels have been reported as common side
effects. In selected PD patients who exhibit protein-energy wasting,
amino acid PD fluids may be tried to improve nutritional status, with
close monitoring of laboratory profile.
Subsequently, instead of nutritional supplementation, amino acid
PD fluids were evaluated as part of a glucose sparing strategy. These
will be discussed in a later section, but the clinical use of amino acid
PD fluids is likely to remain equivocal until further adequately
powered randomized trials can prove benefits. Moreover, in view of
the reduced usage and current low quality of evidence, the company
has removed Nutrineal™ from most of the markets in the world,
except for certain countries in Europe.
4.4 | Glycerol
Glycerol is an osmotic agent with a lower molecular weight and
higher osmotic strength than glucose. It was thought to be theoreti-
cally more biocompatible than glucose as it is able to be sterilized at
a more physiological pH, and avoids hyperinsulinemia that is seen
100
with glucose PD fluids. However, its use has been limited due
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LOW AND LIEW
the need for high glycerol concentration in the PD fluid to achieve
adequate UF, association with hypertriglyceridemia, and accumula-
tion of glycerol that has been associated with hyperosmolar
symptoms.101
5 | T H E I S S U E OF B I O C O M P A T I B I L I T Y I N
PD FLUIDS
The deleterious effects of low pH, high lactate, high GDP-containing
PD fluids on the peritoneal membrane have led to the quest for more
“biocompatible” PD fluids. The definition of biocompatible PD fluids
has been widely debated but the term has generally been used to
refer to PD fluids that have neutral-pH, reduced lactate use and con-
tain low levels of GDPs. The components of currently available PD
fluids that have considered to be biocompatible are summarized in
Table 2. Numerous RCTs have been conducted to evaluate the bene-
fits of biocompatible PD fluids, and several meta-analyses have
reviewed the use of these biocompatible PD fluids compared with
standard glucose-containing PD solutions.67,102–105 The key-findings
of these meta-analyses and systemic reviews have been summarized
in Table 3.
5.1 | Residual kidney function and urine volume
The balANZ study106 was an investigator-initiated, multicenter, open-
label, parallel-design RCT that included 185 incident PD patients ran-
domized to either neutral-pH, lactate-buffered, low-GDP fluid (bio-
compatible group) or conventional, standard, lactate-buffered fluid for
2 years. The primary outcome of slope of RKF decline was not signifi-
cantly different between the two groups, however secondary out-
comes showed significantly longer times to anuria in the
biocompatible group. A Cochrane systematic review subsequently
showed that the use of neutral pH, low GDP PD fluids improved RKF
preservation and residual urine volume preservation with high cer-
tainty evidence,67 where a greater effect was seen with a longer dura-
tion of biocompatible fluid use. Other previously published systemic
reviews and meta-analyses have also demonstrated consistent
findings102–105 (Table 3). Some authors have speculated that the pres-
ervation of RKF seen with the low GDP PD fluids may in part be due
to a less forceful fluid removal compared with conventional glucose
PD fluids.107
5.2 | Peritonitis risk
The balANZ trial reported a lower peritonitis rate in the biocompatible
group compared with control patients (0.30 episodes per year vs. 0.49
episodes per year, p = 0.01), and the median duration of peritonitis-
associated hospitalization was also shorter in the biocompatible group
(6 days vs. 11 days, p = 0.05).106 A subsequent analysis suggested a
broad reduction in peritonitis caused by gram-positive, gram-negative,
 1525139x, 2024, 1, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/sdi.13063 by Fielding Graduate University, Wiley Online Library on [29/01/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
LOW AND LIEW 17

TABLE 3 Summary of systemic reviews of biocompatible PD versus conventional glucose PD fluids

Author, year No. of studies and outcome studied Key results

102
Cho et al., 2013 Total 18 trials: Improved preservation of RRF in
6 trials (n = 360), effect on RRF biocompatible PDS group once follow up
7 trials (n = 520), effect on daily urine reached 12–24 months (SMD 0.31, 95%
volume CI 0.10–0.52, p < 0.01) and >24 months
1 trial (n = 58), effect on inflow pain (SMD 0.25; 95% CI 0.01–0.48; p = 0.04)
Significantly " in biocompatible PDS group
(MD 126.39, 95% CI 26.73–226.05,
p = 0.01)
Trend towards # incidence of inflow pain
with use of biocompatible PDS (RR 0.51,
95% CI 0.24–1.08, p = 0.08)
Seo et al.,103 2014 Total 11 trials: No significant difference to preserve RRF
7 trials (n = 601), short-term data for RRF (MD 0.38, 95% CI 0.10 to 0.86,
preservation (3–6 months) p = 0.12)
9 trials (n = 845), long-term data for RRF Significant " RRF with long-term use of
preservation (12–45 months) biocompatible PDS (MD 0.46, 95% CI
0.25–0.67, p < 0.0001)
Wang et al.,104 2015 Total 6 trials: Much slower rate of RRF decline in
Effect on rate of RRF loss (n = 536) biocompatible PDS group (MD 0.45, 95%
Effect on weekly Kt/V (n = 376) CI 0.10–0.80, p = 0.01)
Effect on urine volume (n = 510) Markedly improved in biocompatible PDS
group (MD 0.13, 95% CI 0.06–0.21,
p = 0.0005)
" in biocompatible PDS group (MD 110.34,
95% CI 8.58–212.10, p = 0.03)
Yohanna et al.,105 2015 Total 11 trials: RRF found to be significantly " in
11 trials (n = 643), effect on RRF biocompatible PDS group (SMD 0.17,
preservation 95% CI 0.01–0.31, p = 0.04).
8 trials (n = 598), effect on urine volume Total daily urine volume significantly " in
6 trials (n = 432), effect on peritoneal biocompatible PDS group (MD 128, 95%
solute transport rate CI 58–198, p = 0.0004), however effect
only significant after 6 months of
treatment
Treatment with biocompatible PDS resulted
in a " D/PCr at ≤6 months of treatment
(MD 0.04; 95% CI, 0.02 to 0.06,
p = 0.0004), but not significantly
different beyond 6 months
Htay et al.,67 2018 Total 29 studies Better preservation of RRF with use of
15 trials (n = 835), effect on RRF biocompatible PDS (SMD 0.19, 95% CI
preservation 0.05–0.33, high certainty evidence), this
11 trials (n = 791), effect on daily urine effect was presented for all follow up
volume durations (<12 months, 12–24 months,
9 trials (n = 414), effect on 4-h peritoneal and >24 months)
UF Daily urine volume " in biocompatible PDS
10 trials (n = 746), effect on 4-h D/PCr group (MD 114.37, 95% CI 47.09–
181.65, high certainty evidence), benefit
observed after 1 year of follow up
Slightly # 4-h peritoneal UF with
biocompatible PDS (SMD 0.42, 95% CI
0.74 to 0.10, low certainty evidence)
4-h D/PCr may be higher in the
biocompatible group (MD 0.01, 95% CI
0.00 to 0.03, low certainty evidence)

Abbreviations: Biocompatible, neutral-pH, low glucose degradation product; D/PCr, dialysate to plasma creatinine ratio; MD, mean difference; PDS, PD
solutions; RRF, residual renal function; SMD, standard mean difference; UF, ultrafiltration.

18
and specifically non-Pseudomonas gram-negative organisms, as well
as less severe peritonitis in patients using biocompatible PD fluids.108
However a systematic review by the Cochrane group and other stud-
ies have not supported this observation, thus the suggestion that bio-
compatible PD fluids reduces the risk of peritonitis cannot be
conclusively substantiated.67
5.3 | Effect on peritoneal solute transport and
ultrafiltration volume
There have been conflicting results regarding the effect of biocompat-
ible PD fluids on peritoneal transport status and UF volume. Several
studies, including a separate analysis of the balANZ trial, have shown
that biocompatible PD fluids were associated with lower UF volume
and increased peritoneal solute transport at initiation, which stayed
stable over time, compared with deterioration in UF volume and
increasing peritoneal solute transport with conventional
109,110
fluids. The recent Cochrane review suggests biocompatible PD
fluids may result in slightly lower UF volume (low evidence due to
high heterogeneity of studies) and may increase peritoneal creatinine
clearance.67 Further studies are required to draw any definitive con-
clusions on UF and peritoneal transport status.
5.4 | Other clinical outcomes
Earlier studies reported significantly reduced inflow pain with neutral
pH, low GDP PD fluids,43,111,112 however these studies had small
sample sizes and similar findings were not reciprocated in later sys-
temic reviews and meta-analyses. Compared with patients using con-
ventional PD fluids, patients using low GDP PD fluids have also been
shown to have an improved serum and effluent profile for adipokines,
resulting in an improvement of local peritoneal homeostasis and allevi-
113
ating systemic inflammation.
There is also no convincing evidence to suggest that biocompatible
PD fluids improve patient or technique survival.67,114 Again, ade-
quately powered studies addressing patient and technique survival as a
primary outcome are required before more conclusions can be drawn.
We believe that there is high-quality evidence for benefits of bio-
compatible PD fluids in RKF preservation. Other clinical benefits,
however, are equivocal but there have not been any safety signals
concerning any clearly identified harm and the use of biocompatible
PD fluids should be considered where possible. Regardless, the avail-
ability and affordability of biocompatible PD fluids vary significantly
between different countries, particularly in many developing countries
where such PD fluids are not easily available.
6 | G LU COS E SP A RI NG ST RAT E GIE S
Excessive glucose exposure in PD fluids is associated with deleterious
effects as eluded earlier, increasing the risks for peritonitis,
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LOW AND LIEW
cardiovascular disease, and vascular calcification.115,116 Consequently,
reducing glucose exposure in the PD treatment has been a keen
endeavor among physicians with a hope of improving clinical out-
comes. Such strategies involve the replacement of glucose-based PD
fluids in part with icodextrin or amino acid solutions.
Yung et al.117 randomized 80 incident PD patients to either 3–
4 standard exchanges of Dianeal™ or a low-glucose PD regimen
containing of Physioneal™, Extraneal™ and Nutrineal™ (PEN group),
followed by a 6-month conversion of the PEN group back to
Dianeal™. At the end of 12 months, improvements in markers of
peritoneal inflammation and significantly higher dialysate/plasma
creatinine ratio were observed in the PEN group. At 18 months,
urine volume was higher in patients in the PEN group. The authors
concluded that the PEN PD regimen may result in better preserva-
tion of mesothelial cell mass, a reduction in intraperitoneal inflam-
mation, and possibly a delay or reduction of peritoneal fibrosis,
however this was not correlated histologically with peritoneal mem-
PD brane histology.
The IMPENDIA/EDEN studies found that the addition of an
amino acid solution and a single icodextrin exchange to a reduced
2 bags of glucose-based PD fluids per day in CAPD patients resulted
in an improved metabolic control with lower HbA1c levels and better
lipid profile.118 However, the effect of these desirable metabolic
effects on long-term clinical outcomes have not been conclusively
established. Moreover, the cost of icodextrin and amino acid solutions
is significantly prohibitive in many countries and is not a sustainable
therapy especially in low resource settings. A low-glucose dialysis reg-
imen such as the PEN PD regimen may have benefits, but like biocom-
patible fluids, logistical and financial challenges limit its widespread
implementation especially in certain jurisdiction where such therapies
are not reimbursed.
7 | E X P E RI M E N T A L P D F L U I D S
As the evidence of the detrimental effect that glucose has on the peri-
toneal membrane grows, investigators have been searching for alter-
native osmotic agents for PD. We describe some updates in these
novel PD fluids.
7.1 | Carnitine
L-carnitine has a molecular weight of 161.2 Da and is highly water
soluble and chemically stable in aqueous solutions, rendering it suit-
able for use in PD fluids.119 PD patients may have a depletion in
muscle and plasma-free carnitine due to losses in the dialysate, and
this could potentially result in skeletal-muscle weakness and fatigue,
cardiomyopathy, dialysis-related hypotension, hyperlipidemia, and
erythropoietin-stimulating agent resistance.120 To date, four open-
label, and one single blinded RCT121–125 have evaluated the use of
carnitine in PD fluids. The open-label trials suggested improved lipid
pattern, improve nitrogen balance, increased peritoneal UF, and

LOW AND LIEW
stable laboratory, metabolic and dialytic parameters.119 Bonimini
et al. showed in the RCT involving 27 PD patients, that the use of
L-carnitine solutions is associated with preserved urine volume and
improved insulin sensitivity when compared with glucose.126 These
studies all had small sample sizes, and further studies are required
to evaluate the long-term safety and efficacy on L-carnitine as an
osmotic agent in PD fluids. These fluids are not currently available
commercially.
7.2 | Dissolved molecular dihydrogen (H2)
Some studies have shown that dihydrogen (H2) has anti-oxidative
and anti-inflammatory properties, and H2 can be dissolved into PD
fluids by placing the bag in H2-enriched electrolyzed water.
Japanese authors showed that H2-dissolved PD fluids could pre-
serve mesothelial cells and peritoneal membrane integrity in rats
undergoing PD.127 The same authors subsequently did a two-week
study on 6 prevalent PD patients using H2-dissolved PD fluids. The
solutions were clinically well tolerated, with a trend towards
improvement in effluent CA125 and mesothelin in some patients,
suggesting enhanced mesothelial regeneration by H2.128 This is a
novel therapy and further clinical trials on long-term safety and out-
comes are required.
7.3 | Hyperbranched polyglycerol (HPG)
HPG is a hydrophilic, nontoxic, non-immunogenic, water-soluble
branched polyether polymer, which is being used in many biomedi-
cal applications. The concentration of HPG in experimental PD
fluids vary from 2.5% to 15%, with an osmolality of 294–
424 mOsm/kg and achieving a neutral pH of 6.6–7.4. It has
recently been demonstrated that it has both clinical efficacy and
greater biocompatibility than glucose in early preclinical studies
performed on rats, with reduced peritoneal inflammation and pre-
served peritoneal histology when compared with glucose-based PD
fluids.129 Long-term human data for HPG-containing PD fluids is
not yet available.
7.4 | Polyglucose solutions
Polydispersity is the ratio of the weight-average to the number-
average molecular weight of the osmotic agent and is a useful mea-
sure of the spread of polymer distribution. The polydispersity for
icodextrin is reported to be 2.6.130 Using the three-pore model for
theoretical calculations, investigators evaluated the use of glucose
polymers with low polydispersity in rabbit models. They were able to
show long-dwell PD fluids containing 11% 18–19 kDa glucose poly-
mers with low polydispersity can provide higher UF without higher
carbohydrate absorption.131 No human studies have been done at
present.
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19
8 | CONC LU SION
PD fluids remain a key component of PD therapy, and various constit-
uents and biocompatibility have local effects on the peritoneum, sys-
temic metabolic alterations, and modifications on clinical outcomes. A
PD fluid that is suitable for one person may not necessarily be the
best choice for another. Prescribing of PD fluids varies significantly
according to local PD practice, availability of PD fluids, and financial
considerations. As described in this review, we can optimize the suc-
cess of PD by employing membrane preserving strategies; and tailor-
ing PD fluid prescription by varying the content of electrolytes, buffer,
and osmotic agent according to individual clinical status. However,
the future development of novel PD fluids remains challenging, espe-
cially in the search for PD fluids that can improve PD technique and
patient's survival.
OR CID
Sanmay Low https://orcid.org/0000-0002-6542-685X
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