Dialysate sodium and sodium gradient in maintenance hemodialysis

Sodium gradient in HD
19. Gomes B, Gysels M, Higginson IJ. What is the latest evidence on
preferences for place of care and place of death? (Abstract). Palliat
Med 2008; 22: 465–466
20. Murtagh FEM, Addington-Hall JM, Edmonds PM et al. Symptoms
in advanced renal disease: a cross-sectional survey of symptom
prevalence in stage 5 chronic kidney disease managed without dialysis.
J Pall Med 2007; 10: 1266–1276
21. Maxwell P, Fitzpatrick R. End-stage renal failure and assessment of
health related quality of life. Qual Health Care, 1998 7:182in PD
patients—decline over time and association with clinical outcomes.
Kidney Int 2002; 61: 239–248
22. Bakewell AB, Higgins RM, Edmunds ME. Quality of life in peritoneal
dialysis patients: decline over time and association with clinical
outcomes. Kidney Int 2002; 61: 239–248
23. Murtagh FE, Marsh JE, Donohoe P et al. Dialysis or not? A comparative survival study of patients over 75 years with chronic kidney dis-
1281
24.
25.
26.
27.
ease stage 5. Nephrol Dial Transplant 2007; 22: 1955–1962. Epub
2007 Apr 4
Morton RL, Tong A, Howard K et al. The views of patients and
carers in treatment decision making for chronic kidney disease: systematic review and thematic synthesis of qualitative studies. BMJ
2010; 340: c112
Burns A, Carson R. Maximum conservative management: a worthwhile treatment for elderly patients with renal failure who choose
not to undergo dialysis. J Palliat Med 2007; 10: 1245–1247
Singer PA, Martin DK, Kelner M. Quality end-of-life care: patients’
perspectives. JAMA 1999; 281: 163–168
Steinhauser KE, Christakis NA, Clipp EC et al. Factors considered
important at the end of life by patients, family, physicians, and other
care providers. JAMA 2000; 284: 2476–2482
Received for publication: 7.1.10; Accepted in revised form: 5.8.10
Nephrol Dial Transplant (2011) 26: 1281–1287
doi: 10.1093/ndt/gfq807
Advance Access publication 8 February 2011
Dialysate sodium and sodium gradient in maintenance hemodialysis:
a neglected sodium restriction approach?
Jair Munoz Mendoza1,2, Sumi Sun2, Glenn M. Chertow1, John Moran1,2, Sheila Doss2 and
Brigitte Schiller1,2
1
Division of Nephrology, Department of Medicine, Stanford University School of Medicine Stanford, CA, USA and 2Satellite
Healthcare, Inc., San Jose, CA, USA
Correspondence and offprint requests to: Brigitte Schiller; E-mail: [email protected]
Abstract
Background. A higher sodium gradient (dialysate sodium
minus pre-dialysis plasma sodium) during hemodialysis
(HD) has been associated with sodium loading; however,
its role is not well studied. We hypothesized that a sodium
dialysate prescription resulting in a higher sodium gradient
is associated with increases in interdialytic weight gain
(IDWG), blood pressure (BP) and thirst.
Methods. We conducted a cross-sectional study on 1084
clinically stable patients on HD. A descriptive analysis of
the sodium prescription was performed and clinical associations with sodium gradient were analyzed.
Results. The dialysate sodium prescription varied widely
across dialysis facilities, ranging from 136 to 149 mEq/L,
with a median of 140 mEq/L. The mean pre-HD plasma
sodium was 136.7 ± 2.9 mEq/L, resulting in the majority
of subjects (n = 904, 83%) being dialyzed against a positive sodium gradient, while the mean sodium gradient was
4.6 ± 4.4 mEq/L. After HD, the plasma sodium increased in
nearly all patients (91%), reaching a mean post-HD plasma
sodium of 141.3 ± 2.5 mEq/L. We found a direct correlation
between IDWG and sodium gradient (r = 0.21, P <
0.0001). After adjustment for confounders and clustering
by facilities, the sodium gradient was independently associated with IDWG (70 g/mEq/L, P < 0.0001). There were
no significant associations among sodium gradient and BP,
whether measured as pre-HD systolic (r = −0.02), diastolic
(r = −0.06) or mean arterial pressure (r = −0.04). Post-HD
thirst was directly correlated with sodium gradient (r =
0.11, P = 0.02).
Conclusion. Sodium gradient is associated with statistically significant and clinically meaningful differences in
IDWG in stable patients on HD.
Keywords: dialysate sodium; hemodialysis; hypertension; interdialytic
weight gain; sodium gradient
Introduction
Patients with end-stage renal disease (ESRD) on hemodialysis (HD) experience exceptionally high rates of cardiovascular mortality and morbidity [1]. Important risk factors
include hypertension (HTN) [2,3] and fluid retention,
© The Author 2010. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved.
For Permissions, please e-mail: [email protected]
1282
measured as interdialytic weight gain (IDWG) [4,5]. The
normal renal regulatory mechanisms to control extracellular fluid volume and osmolality are no longer effective in
patients with ESRD. In the absence of kidney function and
urine output, the burden of maintaining volume homeostasis, electrolyte and acid–base balance falls solely on the HD
procedure [6,7]. A large percentage of patients on HD require multiple antihypertensive agents, yet fail to achieve
satisfactory control of HTN. The degree to which the dialysate prescription, and in particular the dialysate sodium
concentration, influences blood pressure (BP) and IDWG
via changes in sodium flux, plasma volume or other parameters is not well understood.
Sodium is removed during HD by both diffusion and
convection (ultrafiltration). The contribution of diffusion
and the direction of sodium transfer depend on the difference between dialysate and plasma sodium concentrations,
the so called ‘sodium gradient’ [7, 8]. If the sodium gradient is positive, the plasma sodium concentration after HD
will generally increase [9], potentially resulting in higher
IDWG and BP by stimulating thirst [10]. These hypothesized relationships have been studied in only a small number of patients [6, 11].
This study aimed to describe the distribution of prescribed dialysate sodium concentrations in a medium-sized
dialysis provider (Satellite Healthcare, Inc.) and to investigate the relationships among dialysate sodium, sodium
gradient, IDWG, BP and thirst. We hypothesized that
higher sodium gradients would be directly correlated with
IDWG, mean arterial pressure, systolic BP and thirst.
Materials and methods
We conducted a cross-sectional study with data obtained from 1084 HD
patients during the routine monthly blood draw in September 2009 in all
26 satellite healthcare dialysis facilities (21 located in California and 5 in
Texas). We included clinically stable adult prevalent HD patients with
minimal residual kidney function (urine output<100 mL/day) undergoing
conventional thrice weekly in-center HD for at least 3 months. Patients
were excluded if they had any of the following criteria: hospitalization
within the preceding month, more than one missed treatment in the preceding 2 weeks, change in dialysate sodium prescription within the preceding 3 months, spKt/Vurea <1.2, pre-HD plasma glucose > 300 mg/dL,
HD session length shortened by >25% and plasma sodium not measured
on the study day.
The majority of subjects were dialyzed with Fresenius F-180 or F-200
dialyzers, using primarily Fresenius 2008K or 2008H and Gambro Phoenix
delivery systems. Automated BP machines (M-200-NIBP Colin, PressMates BP-8800C Colin or HD-BPM) and Tronix 6102, 6702 scales were
used as per routine care in the facilities.
On the study day, 62% of patients undergoing conventional thrice
weekly HD in participating dialysis facilities and 59% of the actual study
population had a pre-HD BP ≥140/90 mmHg. All patients received dietary
advice to limit salt intake to no >5 g/day as per standard of care. Following
an initial assessment of diet, patients were evaluated monthly or more frequently if the IDWG was >4% of the dry weight. The dialysate sodium and
dry weight were prescribed by the patient's treating nephrologist based
upon clinical evaluation. The study was approved by the Satellite Healthcare Research Committee.
We used the electronic medical record to collect data on patient
demographics, BP (pre- and intradialytic and post-HD), adverse events
(including headache, cramps, nausea and vomiting) and interventions
(Trendelenburg position, saline use, reduction in ultrafiltration rate)
for intradialytic hypotension, dry weight, dialysate sodium concentration
and pre- and postdialysis weight.
Blood samples were collected prior to the first treatment of the week
according to the standard protocol for monthly laboratory monitoring and
J. Munoz Mendoza et al.
processed at Satellite Laboratories (Redwood City, CA). Laboratory tests
included albumin and pre- and post-HD plasma sodium (measured by indirect ion-selective electrode) and blood urea nitrogen (BUN). Pre- and
post-HD BUN were used for formal urea kinetic modeling, which included an estimated total body water and normalized protein equivalent
of nitrogen appearance.
We assessed thirst in subjects from the 10 facilities with the highest
variability in dialysate sodium prescription (>10% of subjects with higher
or lower than 140 mEq/L) in order to capture a wide range of sodium
gradients. All patients from the sampled facilities were asked to indicate
their degree of thirst immediately before and after HD using a visual
analogue scale (with 0 indicating no thirst and 10 very thirsty) in response
to the question, ‘How thirsty are you now?’ Similar tools have been used
in healthy individuals [12] and in HD patients [13].
Operational definitions
We estimated IDWG as the difference between pre-HD weight minus the
post-HD weight reached after the previous HD session, calculated as the
average of the preceding six available intervals, excluding the interdialytic
periods of >3 days. The BP was estimated as the average sitting pre- or
post-HD BPs from the last six HD sessions. We defined intradialytic
hypotension as at least one episode of a fall in systolic BP >20 mmHg
associated with symptoms or with any intervention during the last treatment. We calculated the mean plasma sodium by averaging the last three
available monthly pre-HD plasma sodium concentrations over the preceding 6 months. If the patient was prescribed sodium modeling, we calculated the sodium gradient as the difference between the dialysate sodium
time-averaged concentration (TACNa) [14] and the pre-HD plasma sodium.
Statistical analysis
Continuous variables were summarized as mean ± SD or median with
interquartile range (IQR). Categorical variables were expressed as proportions. Differences in pre-HD plasma sodium among dialysate sodium
groups were compared by one-way analysis of variance. Correlations were
assessed with the Pearson product moment or Spearman rank coefficient.
We used multivariable regression analysis to estimate the effect of sodium
gradient on IDWG, while adjusting for age, sex, race, dialysis vintage
(time since initiation of dialysis) and dry weight. We tested for the presence of interactions between sodium gradient and the other covariates
(age, sex, race and dialysis vintage); no significant interactions were detected. The generalized estimating equations approach was used to account
for clustering of patients at the facility level. Although alternate correlation
structures were explored, the final estimates assumed an exchangeable
correlation structure, meaning that pairs of patients from a given facility
share the same correlation. We considered two-tailed P-values <0.05 as
statistically significant. Statistical analyses were performed using SAS
EG version 4.2 (SAS Institute, Cary, NC).
Table 1. Clinical characteristics of patient population grouped by
dialysate sodium concentrationsa
Dialysate sodium concentration, mEq/L
Characteristic
140
Patients, %
560 (52)
Age, years
65 (53–76)
Male, %
290 (52)
Black, %
48 (8.6)
Diabetes, %
322 (58)
Dry body weight, kg
71.0 ± 18.4
Body water volume, L
32.1 ± 6.6
Vintage, months
45 (24–77)
Sodium modeling, %
20 (3.6)
Pre-HD plasma sodium, mEq/L 136.8 ± 2.9
Albumin, g/dL
3.8 ± 0.3
spKt/V
1.7 ± 0.3
nPNA
1.0 ± 0.1
>140
<140
397 (36)
60 (51–72)
212 (53)
47 (11.8)
239 (60)
74.1 ± 21
33.0 ± 7.4
59 (34–89)
306 (77)
136.6 ± 3.0
3.8 ± 0.4
1.7 ± 0.3
1.0 ± 0.1
127 (12)
58 (50–70)
77 (61)
44 (34.7)
79 (62)
78.1 ± 17.9
36.1 ± 7.1
40 (22–65)
6 (4.7)
137.2 ± 3.1
3.8 ± 0.4
1.6 ± 0.3
1.0 ± 0.1
a
Values are expressed as mean ± SD, numbers (%) or median (25th–75th)
to describe selected characteristics at baseline.
Sodium gradient in HD
Results
Of the 1397 adult prevalent HD patients with minimal residual kidney function undergoing thrice weekly in-center
HD, 313 subjects (22%) were excluded according to one or
more of the criteria outlined above, resulting in a final analytic sample of 1084 subjects.
Dialysate sodium prescription
The median dialysate sodium prescription was 140 mEq/L,
ranging from 136 to 149 mEq/L. More than half of the
patients (n=560, 52%) were dialyzed with a standard dialysate sodium of 140 mEq/L. Nearly one-third (n=332,
31%) were dialyzed with sodium modeling: 158 (47.6%)
with a linear and 174 (52.4%) with a step protocol.
1283
The patient characteristics are shown in Table 1, stratified by dialysate sodium prescription (140, <140 and >140
mEq/L). The patients treated with dialysate sodium concentrations <140 mEq/L were younger, heavier and more
likely to be black, while patients with a dialysate sodium
prescription >140 mEq/L had a longer dialysis vintage
and a high proportion (77%) were prescribed sodium
modeling.
The dialysate sodium prescription practices varied
across facilities (Figure 1). Almost all the subjects (97%,
n=123) prescribed a dialysate sodium <140 mEq/L were
from the five Texas facilities, reflecting the practice of the
treating nephrology group. A dialysate sodium prescription
>140 mEq/L was used for all patients in one facility and
was also used in ≥50% of the patients in another seven
facilities. Sodium modeling was prescribed in nearly all fa-
Fig. 1. Percentage of patients in each facility with dialysate sodium prescriptions greater or lower than 140 mEq/L.
Fig. 2. Frequency distribution of mean pre-HD plasma sodium concentrations in 1084 HD patients (black arrow indicates dialysate sodium of
140 mEq/L).
1284
J. Munoz Mendoza et al.
Fig. 3. Frequency distribution of sodium gradient in 1084 HD patients.
Fig. 4. Correlation between sodium gradient and IDWG (r = 0.21, P < 0.0001).
cilities (24 of 26) with varying proportions: in six facilities
at least 50% of patients were on sodium modeling and in
one facility it was the exclusive prescription.
Plasma sodium and sodium gradient
The mean pre-HD plasma sodium concentration was 136.7
± 2.9 mEq/L. The majority (n = 904, 83%) of patients had
pre-HD plasma sodium concentrations <140 mEq/L, the
most common dialysate sodium prescription (Figure 2).
However, the pre-HD plasma sodium concentration was
not significantly different among the patients dialyzed with
different dialysate sodium concentrations (P = 0.12; Table 1).
After dialysis, the mean plasma sodium concentration
increased to 141.3 ± 2.5 mEq/L. The vast majority (91%)
of patients experienced an increase in plasma sodium concentration (post- versus pre-HD). The mean sodium gradient was 4.6 ± 4.4 mEq/L, with a wide range from −7 to 24
mEq/L (Figure 3). Only a small number of patients (n = 180,
17%) had a sodium gradient ≤0 mEq/L, and, of these, 124
were dialyzed against a negative gradient.
Sodium gradient and IDWG
The mean IDWG was 2.8 ± 1.1 kg, with a range from −0.7
to 7.2 kg. There was a direct correlation between IDWG
and sodium gradient (r = 0.21, P < 0.0001; Figure 4).
When IDWG was indexed to the estimated dry weight
(i.e. estimated as percent IDWG), the correlation with sodium gradient was stronger (r = 0.30, P < 0.0001). Both
Sodium gradient in HD
1285
Table 2. Increase in IDWG/1 mEq/L increase in sodium gradient adjusted for clustering of patients at the
facility level
Increase in IDWG/1 mEq/L increase in sodium gradient
Variable
Estimate
95% CI
P-value
Unadjusted model
Multivariate adjusted modela
Plus facility clustering
0.05
0.06
0.07
0.04–0.06
0.05–0.07
0.06–0.08
<0.0001
<0.0001
<0.0001
a
Adjusted by age, male, black, dry weight and vintage.
correlations remained similar in magnitude and statistically
significant (i.e. non-zero) when excluding subjects on sodium modeling. After adjustment for age, sex, race, dialysis
vintage, dry weight and accounting for clustering at the
facility level, a 1 mEq/L increase in the sodium gradient
was associated with a 70 g increase in IDWG (P < 0.0001).
This was roughly equivalent to a 350 g difference in IDWG
for a 5 mEq/L difference in sodium gradient (Table 2,
Figure 4). Of note, the group of patients with a sodium
gradient ≤0 mEq/L had an IDWG lower than subjects
with positive sodium gradient (2.5 versus 2.9 kg, P < 0.001).
Sodium gradient and BP
We found no significant associations between sodium gradient and BP, whether the latter was measured as pre-HD
systolic (r = −0.02), diastolic (r = −0.06) or mean arterial
pressure (r = −0.04) (P > 0.05 for all comparisons). We
found weak inverse correlations between sodium gradient
and post-HD mean arterial pressure (r = −0.09, P = 0.005)
and post-HD diastolic BP (r = −0.11) (P = 0.004).
We found no increased frequency of intradialytic
hypotension in patients with sodium gradients of zero or
less compared to patients with positive sodium gradients
(22 versus 24%, P = 0.52).
Sodium gradient and thirst
We noted a surprisingly low degree of self-reported thirst
measured by a visual analogue scale (from 0 to 10). The
median thirst score was 2 pre-HD (IQR 1–5) and 2 postHD (IQR 0–5). Post-HD thirst was directly, albeit weakly,
correlated with sodium gradient (r = 0.11, P = 0.02), but
there was no correlation between sodium gradient and preHD thirst (r = −0.04, P = 0.37).
Discussion
Recommending dietary sodium restriction is a part of
routine HD-related care for the management of both HTN
and fluid overload. However, higher dialysate sodium prescriptions have been widely adopted in recent years in an
attempt to decrease hemodynamic instability in patients
undergoing HD [15]. This trend was evidenced in our population, despite variation in prescription practice at the facility level, where high dialysate sodium concentrations and
positive sodium gradients were the rule.
We found a direct correlation between sodium gradient
and IDWG (and percent IDWG), as previously reported in
a smaller sample of 58 HD patients by Keen and Gotch [6].
The effect of sodium gradient on IDWG remained significant after taking into consideration other factors that may
influence IDWG. The association between higher sodium
gradients and higher IDWG is likely attributable to the increased post-HD plasma sodium [9,11,16,17].
Excessive fluid intake manifesting as IDWG can contribute to left ventricular hypertrophy and cardiovascular events.
Kalantar-Zadeh et al. recently found IDWG ≥4.0 kg to be
associated with a 25% increased risk of cardiovascular death
compared to IDWG of 1.5–2.0 kg [4]. Although our current
approach with dietary salt restriction may decrease left ventricular hypertrophy [18], BP [19–21] and IDWG [19,20],
the benefits may be muted due to poor adherence. Individualizing the dialysate sodium prescription by matching dialysate sodium to the patient's pre-HD sodium [10,15] is a simple
complementary strategy to restrict sodium in HD that may
help reduce IDWG in some patients.
We did not find a direct correlation between sodium
gradient and pre-HD BP. However, any correlation may
well be masked by the use of antihypertensive agents—
and indeed, one would expect antihypertensive therapy to
be maximized in those patients who are most prone to
HTN with high IDWG. In a recent analysis of a large
cohort of prevalent HD patients, a 1% increase in IDWG
was only associated with a 1 mmHg increase in systolic
BP [22]. Also, our cross-sectional design may have prevented us from detecting changes in BP that occur weeks
to months after reducing dry weight—the ‘lag phenomenon’
[23,24].
The prescription of lower dialysate sodium concentrations in an attempt to reach eunatremia raises the concern
of provoking intradialytic hypotension. However, as in previous studies [6, 25], we found no increased frequency of
intradialytic hypotension in patients with negative or no
sodium gradient or less (in theory the highest risk group)
compared to patients with positive sodium gradients. Indeed, two other studies have reported a reduction in the
frequency of intradialytic hypotension after decreasing
the dialysate sodium [11, 16]. Additionally, biofeedback
systems that modulate blood volume contraction by adjusting the ultrafiltration and dialysate conductivity have been
shown to decrease intradialytic hypotension without salt
loading [26].
As reported previously, the sodium gradient was associated with post-HD thirst [11,16]. The low degree of thirst
scores reported here may be related to the timing of the
self-assessment. It has been previously shown that thirst
is more commonly experienced 4–6 h after the end of
1286
HD [27], rather than immediately before and after HD as
in our study. In addition, our visual analogue instrument
may have had limited discriminatory power.
Some authors have suggested the concept of a unique
pre-HD plasma sodium, the so called sodium ‘set-point’
for each patient [6,10,15,17]. Supporting this hypothesis,
recently, Peixoto et al. [28] observed stable long-term
pre-HD sodium concentrations in a veterans population
predominantly using a single dialysate sodium prescription.
In our larger and more diverse patient population, we found
no differences in the pre-HD plasma sodium concentrations
among patients grouped by dialysate sodium prescription
ranges, but we need prospective studies to confirm this
observation. Whether lower pre-HD plasma sodium is
the cause or the consequence of excess fluid intake remains
unanswered. Lindley [29] postulated that there are two
groups of patients on HD: one group with normal plasma
sodium drinking water in response to sodium-induced
osmometric thirst and another group with low plasma sodium ingesting fluid due to non-salt-related reasons, such
as xerostomia, comfort or social drinking.
To the best of our knowledge, this is the largest reported
study of clinically stable adult patients on HD with minimal
residual kidney function dialyzed under current techniques
with different dialysate sodium concentrations and a broad
range of sodium gradients, demonstrating an association of
sodium gradient and IDWG.
There are several important limitations to this study. The
cross-sectional design precludes the establishment of a
causal relationship between sodium gradient and IDWG.
Sodium balance was not calculated by including fluid
and salt intake, and actual dialysate and ultrafiltrate sodium
were not measured. Thirst and intradialytic hypotension
data were obtained in a subset of patients; comorbidities
and antihypertensive agent use were not captured. Finally,
the absence of an association between sodium gradient
and BP could reflect the limited precision and lack of uniformity with which BP was measured, as well as the effect of
prescribed antihypertensive medication. In future studies,
more comprehensive determinations of BP, including ambulatory BP monitoring, could be employed [30]. Moreover, interventional studies would help to determine
whether changes in sodium gradient and IDWG induced
by lower dialysate sodium prescriptions would yield lower
BPs over time.
In conclusion, the sodium gradient is associated with
statistically significant and clinically meaningful differences in IDWG in stable patients on HD and possibly with
post-HD thirst. Prospective studies altering dialysate sodium prescription to reduce the sodium gradient with or
without matching the dialysate sodium to the patient's
pre-HD plasma sodium are needed to determine a causal
relationship and estimate clinical benefit.
Conflict of interest statement. My statement (on behalf of all the authors) is
as follows: we have had no involvements that might raise the question of
bias in the work reported or in the conclusions, implications or opinions
stated.
J.M.M. MD: ‘The results presented in this paper have not been published previously in whole or part, except in abstract form’.
J. Munoz Mendoza et al.
(See related article by Lomonte et al. Do not forget to individualize dialysate sodium prescription. Nephrol Dial Transplant 2011; 26: 1126–1128)
References
1. Foley RN, Parfrey PS, Sarnak MJ. Clinical epidemiology of cardiovascular disease in chronic renal disease. Am J Kidney Dis 1998; 32
(5 Suppl. 3) S112–S119
2. Horl MP, Horl WH. Hemodialysis-associated hypertension:
pathophysiology and therapy. Am J Kidney Dis 2002; 39: 227–244
3. Agarwal R, Nissenson AR, Batlle D et al. Prevalence, treatment, and
control of hypertension in chronic hemodialysis patients in the United
States. Am J Med 2003; 115: 291–297
4. Kalantar-Zadeh K, Regidor DL, Kovesdy CP et al. Fluid retention is
associated with cardiovascular mortality in patients undergoing longterm hemodialysis. Circulation 2009; 119: 671–679
5. Foley RN, Herzog CA, Collins AJ. Blood pressure and long-term
mortality in United States hemodialysis patients: USRDS Waves 3
and 4 Study. Kidney Int 2002; 62: 1784–1790
6. Keen ML, Gotch FA. The association of the sodium “setpoint” to
interdialytic weight gain and blood pressure in hemodialysis patients.
Int J Artif Organs 2007; 30: 971–979
7. Pozzoni P, DI Fillipo S, Pontoriero G et al. Effectiveness of sodium
and conductivity kinetic models in predicting end-dialysis plasma
water sodium concentration: preliminary results of a single-center
experience. Hemodial Int 2007; 11: 169–177
8. Kimura G, Van Stone JC, Bauer JH et al. A simulation study on
transcellular fluid shifts induced by hemodialysis. Kidney Int 1983;
24: 542–548
9. Flanigan MJ, Khairullah QT, Lim VS. Dialysate sodium delivery can
alter chronic blood pressure management. Am J Kidney Dis 1997; 29:
383–391
10. Santos SF, Peixoto AJ. Revisiting the dialysate sodium prescription as
a tool for better blood pressure and interdialytic weight gain management in hemodialysis patients. Clin J Am Soc Nephrol 2008; 3:
522–530
11. de Paula FM, Peixoto AJ, Pinto LV et al. Clinical consequences of an
individualized dialysate sodium prescription in hemodialysis patients.
Kidney Int 2004; 66: 1232–1238
12. Rolls BJ, Wood RJ, Rolls ET et al. Thirst following water deprivation
in humans. Am J Physiol 1980; 239: R476–R482
13. Mistiaen P. Thirst, interdialytic weight gain, and thirst-interventions
in hemodialysis patients: a literature review. Nephrol Nurs J 2001; 28:
601–604, 610–613; quiz 614–615
14. Song JH, Lee SW, Suh CK et al. Time-averaged concentration of
dialysate sodium relates with sodium load and interdialytic weight
gain during sodium-profiling hemodialysis. Am J Kidney Dis 2002;
40: 291–301
15. Flanigan MJ. Role of sodium in hemodialysis. Kidney Int Suppl 2000;
76: S72–S78
16. Dominic SC, Ramachandran S, Somiah S et al. Quenching the thirst
in dialysis patients. Nephron 1996; 73: 597–600
17. Gotch FA, Lam MA, Prowitt M et al. Preliminary clinical results with
sodium-volume modeling of hemodialysis therapy. Proc Clin Dial
Transplant Forum 1980; 10: 12–17
18. Kayikcioglu M, Tumuklu M, Ozkahya M et al. The benefit of salt
restriction in the treatment of end-stage renal disease by haemodialysis. Nephrol Dial Transplant 2009; 24: 956–962
19. Maduell F, Navarro V. [Assessment of salt intake in hemodialysis].
Nefrologia 2001; 21: 71–77
20. Ahmad S. Dietary sodium restriction for hypertension in dialysis patients. Semin Dial 2004; 17: 284–287
21. Scribner BH. A personalized history of chronic hemodialysis. Am J
Kidney Dis 1990; 16: 511–519
22. Inrig JK, Patel UD, Gillespie BS et al. Relationship between
interdialytic weight gain and blood pressure among prevalent
hemodialysis patients. Am J Kidney Dis 2007; 50: 108–118, 118
e1–118 e4
Comparison of nocturnal haemodialysis and conventional haemodialysis
1287
23. Shaldon S, Vienken J. The long forgotten salt factor and the benefits
of using a 5-g-salt-restricted diet in all ESRD patients. Nephrol Dial
Transplant 2008; 23: 2118–2120
24. Charra B, Bergstrom J, Scribner BH. Blood pressure control in dialysis patients: importance of the lag phenomenon. Am J Kidney Dis
1998; 32: 720–724
25. Daugirdas JT, Al-Kudsi RR, Ing TS et al. A double-blind evaluation
of sodium gradient hemodialysis. Am J Nephrol 1985; 5: 163–168
26. Basile C, Giordano R, Vernaglione L et al. Efficacy and safety of
haemodialysis treatment with the hemocontrol biofeedback system: a
prospective medium-term study. Nephrol Dial Transplant 2001; 16:
328–334
27. Giovannetti S, Barsotti G, Cupisti A et al. Dipsogenic factors operating in chronic uremics on maintenance hemodialysis. Nephron
1994; 66: 413–420
28. Peixoto AJ, Gowda N, Parikh CR et al. Long-term stability of serum
sodium in hemodialysis patients. Blood Purif 2010; 29: 264–267
29. Lindley EJ. Reducing sodium intake in hemodialysis patients. Semin
Dial 2009; 22: 260–263
30. Agarwal R, Peixoto AJ, Santos SF et al. Pre- and postdialysis blood
pressures are imprecise estimates of interdialytic ambulatory blood
pressure. Clin J Am Soc Nephrol 2006; 1: 389–398
Received for publication: 22.9.10; Accepted in revised form: 13.12.10
Nephrol Dial Transplant (2011) 26: 1287–1296
doi: 10.1093/ndt/gfq724
Advance Access publication 9 December 2010
Comparison of 4- and 8-h dialysis sessions in thrice-weekly
in-centre haemodialysis
Ercan Ok1, Soner Duman1, Gulay Asci1, Murat Tumuklu2, Ozen Onen Sertoz3, Meral Kayikcioglu4,
Huseyin Toz1, Sıddık M. Adam5, Mumtaz Yilmaz1, Halil Zeki Tonbul6, Mehmet Ozkahya1
and On behalf of the ‘Long Dialysis Study Group’
1
Division of Nephrology, Ege University School of Medicine, Izmir, Turkey, 2Department of Cardiology, Kent Hospital, Izmir, Turkey,
Department of Psychiatry, 4Department of Cardiology, Ege University School of Medicine, Izmir, Turkey, 5Division of Nephrology,
Adana Training and Research Hospital, Adana, Turkey and 6Division of Nephrology, Selcuk University School of Medicine, Konya,
Turkey
3
Correspondence and offprint requests to: Ercan Ok; E-mail: [email protected]
Abstract
Background. Longer dialysis sessions may improve outcome in haemodialysis (HD) patients. We compared the
clinical and laboratory outcomes of 8- and 4-h thriceweekly HD.
Methods. Two-hundred and forty-seven HD patients who
agreed to participate in a thrice-weekly 8-h in-centre nocturnal HD (NHD) treatment and 247 age-, sex-, diabetes
status- and HD duration-matched control cases to 4-h
conventional HD (CHD) were enrolled in this prospective
controlled study. Echocardiography and psychometric
measurements were performed at baseline and at the
12th month. The primary outcome was 1-year overall
mortality.
Results. Overall mortality rates were 1.77 (NHD) and 6.23
(CHD) per 100 patient-years (P = 0.01) during a mean
11.3 ± 4.7 months of follow-up. NHD treatment was associated with a 72% risk reduction for overall mortality compared to the CHD treatment (hazard ratio = 0.28, 95%
confidence interval 0.09–0.85, P = 0.02). Hospitalization
rate was lower in the NHD arm. Post-HD body weight
and serum albumin levels increased in the NHD group.
Use of antihypertensive medications and erythropoietin
declined in the NHD group. In the NHD group, left atrium
and left ventricular end-diastolic diameters decreased and
left ventricular mass index regressed. Both use of phosphate binders and serum phosphate level decreased in
the NHD group. Cognitive functions improved in the
NHD group, and quality of life scores deteriorated in the
CHD group.
Conclusions. Eight-hour thrice-weekly in-centre NHD
provides morbidity and possibly mortality benefits compared to conventional 4-h HD.
Keywords: in-centre haemodialysis; nocturnal; outcomes; survival
Introduction
The mortality rate of patients treated with haemodialysis
(HD) remains unacceptably high despite several improvements in dialysis technology and general medical care [1].
The low level of quality of life (QOL) is also an important
concern in this population.
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