NDT Advance Access published online on July 7, 2008
Nephrology Dialysis Transplantation, doi:10.1093/ndt/gfn384
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Acute central haemodynamic effects induced by intraperitoneal glucose instillation
1 Renal Division, Department of Internal Medicine, Ghent University Hospital 2 Heymans Institute of Pharmacology, Ghent University, Belgium
Correspondence and offprint requests to: Wim Van Biesen, Renal Division, Department of Internal Medicine, University Hospital Ghent, De Pintelaan 185, 9000 Ghent, Belgium. Tel: +32-9-2404509; Fax: +32-9-2404599; E-mail: wim.vanbiesen{at}ugent.be
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Abstract |
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Background. The supposed lack of a haemodynamic impact of peritoneal dialysis (PD) has been challenged recently by the finding of a mild increase of peripheral blood pressure (BP) during an acute dwell. It is not clear whether, besides the effect of changes in intraperitoneal (IP) volume and/or pressure, IP glucose instillation and absorption plays a role in this. Therefore, we tested the impact of IP instillation of glucose on the evolution of central haemodynamic parameters, using SphygmoCor®, during an acute dwell with two different glucose concentrations.
Methods. Stable, non-diabetic PD patients (N = 22) were treated consecutively in a randomized, cross-over design (A then B or B then A) with one 1.36% (A) and one 3.86% (B) physioneal dwell of 100 min. Central BP was measured with SphygmoCor® and blood was sampled for serum glucose and insulin levels every 20 min. Insulin resistance was defined as a Homeostatic Model Assessment Index (HOMA-index) >1.4.
Results. Serum glucose levels rose during both the 1.36% and the 3.86% dwell, whereas insulin levels rose only during the 3.86% dwell. The increase of both glucose and insulin levels was more pronounced in patients with insulin resistance (11/22 patients). There was, however, no accompanying change versus baseline in haemodynamic parameters (carotid systolic blood pressure, diastolic BP, heart rate or augmentation index).
Conclusion. Despite substantial increases in blood glucose and insulin levels, there was no accompanying change in central haemodynamic parameters during an acute PD dwell with low or high glucose concentrations.
Keywords: central blood pressure; glucose; haemodynamic; peritoneal dialysis; tonometry
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Introduction |
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Mortality from cardiovascular disease is higher in patients with renal impairment than in the general population [1–3] and is the major cause of death in patients on renal replacement therapy [4]. Haemodynamic alterations such as volume overload and hypertension contribute to the accelerated progression of cardiovascular disease in dialysis patients [5–7].
It is a generally held belief that no acute haemodynamic changes are provoked during peritoneal dialysis (PD). The few studies evaluating changes in haemodynamic parameters indicate, however, that some mild changes in blood pressure (BP) and vascular tone do occur during an acute dwell [8,9]. These changes can theoretically be attributed to different potential mechanisms: (i) a change in intra-abdominal volume and/or pressure [10]; (ii) the absorption of glucose and the ensuing insulin release [11] and (iii) a pure bio-incompatibility of the dialysis solution [12].
The role of intraperitoneal (IP) volume and/or pressure has been elucidated in a previous study demonstrating that volume instillation with a non-glucose-containing solution (icodextrin, Baxter Healthcare, Ireland) induced an increase in IP pressure and a related change in haemodynamic parameters [10]. As in these experiments no glucose load was given, this does not exclude an additional role of glucose absorption in acute haemodynamic changes during PD. In healthy volunteers, it appears that intravenous glucose loading does not alter BP [12]. It is important to know whether glucose has a role in these haemodynamic effects, as this would be an argument for the further search for non-glucose osmotic agents [13], and for the avoidance of hypertonic glucose by appropriate dietary salt restriction and use of icodextrin.
Previous studies in this field only measured peripheral BP and not central haemodynamic parameters, whereas the latter have been shown to be the most predictive of mortality in clinical trials involving both renal [14] and non-renal populations. It appears thus appropriate to use central haemodynamic parameters as sensitive and clinically relevant markers of haemodynamic changes during an acute dwell in PD.
We performed experiments using the SphygmoCor® system to assess central BP and haemodynamic parameters and their evolution in PD patients during acute dwell situations.
The aim of the present study was to investigate the acute effect of a glucose-containing PD dwell on central haemodynamic parameters, using applanation tonometry of the carotid artery. Two dialysate fluids with different glucose concentrations were compared, assuming that the potential effects would be dose dependent and detectable by correlating changes in the haemodynamic parameters with changes in parameters of glucose metabolism.
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Patients and methods |
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Patients over 18 years old, on PD for at least 1 month and in stable clinical condition were eligible for the study. Patients with documented congestive heart failure or with diabetes requiring insulin were excluded. Patients were considered euvolemic, as assessed by their nephrologist. All patients were oedema free at the day of the study.
The study was approved by the Local Research Ethics Committee and written informed consent was obtained from each participant.
Study protocol
Patients were asked to refrain from food intake, caffeine-containing beverages and smoking at least 12 h before start of the study. All anti-hypertensive medication was withheld 24 h before the experiments and delayed until the end of the study session. The study started at 8.00 a.m. with a standardized breakfast, to avoid influence of differences in intestinal glucose absorption. The preceding overnight dwell was standardized to 1.36% to avoid patients being relatively dehydrated or too much glucose loaded. The antecubital vein was punctured with a venflon catheter for repeated blood sampling. After this, a complete drainage of the overnight dwell was performed, immediately after which the fill for the experiments was started. Drainage was considered complete if no more fluid was drained during 2 min. No additional manipulations or movements were performed during drainage, as this could interfere on itself with haemodynamic parameters.
Glucose 1.36% and glucose 3.86% dialysates with low glucose degradation products (GDP) content and physiologic pH (Physioneal, Baxter Healthcare S.A., Ireland) were used.
The patients were randomized to one of the two following possibilities: (i) regimen A, immediately followed by regimen B or (ii) regimen B, immediately followed by regimen A (randomized, cross-over design). Regimens A and B were performed consecutively on the same day.
Regimen A: infusion of 2 l of glucose 1.36%, followed by a dwell of 100 min.
Regimen B: infusion of 2 l of glucose 3.86%, followed by a dwell of 100 min.
Baseline measurements (t0) were started after at least 10 min of supine rest. After instillation of the dialysate, blood sampling for biochemistry and haemodynamic measurements were performed every 20 min for 2 x100 min.
Brachial BP was measured with a validated oscillometric device (Omron M4-I; Omron Healthcare Europe) and the mean of three stable (coefficient of variation 
5%) consecutive measurements was used.
Local carotid systolic blood pressure (CSP) was measured by applanation tonometry using the SphygmoCor® device (AtCor Medical, Sydney, Australia). Carotid pressure waves were calibrated on diastolic and mean arterial pressure (MAP), obtained from the numeric integral of a brachial artery tonometric pressure wave over time, as previously described [15], to obtain CSP. Such calibration assumes that the MAP minus diastolic BP is constant throughout the large artery tree and yields values that are valid surrogates for central measures [16] that are not prone to errors from centrifugal pulse pressure (PP) amplification or transfer algorithms. Augmentation pressure (AGP) and aortic pressure (AP) were obtained from pulse wave analysis of a carotid waveform as described earlier using the SphygmoCor® software (AtCor Medical, Sydney, Australia) [15]. AGP was defined as the pressure difference between the first and the second shoulder of the pulse wave. PP was defined by subtracting the minimal (diastolic) pressure from the maximal (systolic) pressure, both measured centrally as derived from the pulse wave analysis. Augmentation index (AI) was defined as the ratio of AGP and PP. All haemodynamic measurements were done at baseline, and repeated every 20 min thereafter.
Ultrafiltration volumes were measured immediately after complete drainage. Patients remained in the supine position during the complete dwell.
Immediately before infusion, and every 20 min after, blood was sampled from the antecubital vein, for the assessment of glucose and insulin. At each time point, 5 ml blood was taken and centrifuged at 3000 rpm during 10 min. Afterwards, serum was frozen at –80°C awaiting analysis in one single batch.
The glucose and insulin measurements were performed on a Roche–Hitachi Modular Analytics P machine, using the hexokinase-based method for glucose and the immunochemical method for insulin.
From these values, the Homeostatic Model Assessment Index (HOMA-index) was calculated to express insulin sensitivity:
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A value >1.4 at baseline (t0) was considered to indicate insulin resistance [17].
In addition, serum albumin, C-reactive protein (CRP) and haemoglobin were determined on the baseline samples.
Statistical analysis
Data were analysed using SPSS for Windows version 12.0. Statistical methods were used to evaluate differences between the 1.36 and the 3.86% glucose dwell (where treatment differences were evaluated) and to evaluate the relation between haemodynamic and metabolic parameters (where individual data points were considered, irrespective of treatment). As insulin resistance was hypothesized to play a role, the analysis was repeated separately for patients with and without insulin resistance.
Power analysis.
We calculated that, for a maximum variance of 20% for all parameters of interest, and to obtain a power of 80% for an alpha error of 0.05 (two sided), we would need 20 subjects to find a treatment-induced difference of 12%. Under the assumption that the use of a 3.86% glucose PD would increase BP (which was in fact the working hypothesis), thus a one-sided alpha error, the same number of patients would result in a detection of a 10% difference with the treatment.
As a first step, baseline parameters were compared between 1.36% and 3.86% glucose experiments using the paired Student's t-test, to exclude differences pre-instillation of dialysate despite randomization.
As a second step, a one-way ANOVA for repeated measures was performed to analyse changes from baseline over the different time points in both groups (1.36% and 3.86% glucose) for the different parameters.
As a third step, Wilcoxon signed ranks tests were carried out to compare at each time point the parameters obtained in the 1.36% and the 3.86% glucose dwell.
In addition, after verifying that the difference in baseline parameters between 1.36% and 3.86% was not different from zero, a one-way ANOVA for repeated measures of the paired differences between 1.36% and 3.86% over time was done to analyse eventual individual differences in response.
Data are reported as means and standard deviations. Tests were two-sided and a P-value <0.05 was considered significant.
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Results |
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The demographic data and baseline biochemical parameters of the patients (male n=13, female n=9) are listed in Table 1. Of these patients, 2 had no maintenance anti-hypertensives, 3 were on one, 13 on two, 2 on three and 2 on four different classes. Insulin resistance was present in 11 patients.
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Baseline haemodynamic and biochemical parameters immediately before the start of the first dwell are shown in Table 2, separately for those starting with a 1.36% or a 3.86% dwell. There was no difference in baseline parameters between these two groups.
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To exclude time-dependent effects between the first and second dwell despite randomization, the haemodynamic and biochemical parameters before the first and the second dwell were compared (Table 3), separated for patients having the 1.36% or the 3.86% glucose as the first dwell. There was a carry-over effect for insulin and HOMA-index, but not for the haemodynamic parameters.
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Ultrafiltration at the end of the dwell was 2295 ± 200 versus 2822 ± 216 ml in the 1.36% and 3.86%, respectively (P < 0.001).
Time-dependent changes during glucose 1.36% and glucose 3.86%
When analysing the evolution over time of parameters during a 1.36% glucose dwell (Figure 1, left panels), only significant changes were found in the evolution of blood glucose (P = 0.004). There were no significant changes in insulin levels, CSP, diastolic BP, heart rate or AI.
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When analysing the evolution over time of parameters during the 3.86% glucose dwell (Figure 1, right panels), significant changes were found for the evolution of blood glucose (P = 0.002) and insulin levels (P < 0.0001), but not for the haemodynamic parameters CSP, diastolic BP, heart rate or AI.
Differences between glucose 1.36% and glucose 3.86% over time
As there was no difference between any of the parameters at baseline between the 1.36% and the 3.86% group, we tested the hypothesis that at all time points this difference remained zero by using a one-way ANOVA for repeated measures analysis for the difference between the parameters in the 1.36% and the 3.86%, as a surrogate measure of the impact of glucose loading. Only a difference was found for blood glucose, which increased more over time in the 3.86% group (P = 0.05). This more pronounced increase in blood glucose during the 3.86% dwell, however, was not associated with a different evolution of haemodynamic parameters.
To evaluate the impact of insulin resistance, a separate analysis was performed. During the 3.86% glucose dwell, there was no change in blood glucose, insulin levels or haemodynamic parameters over time in patients without insulin resistance. In contrast, in those with insulin resistance, an increase over time in blood glucose (P < 0.0001), insulin levels (P = 0.01) and AI (P = 0.01) was observed, but again, no change in heart rate, CSP, diastolic BP or mean arterial pressure.
Evaluation of relation between changes in haemodynamic and metabolic parameters
The R2 values of the correlations between haemodynamic parameters and metabolic parameters, both for patients with and without insulin resistance separately, were all below 0.1, meaning that <10% of the variance in haemodynamic parameters was explained by changes in metabolic parameters.
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Discussion |
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This study investigates the acute central haemodynamic effects of a PD dwell containing low (1.36%) and high (3.86%) glucose, as measured with the SphygmoCor® system. Despite a significant rise in serum glucose and insulin levels over time, which was more pronounced during the high glucose dwell and in patients with pre-existing insulin resistance, there was no demonstrable effect on central systolic or diastolic BP. We confirm the higher HOMA-index values in PD patients [18], which are probably related to a carry-over effect induced by the absorption of intra-abdominal glucose, resulting in a continuous non-fasting state of the patient.
The acute haemodynamic effects of a PD dwell have only been investigated to a limited extent [8,19–22], probably because it is assumed that PD is a technique with a protracted slow ultrafiltration, resulting in haemodynamic stability. However, instillation of dialysate might by itself induce acute haemodynamic changes, which might be clinically important in view of the high cumulative number of exchanges performed over time and the decreased cardiovascular reserve of this population.
Using the Finometer technology, Selby et al. [19] demonstrated an increase in BP after instillation of 2 l of PD fluid but could not determine whether this effect was due to glucose, volume, a combination of both or some other factors. Using peripheral BP and cardiac output monitoring with foreign gas rebreathing, Ivarsen et al. [22] showed that cardiac output decreased and peripheral resistance increased when increasing the fill volume from 2 to 3 l in supine position. Also Boon et al. [8] demonstrated an increase in peripheral resistance and brachial BP after instillation of 2 l of glucose-based peritoneal dialysate. Both authors hypothesized that the underlying mechanism was related to a volume-mediated effect. However, in both studies, a glucose-containing PD solution was used, so an eventual additional effect of glucose loading cannot be excluded. Covic et al. [9] assessed central BP in PD patients and also took into consideration the potential impact of the IP presence of dialysate. Unfortunately, they only compared haemodynamic parameters during full and empty abdomen in different patients.
Verbeke et al. [10] demonstrated an increase in central BP, related to an increase in IP pressure, during an acute dwell with a glucose-free dialysis solution (icodextrin). In that study, a temperature-mediated effect was excluded by warming the icodextrin solution to body temperature, and a pH-mediated effect was excluded by adjusting the pH to 7.4 using bicarbonate. As the volume effect appeared within 20 min after instillation, but remained more than an hour after emptying the abdomen, the authors hypothesized that an increase in preload by recruitment of IP vessels was the underlying mechanism. In our present study, the volume effect was cancelled by using the same volume for the low and high glucose dwell, and by not allowing an empty abdomen between dwells by immediate refilling after drainage.
It might be that the bio-incompatibility related to the low pH and the presence of GDPs in conventional solutions induces by itself some haemodynamic reaction. Kawabe et al. [23] found in in vitro experiments that exposure to PD solutions resulted in contraction of large vessels and relaxation of microvessels. In vivo, the haemodynamic response appears to be different when using conventional versus low GDP solutions [12]. In our present study, we used only low GDP, neutral pH solutions to avoid this interference.
Whereas Selby et al. [12] found a difference in haemodynamic response between the low and high glucose groups, we, just like Boon et al. [8], were not able to confirm this finding.
We observed a large increase in serum glucose levels over time after instillation of the PD fluid. As expected, this increase was more pronounced in the high versus the low glucose group, and in those patients with versus without insulin resistance. Nevertheless, no consistent effects on haemodynamic parameters could be observed, neither by analysis of the evolution of the individual patient values nor of the mean values.
As we hypothesized a potential influence of insulin resistance, we did a separate analysis in patients with insulin resistance. Although the increases in blood glucose and insulin levels in this subgroup were more pronounced, again we could not detect significant changes in haemodynamic parameters, nor differences in haemodynamic response during the high compared to the low glucose dwells. In healthy volunteers, a constant intravenous infusion of a glucose concentration fivefold higher than the maximal absorption rate during a PD dwell with 1.36% glucose resulted in disturbances of nocturnal heart rate variability but did not cause BP changes [11].
There are several potential explanations for the discrepancy between our study and that of Selby et al. [12].
First, we used a randomized cross-over design, whereas in the Selby study, the high glucose was always preceded by the 1.36%. In a previous study, using non-glucose-containing, pH-adjusted PD solutions (icodextrin), a circadian effect on haemodynamic parameters was found, with an increase around noon [10]. Therefore, the higher BP in the 3.86% group might rather be induced by the timing than by the higher glucose concentration. Since in the present study, a randomized cross-over design was followed, a bias due to such time effect was obviated. In addition, when comparing baseline values before the first and the second dwell, only an increase in metabolic, but not in haemodynamic parameters, was observed in the current study. It is likely that the more protracted and complicated regime used in previous studies [10,12] induces stress-related changes in the patients.
Second, the differences between 1.36% and 3.86% glucose, as observed by Selby et al., might merely have been the consequence of a more pronounced ultrafiltration in the 3.86% group, creating a larger IP volume. Also in our study a larger IP volume at the end of the dwell was observed. It has been demonstrated that the effect of IP volume is mostly induced in the beginning of the filling procedure, where large changes in IP pressure are induced, whereas the gradual and moderate further increase of IP volume because of ultrafiltration during the dwell has less or even no further impact. In addition, if any effect should be attributed to the higher IP volume, it would have resulted in a higher BP in the 3.86% group, as more ultrafiltration was obtained in this dwell, an effect that we did not observe.
Third, Selby et al. used the Finometer®, reflecting peripheral BP, to measure the haemodynamic parameters, whereas we used SphygmoCor®, reflecting central BP. The differences in approach of these methods have been discussed previously [10] and might be the source of the observed difference in conclusions, as baseline measurements and changes after intervention of peripheral and central BP may significantly differ [24]. From the cardiovascular standpoint, however, the central BP is the most important one, as this is the pressure that the left ventricle actually has to produce (afterload) and that impacts on the wall of the large central vessels. Therefore, we performed applanation tonometry at the carotid artery using the SphygmoCor® system as this noninvasive approach yields accurate estimates of central haemodynamic measures [16].
The values for baseline insulin and HOMA-index were higher as compared to a haemodialysis population, but comparable to values reported in other studies in PD patients [18]. Gursu et al. [25] found that the HOMA-index in fasting patients was higher after a long-term dwell with glucose when compared to icodextrin. Similarly, we found a substantial impact of a previous dwell on the HOMA-index. For the PD patient population, these observations point to a conceptual problem with the HOMA-index, because it is supposed to be determined in fasting condition. As PD patients have a continuous source of glucose in their abdomen, this creates some bias in the interpretation of the HOMA-index. It is not clear whether the higher HOMA-index in PD correlates also with a higher cardiovascular mortality, or whether other reference values should be used. In view of the substantial carry-over we have observed, it can be questioned whether determining the HOMA-index in PD patients while having an empty abdomen can solve the problem. Further research on this topic is certainly warranted.
Limitations of the study
We did not measure IP pressure in this study, nor did we exclude the presence of residual IP volume after drainage. Thus, it might be that differences in IP pressure were present during the two dwells, which might have effects on haemodynamic parameters [10]. In that study, it was also clear that an increase in central haemodynamic parameters and IP pressure is most present during the fast IP instillation of fluid and to a much more limited extent during the dwell itself. In addition, this potential explanation does not abolish our conclusion of the current paper that we did not observe an additional haemodynamic effect induced by the use of high or low glucose strength dialysate solutions, and this despite marked differences in serum glucose levels. If any difference in IP pressure were present during the low and high glucose dwell, we would expect that IP pressure would be higher during the high glucose dwell. If this were the case, the conclusion would be that a higher glucose exposure decreases central haemodynamic parameters. Whereas this is rather unlikely, it cannot be excluded with the current experiments. To evaluate this, experiments using intravenous glucose loading, thus completely avoiding bias induced by IP pressure, should be performed.
In conclusion, we did not find clinically relevant differences in haemodynamic response to acute IP instillation of dialysate solutions with different glucose concentrations, in spite of substantial increases in serum glucose and insulin levels. The HOMA-index in PD patients seems to be disturbed, most likely (at least in part) because of the presence of glucose in their abdomen.
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Acknowledgments |
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The abstract of this paper has been accepted for presentation for the meeting of the American Society of Nephrology in San Francisco, 2007.
Conflict of interest statement. All authors testify that they have no conflicts of interest with regards to the content of this paper. W. Van Biesen has received travel grants and speaker fees from Gambro, Baxter and Fresenius for lectures regarding peritoneal dialysis in general. Raymond Vanholder has received travel grants and speaker fees from Gambro and Fresenius for lectures on general nephrology and dialysis lectures. Francis Verbeke has received travel grants and speaker fees from Genzyme for coordination of the CORD trial.
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Accepted in revised form: 16. 6.08
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