Open Journal of Nephrology, 2012, 2, 29-34
http://dx.doi.org/10.4236/ojneph.2012.23005 Published Online September 2012 (http://www.SciRP.org/journal/ojneph)
Do We Have a Biocompatible Peritoneal Dialysis Fluid?
Shadi Hassan1, Batya Kristal2,3, Khalid Khazim3, Fadi Hassan4, Dunia Hassan5, Kamal Hassan2,3
1Internal Medicine Department, Carmel Medical Center, Haifa, Israel
2Faculty of Medicine in the Galilee, Bar-Ilan University, Safed, Israel
3Nephrology and Hypertension Department, Western Galilee Hospital, Nahariya, Israel
4Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel
5The Ruth and Bruce Faculty of Medicine, Technion Israel Institute of Technology, Haifa, Israel
Received April 21, 2012; revised June 7, 2012; accepted June 21, 2012
ABSTRACT
Objective: Cardiovascular disease remains the leading cause of morbidity and mortality in patients on maintenance
dialysis. Diabetes mellitus, dyslipidemia, hypertension, inflammation and hyperhomocyteinemia are major cardiovas-
cular risk factors. Aim: To evaluate the effects of Icodextrin and amino acid peritoneal dialysis fluid (AAPDF) on these
major cardiovascular risk factors looking for a more biocompatible PDF formula. Methods: 20 adult stable peritoneal
dialysis patients were included in the study. 10 patients received 2 L Icodextrin and other 10 patients received 2 L
AAPDF in their dialysis prescription for 8 weeks. Results: Icodextrin decreased fasting plasma glucose (p < 0.001),
LDL-C (p = 0.03), SBP (p < 0.01), DBP (p < 0.05) and plasma homocysteine (p = 0.002), and increased HDL-C (p =
0.009), CRP (p = 0.035) and fibrinogen (p = 0.009). AAPDF did not affect fasting plasma glucose, LDL-C, HDL-C,
CRP and fibrinogen but increased serum albumin (p = 0.03), SBP (p < 0.01), DBP (p < 0.05) and PHcy (p = 0.03).
Conclusions: A biocompatible PDF should provide not only adequate dialysis and ultrafiltration but should also
improve nutritional and metabolic status, blood pressure control and reduce inflammation and plasma homocyteine.
Keywords: Icodextrin; Amino Acids PDF; Homocyteine; Carbohydrates; Lipids; Inflammation
1. Introduction
Cardiovascular disease (CVD) remains the leading cause
of morbidity and mortality in end-stage renal disease
patients on maintenance dialysis [1]. Diabetes mellitus,
dyslipidemia, hypertension, inflammation and hyperho-
mocyteinemia are major cardiovascular risk factors. Re-
cent studies have suggested that novel risk factors, ure-
mia or dialysis-related, are of great importance, as they
act synergistically with the highly prevalent traditional
risk factors for CVD in chronic kidney disease (CKD)
patients [2]. Glucose based peritoneal dialysis fluids
(PDFs) are usually associated with progressive loss of
the osmotic gradient, concomitant reduction in ultrafil-
tration (UF) and to the development of hyperglycemia
and dyslipidemia. Dyslipidemia increases the risk of
CVD and becomes worse in peritoneal dialysis (PD) pa-
tients [3]. Up to 80% of peritoneal dialysis patients are
hypertensive [4]. Hypertension plays an important role in
the development of CVD in this population [4]. Elevated
plasma inflammation markers associated with increased
risk for CVD [5]. Almost all (97% - 98%) PD and hemo-
dialysis patients have hyperhomocyteinemia that known
to be associated with an increased risk of cardiovascular,
cerebrovascular and venous thromboembolic diseases
[6-8]. Icodextrin and Amino acid PDF (AAPDF) consid-
ered more biocompatible PDFs. Icodextrin PDF is tar-
geted to have more sustained oncotic effect, to reduce
plasma glucose and glucose-induced lipid abnormalities,
and to avoid the production of glucose degradation
products (GDPs) [9,10]. Generally, there is some concern
that Icodextrin treatment may induce a subclinical in-
flammatory response, both intraperitoneally and sys-
temically [10-12]. AAPDF was designed to correct nu-
triational status by supplying extra nitrogen through the
intraperitoneal route [13]. Although the effects of Ico-
dextrin and AAPDF on metabolic status, blood pressure
control, inflammation and plasma homocyteine were
studied but some issues still controversial. Aim of this
study was to evaluate the effects of Icodextrin and
AAPDF on these major cardiovascular risk factors.
2. Patients and Methods
Randomly, 20 adult stable PD patients on continuous
ambulatory peritoneal dialysis (CAPD) or automated
Peritoneal Dialysis (APD) for at least 3 months and with
Kt/V > 1.8 were included in the study. Demographic and
clinical characteristics of the enrolled subjects are listed
in Table 1. The study protocol was approved by the local
C
opyright © 2012 SciRes. OJNeph

S. HASSAN ET AL.
30
Ethics Committee and all patients gave written informed
consent before participating in the study. The patients
randomly assigned to receive Icodextrin or AAPDF. Ten
patients received 2 L Icodextrin in their dialysis prescrip-
tion for 8 weeks, the night dwells in CAPD subjects were
substituted with 2 L Icodextrin and in APD subjects 2 L
from their regular regimen were substituted with 2 L
Icodextrin given as last fill. Ten patients received 2 L
AAPDF in their dialysis prescription for 8 weeks, the
second dwells in CAPD subjects were substituted with 2
L AAPDF and in APD subjects 2 L from their regular
regimen were substituted with 2 L AAPDF given at noon.
The residual renal function (RRF) was estimated by
mean urea and creatinine clearance (CUC) and by the
Modification of Diet in Renal Disease (MDRD) equation
study [14]. At baseline the standard peritoneal equilibra-
tion test (PET) [15], and estimation of Kt/V were perfor-
med using PD-Adequest 2.0 for Windows program
(Baxter Healthcare Co., Deerfield, IL) [16]. Blood, urine
and dialysate analysis were performed in both groups at
baseline and 8 weeks. Blood analysis included complete
blood count (CBC), glucose, low density lipoprotein
cholesterol (LDL-C), high density lipoprotein cholesterol
(HDL-C), triglycerides, albumin, CRP, fibrinogen, plasma
homocysteine (PHcy), folic acid, vitamin B12, and PTH.
Urine analysis included 24-hour urinary collections for
creatinine (mg/dl) (UCr) and urea (mg/dl) (UUrea). Dialy-
sate analysis included creatinine (mg/dl) (DCr) and glucose
(mg/dl) (DGlu). Daily urinary output (ml/day) (DUO),
PET and Kt/V were also evaluated at baseline and 8
weeks. PHcy was determined using AxSYM Homocysteine
Table 1. Characteristics of the study population.
Icodextrin group AAPDFa group
Number 10 10
Age (years) 61.3 ± 11.9 59.6 ± 20.0
Male/female 5/5 5/5
CAPDb/APDc 5/5 5/5
Dialysis duration (months) 29.2 ± 33.6 28.8 ± 17.3
PETd: HATse/LATsf 5/5 5/5
Kt/V 2.41 ± 0.4 2.39 ± 0.4
Vitamin B12 (pg/ml)
(Normal:160 - 680) 598.3 ± 280.3 610.9 ± 330.5
Folic acid (ng/mL)
(Normal:150 - 700) 760.0 ± 385.0 771.2 ± 318.1
PTH (pg/ml) (normal:10 - 60) 313 ± 185 301 ± 158
Underlying cause:
Diabetes mellitus 5 5
Primary hyperoxaluria type 1 2 2
APKDg 1 1
Unknown 2
2
a: Amino Acid Peritoneal Dialysis Fluid; b: Continuous ambulatory perito-
neal dialysis; c: Automated peritoneal dialysis; d: Peritoneal equilibration test;
e: High average transporters; f: Low average transporters; g: Adult Polycys-
tic Kidney Disease.
assay (Produced by Axis-Shied, Dundee, UK for Abbott
laboratories, Abbott park, IL 60064, USA). Statistical
methods: Qualitative variables were described as incide-
nces and percentages. Quantitative variables were descri-
bed as means and standard deviations. Repeated Measures
tests were used to evaluate the effects of Icodextrin and
AAPDF on RRF, DUO, UF, D/PCr, DGlu, DCr, fasting
glucose, plasma lipids, plasma inflammation markers,
body weight, blood pressure and PHcy. Repeated Measures
tests were also used to evaluate the effects of PD
modality, peritoneal membrane characteristics, Kt/V, ge-
nder, cause of CKD and hemoglobin on PHcy. Linear
regression was used to evaluate the correlation between
PHcy and RRF, DUO, PD duration, age, body weight,
PTH and hemoglobin levels. Linear regression was also
used to evaluate the correlation between degree of incre-
ment in UF (∆Net UF) and the degree of reduction in PHcy
(∆PHcy) as well as between the degree of increment in
D/PCr (∆D/PCr ) and ∆PHcy.
3. Results
Repeated measures analysis revealed that Icodextrin and
AAPDF did not affect the RRF or DUO (Table 2). No
linear correlation was found between the RRF and PHcy.
Icodextrin increased UF (p = 0.003) and D/PCr (p < 0.001)
(Table 2). Icodextrin, as well AAPDF decreased DGlu (p
= 0.02) (Table 2).
Table 2. Effects of Icodextrin and AAPDF on RRF, DUO,
UF, D/PCr and DGlu.
Icodextrin group
Baseline 8 Weeks p
PHcy (µmol/L) 29.1 ± 21.8 14.8 ± 5.3 0.002
CUC (ml/min/1.73m2) 10.1 ± 2.3 9.5 ± 2.9 n.s.
eGFRMDRD
(ml/min/1.73m2) 8.3 ± 2.4 8.1 ± 2.0 n.s.
DUO (L/day) 0.8 ± 0.4 0.75 ± 0.3 n.s.
UF (L/day) 0.98 ± 0.1 1.22 ± 1.3 0.003
D/PCr 0.54 ± 0.1 0.79 ± 0.1 <0.001
DGlu (mg/dl) 1035.8 ± 438.1 901.8 ± 354.90.016
AAPDF group
Baseline 8 weeks p
PHcya (µmol/L) 26.6 ± 17.0 36.4 ± 15.6 0.03
CUCb (ml/min/1.73m2) 10.2 ± 3.7 9.7 ± 3.3 n.s.
eGFRMDRDc
(ml/min/1.73m2) 8.1 ± 2.3 8.0 ± 2.0 n.s.
DUOd (L/day) 0.7 ± 0.3 0.6 ± 0.4 n.s.
UFe (L/day) 0.99 ± 0.2 0.97 ± 0.2 n.s.
D/PCrf 0.64 ± 0.1 0.61 ± 0.2 n.s.
DGlug (mg/dl) 981.4 ± 446.8 854.5 ± 435.50.02
a: Plasma homocysteine; b: Mean urea and creatinine clearance; c: estimated
GFR using the Modification of Diet in Renal Disease equation study; d:
Daily Urinary Output; e: Ultrafiltration, f: Dialysate creatinine/plasma creat-
inine; g: Dialysate glucose level.

S. HASSAN ET AL. 31
The basal levels of HbA1C in the two study groups
were similar (4.9% ± 0.7% in Icodextrin group and 5.1%
± 1.5% in AAPDF group). Icodextrin decreased fasting
glucose (p < 0.001), LDL-C (p = 0.03) and triglycerides
(p = 0.04), and increased HDL-C levels (p = 0.009)
(Table 3). AAPDF did not affect glucose and lipid
metabolism (Table 3).
Basal levels of inflammation markers were similar in
both study groups. Basal serum CRP and fibrinogen
levels were elevated in both study groups. Compared to
AAPDF, Icodextrin increased serum CRP (p = 0.035) and
fibrinogen levels (p = 0.009) (Table 3). AAPDF, in con-
trast to Icodextrin, increased serum albumin (p = 0.03)
(Table 3). Icodextrin decreased body weight (p=0.002),
SBP (p < 0.01) and DBP (p < 0.05) while AAPDF incre-
ased body weight (p = 0.002), SBP (p < 0.01) and DBP
(p < 0.05) (Table 3).
Table 3. Effects of Icodextrin and AAPDF on carbohydrates,
lipids, inflammation and blood pressure.
Icodextrin group
Baseline 8 weeks p
Fasting glucose (mg/dl) 141.1 ± 39.9 119.3 ± 29.1 <0.00
1
LDL-C (mg/dl) 102.3 ± 33.3 89.6 ± 22.0 0.03
HDL-C (mg/dl) 35.6 ± 10.1 40.7 ± 11.8 0.009
TG (mg/dl) 272.4 ± 67.0 221.4 ± 74.8 0.04
Albumin(gr/dl) 3.6 ± 0.4 3.6 ± 0.3 n.s.
CRP (0 - 5 mg/L) 9.5 ± 6.5 22.4 ± 16.5 0.035
Fibrinogen
(200 - 400 mg/dl) 835.1 ± 126.5 1066.1 ± 199.80.009
Body weight (kg) 80.4 ± 14.1 78.5 ± 14.7 0.002
SBP (mmHg) 149.5 ± 35.5 131.4 ± 21.9 <0.01
DBP (mmHg) 79.0 ± 14.5 72.8 ± 9.9 <0.05
AAPDF group
Baseline 8 weeks p
Fasting glucose (mg/dl) 138.4 ± 76.2 142.2 ± 86.6 n.s.
LDL-Ca (mg/dl) 117.6 ± 25.9 112.97 ± 21.1n.s.
HDL-Cb (mg/dl) 42.0 ± 9.4 45.0 ± 11.6 n.s.
TGc (mg/dl) 186.4 ± 96.6 176.3 ± 62.7 n.s.
Albumin (gr/dl) 3.5 ± 0.4 4.3 ± 0.5 0.03
CRP (0 - 5 mg/L) 12.6 ± 26.0 10.4 ± 18.3 n.s.
Fibrinogen
(200 - 400 mg/dl) 999.6 ± 189.6 973.0 ± 231.4n.s.
Body weight (kg) 71.6 ± 15.0 72.5 ± 15.0 0.002
SBPd (mmHg) 138.7 ± 28.4 146.6 ± 26.4 <0.01
DBPe (mmHg) 75.4 ± 12.3 80.1 ± 11.8 <0.05
a: Low density lipoprotein cholesterol; b: High density lipoprotein cholest-
erol; c: Triglycerides; d: Systolic blood pressure; e: Diastolic blood pressure.
Hyperhomocysteinemia was identified in 84% of the
study subjects at baseline. Icodextrin decreased PHcy (p =
0.002) (Table 2). AAPDF increased PHcy (p = 0.03) (Table
2). Furthermore, in Icodextrin group, a linear corre-
lation was found between the degree of increment in UF
(∆UF) and the degree of reduction in PHcy (∆PHcy) (p <
0.001, R2 = 0.962) (Figure 1), and between the degree of
increment in D/PCr (∆D/PCr) and ∆PHcy (p < 0.001, R2 =
0.836) (Figure 2).
Icodextrin decreased PHcy in both CAPD and APD
patients (p = 0.033), in low average transporter patients
(LATs) (p = 0.006), in PD patients with Kt/V > 2 (p =
0.04) or Kt/V ≤ 2 (p = 0.003) and in non diabetic patients
(p = 0.039) (Table 4). LATs had a higher basal PHcy
compared with high-average transporter patients (HATs)
(p = 0.015) (Table 4). HATs had lower PHcy which were
in the upper normal limits (Table 4).
Figure 1. The correlation between ∆PHcy and ∆Net UF in the
extraneal group.
Figure 2. The correlation between ∆PHcy and ∆D/PCr in the
extraneal group.

S. HASSAN ET AL.
32
Table 4. Effects of PDa modality, peritoneal membrane
characteristics, Kt/V, gender and diabetes mellitus on PHcy.
PHcyb (µmol/L) in Icodextrin group
Baseline 8 weeks p
CAPDc 33.0 ± 26.3 14.7 ± 6.2 0.033
APDd 24.3 ± 17.0 14.8 ± 5.0 0.033
p n.s.
LATse 46.4 ± 23.2 17.2 ± 5.3 0.006
HATsf 15.3 ± 3.0 12.8 ± 5.1 n.s.
P 0.015
Kt/V ≤ 2 46.9 ± 32.5 19.5 ± 2.7 0.003
Kt/V > 2 20.2 ± 7.3 15.9 ± 6.2 0.04
p 0.05
DMg 24.5 ± 7.9 17.0 ± 7.4 n.s.
Non DM 31.4 ± 6.7 13.7 ± 4.4 0.039
p n.s.
PHcy (µmol/L) in AAPDF group
Baseline 8 weeks p
CAPD 26.72 ± 7.2 33.6 ± 15.7 n.s.
APD 26.52 ± 24.5 31.12 ± 34.9 n.s.
p n.s.
LATs 37.5 ± 18.8 48.5 ± 28.5 n.s.
HATs 15.8 ± 2.1 16.2 ± 3.1 n.s.
p 0.015
Kt/V ≤ 2 32.3 ± 25.5 38.5 ± 36.6 n.s.
Kt/V > 2 22.8 ± 9.4 28.3 ± 17.9 n.s.
p 0.05
DM 28.7 ± 5.1 37.0 ± 3.9 n.s.
Non DM 30.0 ± 19.5 38.9 ± 28.4 n.s.
p n.s.
a: Peritoneal dialysis; b: Plasma homocysteine; c: Continuous ambulatory
peritoneal dialysis; d: Automated peritoneal dialysis, HATs = High average
transporters; e: Low average transporters; f: High average transporters; g:
Diabetes mellitus.
AAPDF increased PHcy (p = 0.03) (Table 2).
Linear regression analysis did not show any correla-
tion between PHcy and age, gender, body weight, duration
of PD, DUO, hemoglobin and PTH levels in both Icode-
xtrin and AAPDF groups.
4. Discussion
Long-term systemic exposure of glucose caused by con-
ventional PD solutions has been well recognized to cause
metabolic and cardiovascular abnormalities, which con-
tribute to the morbidities seen in PD patients. Several
studies have shown that conventional solutions damage
mesothelial cells and peritoneal blood vessels leading to
functional impairment [17,18]. Besides its effects on the
peritoneal membrane, rapid absorption of glucose during
a dwell leads to loss of osmotic gradient and diminished
ultrafiltration as well as to the development of hypergly-
cemia and associated hyperinsulinemia in both diabetic
as well as nondiabetic patients [19]. The high levels of
dextrose and the lactate acidic buffer make the conven-
tional solutions nonphysiologic and nonbiocompatible.
Introducing the newer solutions that designed to be more
biocompatible by either, containing physiologic buffer
bicarbonate, or having lower GDP concentration, and/or
substituting glucose with alternative osmotic agents, like
polyglucose or amino acids were targeted to ameliorate
the complications of conventional dextrose solutions
[20-22]. It is postulated that newer PD solutions contain-
ing lower levels of GDPs are less nephrotoxic, and hence
may preserve RRF longer. Additionally, the effect of
fluid status on preservation of RRF cannot be ignored.
In the present study, Icodextrin and AAPDF did not
affect RRF (Table 2). Icodextrin improved glucose con-
trol and lipid profile including significant decrease in
LDL-C and triglyceride levels as well as significant in-
crease in HDL-C (Table 3). Similar results were reported
by Bredie et al. [23].
It is well known that the major reason for the elevation
of blood pressure in PD patients is volume overload.
Icodextrin improved blood pressure control by improving
UF and decreasing body weight (Tables 2 and 3).
The effects of Icodextrin on inflammation status in PD
patients are controversial [11,12]. Martikainen et al.
showed that Icodextrin use was resulted in subclinical
inflammatory response [11]. In contrast, Lin et al. re-
ported that Icodextrin decreased CRP [12]. In this study
the basal serum CRP and fibrinogen levels were similar
and elevated in both study groups (Table 3). Icodextrin
use was accompanied by a rise in plasma CRP and fi-
brinogen levels (Table 3). There is a concern that Ico-
dextrin use may induce a subclinical inflammatory re-
sponse, both intraperitoneally and systemically. Accord-
ingly, Icodextrin that lowered GDPs levels and designed
to preserve the peritoneal membrane and to improve
glucose and lipid control, seems to intensify systemic
inflammation.
Hyperhomocysteinemia was identified in 84% of our
study subjects compared to the 97% - 98% reported by
Van Guldener [24]. The significant rise in D/PCr and UF
as well as the linear correlations between ∆PHcy and
∆NetUF, and between ∆PHcy and ∆D/PCr in the Icodextrin
group, suggest better peritoneal clearances of Hcy com-
pared to standard glucose-based fluids and AAPDF (Ta-
ble 2, Figures 1 and 2). Similar results were reported by
Czupryniak et al. [25].
It is well known that AAPDF improve nutritional
status in malnourished PD patients. Although increased
serum albumin levels and did not affect UF, glucose and
lipid metabolism, and inflammation status, AAPDF in-
creased body weight, SBP, DBP and PHcy levels (p =

S. HASSAN ET AL. 33
0.002, p < 0.01, p < 0.05, p = 0.03—respectively) (Ta-
bles 2 and 3). The increase in PHcy in the AAPDF group
is, most likely, related to methionine, a precursor of Hcy,
absorption as well as to the decrease in D/PCr and UF in
the AAPDF group (Table 2). Then, AAPDF that intro-
duced to improve nutritional status and survival may
contribute to the unfavorable rise of PHcy. The rise in PHcy
in PD patients treated with AAPDF described also in
previous studies [26,27].
End stage renal disease patients are unable to excrete
the daily acid load. The standard PDFs, Icodextrin and
AAPDF use lactate as a buffer that, by its acidic pH,
causes harmful effects on the peritoneal cells [17]. In
contrast, bicarbonate-based PDFs include a physiologic
buffer with neutral pH, cause less peritoneal damage [28].
The relationships between the PD modality, the peri-
toneal membrane characteristics and Kt/V, and PHcy re-
main a controversial issue [29,30]. Basal PHcy was elevated
and not different in the two study groups and all sub-
groups apart from HATs (Table 4). In the Icodextrin
group PHcy decreased in both PD modalities (p = 0.033)
(Table 3). On the other hand, AAPDF increase PHcy (p =
0.033) (Table 2). This may be due to its low osmotic
drive and as a result of the absorption of methionine
through the peritoneal membrane. These results suggest
that the peritoneal membrane characteristics and the
composition of the PDF have an important role in the
peritoneal elimination of Hcy.
Basal PHcy in HATs were near normal in both study
groups (Table 4). It may be related to the higher solute
clearances across the peritoneal membrane in HATs.
Basal PHcy was marginally lower in subjects with Kt/V
> 2 compared to those with Kt/V ≤ 2 (p = 0.05) (Table 4).
Icodextrin, but not AAPDF, significantly decreased PHcy
in PD patients with Kt/V > 2, in those with Kt/V ≤ 2 and
in non diabetic patients (Table 4). Therefore, Icodextrin
may influence the atherosclerotic outcomes through
Hcy-lowering effects, as it was stated previously by Do-
cloux et al [29].
No associations between age, gender, body weight, du-
ration of PD, hemoglobin, PTH, RRF and DUO and PHcy
were found.
In summary: Higher UF, higher D/PCr, HATs, Kt/V >
2, non diabetic patients and Icodextrin use were associ-
ated with decline in PHcy. Conversely, lower UF, lower
D/PCr, LATs, Kt/V ≤ 2, diabetic patients and AAPDF use
were associated with rise in PHcy.
Although it exhibited favorable effects on metabolic
status, blood pressure control and PHcy levels, Icodextrin
seems to intensify systemic inflammation. On the other
hand, although it did not seem to affect adversely the
metabolic status and systemic inflammation, AAPDF
increased PHcy and blood pressure.
The results of the present study suggested that the use
of Icodextrin and AAPDF was associated with beneficial
effects as well as with considerable harmful consequences
that may adversely affect the prognosis and survival of
PD patients.
5. Conclusion
A new PDF containing a mixture of a biocompatible sub-
stance, amino acids without methionine, lower glucose
and GDPs content, and neutral pH will provide sustained
oncotic effect, adequate dialysis and ultrafiltration as
well as will improve nutritional status and metabolic
profile, reduce inflammation, plasma homocyteine and
blood pressure. A PDF with those properties will preserve
the peritoneal membrane and improve the prognosis and
survival of peritoneal dialysis patients.
6. Acknowledgements
The authors would like to thank Prof. Ben Ami Sela,
Clinical Biochemistry Laboratory-Sheba Medical Center,
Tel Hashomer, Israel for his assistance in determination
of PHcy. We also would like to thank Tobie Kuritsky for
her assistance in editing our manuscript.
REFERENCES
[1] P. S. Parfrey and J. D. Harnett, “Long Term Cardiac
Morbidity and Mortality during Dialysis Therapy,” Ad-
vanced Nephrology, Vol. 23, 1994, pp. 311-330.
[2] S. H. Park, P. Stenvinkel and B. Lindholm, “Cardiovas-
cular Biomarkers in Chronic Kidney Disease,” Journal of
Renal Nutrition, Vol. 22, No. 1, 2012, pp. 120-127.
doi:10.1053/j.jrn.2011.10.021
[3] A. H. Mitwalli, A. A. Alam, J. S. Al Wakeel and A. C.
Isnani, “Dyslipidemia in Dialysis Patients,” Saudi Jour-
nal of Kidney Disease and Transplantation, Vol. 22, No.
4, 2011, pp. 689-694.
[4] L. M. Ortega and B. J. Materson, “Hypertension in Peri-
toneal Dialysis Patients: Epidemiology, Pathogenesis, and
Treatment,” Journal of the American Society of Hyper-
tension, Vol. 5, No. 3, 2011, pp. 128-136.
doi:10.1016/j.jash.2011.02.004
[5] M. Moriishi and H. Kawanishi, “Icodextrin and Intrap-
eritoneal Inflammation,” Peritoneal Dialysis Interna-
tional, Vol. 28, Suppl. 3, 2008, pp. S96-S100.
[6] T. Huang, G. Yuan, Z. Zhang, Z. Zou and D. Li, “Car-
diovascular Pathogenesis in Hyperhomocysteinemia,”
Asia Pacific Journal of Clinical Nutrition, Vol. 17, No. 1,
2008, pp. 8-16.
[7] C. van Guldener and F. Stam, “Stehouwer CDA. Homo-
cysteine Metabolism in Renal Failure,” Kidney Interna-
tional, Vol. 59, Suppl. 78, 2001, pp. S234-S237.
doi:10.1046/j.1523-1755.2001.07859.x
[8] M. M. Sagheb, M. A. Ostovan, Z. Sohrabi, E. Atabati, G.
A. Raisjalai and J. Roozbeh, “Hyperhomocysteinemia and
Cardiovascular Risks in Hemodialysis Patients,” Saudi

S. HASSAN ET AL.
34
Journal of Kidney Diseases and Transplantation, Vol. 21,
No. 5, 2010, pp. 863-866.
[9] L. A. Cooker, C. J. Holmes and C. M. Hoff, “Biocom-
patibility of Icodextrin,” Kidney International, Vol. 62,
Suppl. 81, 2002, pp. S34-S45.
doi:10.1046/j.1523-1755.62.s81.6.x
[10] M. Canbakan and G. M. Sahin, “Icodextrine and Insulin
Resistance in Continuous Ambulatory Peritoneal Dialysis
Patients,” Renal Failure, Vol. 29, No. 3, 2007, pp. 289-
293. doi:10.1080/08860220601166271
[11] T. A. Martikainen, A. M. Teppo, C. Grönhagen-Riska and
A. V. Ekstrand, “Glucose-Free Dialysis Solutions: In-
ductors of Inflammation or Preservers of Peritoneal
Membrane?” Peritoneal Dialysis International, Vol. 25,
No. 5, 2005, pp. 453-460.
[12] W. Lin, Y. C. Chen, M. S. Wu, H. J. Hsu, C. Y. Sun, Y.
K.Lin and I. W. Wu, “Icodextrin Dialysate Improves Nu-
tritional and Inflammatory Profiles in Peritoneal Dialysis
Patients,” Renal Failure, Vol. 31, No. 2, 2009, pp. 98-105.
doi:10.1080/08860220802595500
[13] F. K. Li, L. Y.Chan , J. C. Woo, et al., “A 3-Year, Pro-
spective, Randomized, Controlled, Study on Amino Acid
Dialysate in Patients on CAPD,” American Journal of
Kidney Diseases, Vol. 42, No. 1, 2003, pp. 173-183.
doi:10.1016/S0272-6386(03)00421-9
[14] A. S. Levey, J. P. Bosch, J. B. Lewis, T. Greene, N.
Rogers and D. Roth, “A More Accurate Method to Esti-
mate Glomerular Filtration Rate from Serum Creatinine:
A New Prediction Equation, Modification of Diet in Re-
nal Disease Study Group,” Annals of Internal Medicine,
Vol. 130, No. 6, 1999, pp. 461-470.
[15] Z. J. Twardowski, “Clinical Value of Standardized
Equilibration Tests in CAPD Patients,” Blood Purifica-
tion, Vol. 7, No. 2-3, 1989, pp. 95-108.
doi:10.1159/000169582
[16] G. Amici, S. Mastrosimone, G. Da Rin, C. Bocci and A.
Bonadonna, “Clinical Validation of PD Adequest Soft-
ware: Modeling Error Assessment,” Peritoneal Dialysis
International, Vol. 18, No. 3, 1998, pp. 317-321.
[17] H. Ha, M. R. Yu, H. N. Choi, M. K. Cha, H. S. Kang, M.
H. Kim and H. B. Lee, “Effects of Conventional and New
Peritoneal Dialysis Solutions on Human Peritoneal Meso-
thelial Cell Viability and Proliferation,” Peritoneal Di-
alysis International, Vol. 20, Suppl. 5, 2000, pp. S10-
S18.
[18] R. T. Krediet, M. M. Zweers, A. C. vander Wal and D. J.
Struijk, “Neoangiogenesis in the Peritoneal Membrane,”
Peritoneal Dialysis International, Vol. 20, Suppl. 2, 2000,
pp. S19-S25.
[19] J. Delarue and C. Maingourd, “Acute Metabolic Effects
of Dialysis Fluids during CAPD,” American Journal of
Kidney Diseases, Vol. 37, Suppl. 2, 2001, pp. S103-S107.
doi:10.1053/ajkd.2001.20762
[20] N. Posthuma, P. M. ter Wee, A. J. Donker, P. L. Oe, E. M.
Peers and H. A. Verbrugh, “Assesement of the Effective-
ness, Safety, and Biocompatibility of Icodextrin in Auto-
mated Peritoneal Dialysis. The Dextrin in APD in Am-
sterdam (DIANA) Group,” Peritoneal Dialysis Interna-
tional, Vol. 20, Suppl. 2, 2000, pp. S106-S113.
[21] T. W. Kao, H. F. Chuang, K. Y. Hung, K. D. Wu and T. J.
Tsai, “Rate of Decline of Residual Renal Function is As-
sociated with All-Cause Mortality and Technique Failure
in Patients on Long-Term Peritoneal Dialysis,” Nephrol-
ogy Dialysis Transplantation, Vol. 24, No. 9, 2009, pp.
2909-2914. doi:10.1093/ndt/gfp056
[22] S. Kim, J. Oh, S. Kim, W. Chung, C. Ahn, S. G. Kim and
K. H. Oh, “Benefits of Biocompatible PD Fluid for Pres-
ervation of Residual Renal Function in Incident CAPD
Patients: A 1-Year Study,” Nephrology Dialysis Trans-
plantation, Vol. 24, No. 9, 2009, pp. 2899-2908.
doi:10.1093/ndt/gfp054
[23] S. J. Bredie, F. H. Bosch, P. N. Demacker, A. F. Stalen-
hoef and R. Van Leusen, “Effects of Peritoneal Dialysis
with an Overnight Icodextrin Dwell on Parameters of
Glucose and Lipid Metabolism,” Peritoneal Dialysis In-
ternational, Vol. 21, No. 3, 2001, pp. 275-281.
[24] C. Van Guldener, “Why is Homocysteine Elevated in
Renal Failure and What Can Be Expected from Homo-
cysteine-Lowering?” Peritoneal Dialysis International,
Vol. 21, No. 5, 2006, pp. 1161-1166.
doi:10.1093/ndt/gfl044
[25] A. Czupryniak, M. Nowicki, G. Chwatko, A. Jander and
E. Bald, “Peritoneal Clearance of Homocysteine with Ico-
dextrin or Standard Glucose Solution Exchange,” Ne-
phrology (Carlton), Vol. 10, No. 6, 2005, pp. 571-575.
[26] H. F. Brulez, C. van Guldener, A. J. Donker and P. M.
Ter Wee, “The Impact of an Amino Acid-Based Perito-
neal Dialysis Fluid on Plasma Total Homocysteine Levels,
Lipid Profile and Body Fat Mass,” Nephrology Dialysis
Transplantation, Vol. 14, No. 1, 1999, pp. 154-159.
doi:10.1093/ndt/14.1.154
[27] S. Y. Yang, J. W. Huang, K. Y. Shih, et al., “Factors
Associated with Increased Plasma Homocysteine in Pa-
tients Using an Amino Acid Peritoneal Dialysis Fluid,”
Nephrology Dialysis Transplantation, Vol. 20, No. 1,
2005, pp. 161-166. doi:10.1093/ndt/gfh554
[28] S. Haas, C. P. Schmitt, K. Arbeiter, K. E. Bonzel, M.
Fischbach, U. John, A. K. Pieper, T. P. Schaub, J.
Passlick-Deetjen and O. Mehls, “Schaefer FImproved
Acidosis Correction and Recovery of Mesothelial Cell
Mass with Neutral-pH Bicarbonate Dialysis Solution
among Children Undergoing Automated Peritoneal Di-
alysis,” Journal of the American Society of Hypertension,
Vol. 14, No. 10, 2003, pp. 2632-2638.
doi:10.1097/01.ASN.0000086475.83211.DF
[29] D. Ducloux, L. Heuze-Lecornu, R. Gibey, C. Bresson-
Vautrin, P. Vautrin and J. M. Chalopin, “Dialysis Ade-
quacy and Homocyst(e)ine Concentrations in Peritoneal
Dialysis Patients,” Nephrology Dialysis Transplantation,
Vol. 14, No. 3, 1999, pp. 728-731.
doi:10.1093/ndt/14.3.728
[30] A. Vychytil, M. Fodinger, M. Papagiannopoulos, et al.,
“Peritoneal Elimination of Homocysteine Moieties in
Continuous Ambulatory Peritoneal Dialysis Patients,”
Kidney International, Vol. 55, No. 5, 1999, pp. 2054-
2061. doi:10.1046/j.1523-1755.1999.00437.x