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Determinants of Arterial Stiffness progression in Peritoneal Dialysis Patients with Strict Volume Control

Impact of Mean Arterial Pressure on Progression of Arterial Stiffness in Peritoneal Dialysis Patients under Strict Volume Control Strategy


Meltem Sezis Demirci 1, Ozkan Gungor 1, Fatih Kircelli 1, Juan Jesus Carrero 2, Erhan Tatar 1, Cenk Demirci 1, Meral Kayikcioglu 3, Gulay Asci 1, Huseyin Toz 1 , Mehmet Ozkahya 1, Ercan Ok 1


1 Ege University School of Medicine, Division of Nephrology, Izmir, Turkey

2 Divisions of Renal Medicine and Baxter Novum, Center for Gender Medicine and Center for Molecular Medicine, Karolinska Institute, Sweden

3 Ege University School of Medicine, Division of Cardiology, Izmir, Turkey



Running Title: Arterial stiffness progression in peritoneal dialysis patients



Corresponding Author:

Ozkan Gungor

Ege University School of Medicine, Division of Nephrology

35100, Bornova, Izmir

Phone: ++90.232.3904254

Email: [email protected].tr



ABSTRACT

Introduction: Arterial stiffness is an important contributor to the increased cardiovascular burden of uremia. The aim of the study was to identify determinants of arterial stiffness progression in peritoneal dialysis (PD) patients with strict volume control.

Patients-Methods: Eighty-nine prevalent PD patients were enrolled. Assessment of arterial stiffness was performed at baseline and after nine months on average (range 8-12 month) by carotid-femoral pulse wave velocity (cf-PWV).

Results: Mean age was 51±13 years; preceeding time on PD was 40±34 months. Fifty-seven percent of the patients were men and 9% were diabetic. At baseline, mean cf-PWV was 8.7±2.7 m/s and was significantly higher in patients with diabetes and on automated PD therapy. Cf-PWV was positively correlated with age, history of cardiovascular disease, mean arterial pressure (MAP), blood glucose, left atrium diameter and left ventricular mass index. Sixty patients underwent a second cf-PWV measurement. Thirty-six percent had progression of arterial stiffness. Delta cf-PWV value was 2.08±1.89 m/s for progressors and -1.25 ± 1.43 m/s p<0.01 for non-progressors (p<0.01). In logistic regression analysis, the change in MAP was the only predictor for progression of arterial stiffness.

Conclusions: MAP is the main determinant of arterial stiffness progression. Our results lead us to suggest that efficient blood pressure control may contribute to preserved or reduced arterial stiffness in PD patients.

Keywords: Peritoneal dialysis, blood pressure, arterial stiffness, mean arterial pressure.

Introduction

Peritoneal dialysis (PD) patients have increased cardiovascular (CV) burden, and CV disease is in fact the most frequent cause of death [1, 2]. Problems in control of blood volume, dyslipidemia and greater oxidative stress caused by glucose-based PD solutions are factors specific to PD therapy that have been suggested to affect these adverse outcomes [3]. Arterial stiffness (AS) has also been depicted as an important contributor to the increased CV burden [4,5]. The underlying mechanisms of AS are, nevertheless, not well defined, but elevated levels of oxidative stress and inflammation markers, hypervolemia, arterial calcification, activation of the renin–angiotensin–aldosterone system, sympathetic nervous system overactivity are all anticipated to play a role in stiffening of the arterial bed [6]. Increased left ventricular stress and reduced coronary perfusion (which are both consequences of arterial stiffness) lead to cardiac hypertrophy and myopathy resulting in congestive heart failure and sudden death in dialysis patients [7].

Hypertension is an important contributor to the increased cardiovascular morbidity and mortality of dialysis patients, and we have previously shown that a strict volume control strategy may be an effective method to reach better control of hypertension and preservation of cardiac functions in both PD and hemodialysis patients [8-10]. Strong associations between mean arterial pressure (MAP) and arterial stiffness have been reported in both dialysis and renal transplant patients [11-13]. However, the determinants of arterial stiffness and its progression in PD patients are not well-defined. In this study we evaluated the changes of carotid-femoral pulse wave velocity (cf-PWV) during 9 months on PD as an attempt to elucidate factors associated PWV progression in a cohort of patients under strict volume control.


Materials and Methods

Patients

Of the ninety-five patients undergoing PD at our institution, eighty-nine PD patients being treated at our unit for at least 6 months were enrolled in this study (3 patients did not want to participate, 2 had atrial fibrillation and 1 had a new onset peritonitis), which included a second examination on average 9 months after (range 8-12 months). Seventy-three patients were on Continuous Ambulatory PD (CAPD) and 16 on automated PD (APD). CAPD patients were dialyzed using Baxter Twin Bag (Baxter Healthcare SA, Castlebar, County Mayo, Ireland) and Fresenius A.N.D.Y Plus or Stay-safe systems. (Fresenius Medical Care GmbH, Bad Homburg, Germany). APD patients were treated with Baxter Home-Choice or Fresenius PD Night cyclers.

Baseline data including age, sex, body mass index (BMI), systolic and diastolic blood pressure, weekly creatinine clearance, and peritoneal Kt/V urea, type of PD therapy and duration of PD therapy, medications and biochemical parameters were recorded from patients’ charts. Blood chemistry parameters were assayed by standardized and automated techniques in the Hospital’s analytical laboratory, which is adhered to several external quality control programs. Blood pressure and biochemical parameters (fasting) were measured at 2-month intervals during the follow-up and time-averaged values were calculated. Blood pressures were measured during the clinic visits by the same physician using an Erka sphygmomanometer in the morning period and while the patient was sitting/resting at least for 5 minutes. The reported measurement measurements are the average of two measurements taken 5 minutes apart. Mean arterial pressure was calculated by adding the systolic pressure reading to two times the diastolic reading and dividing the sum by 3. Fifty healthy individuals with a similar age and sex distribution were used as controls.

The study was approved by Local Ethics Committee, informed consent was obtained from all patients and was performed according to the recommendations of the Declaration of Helsinki.


Center’s Strict Volume Control Strategy

Our center applies a strict volume control strategy consisting of dietary salt restriction and ultrafiltration in order to reach blood pressure levels below 130/85 mmHg and cardiothoracic index below 0.50. To reach these targets, detailed oral and written information on moderate salt restriction (NaCl intake 4-5 g/day) is given to the patients. Patients are allowed to drink as much as their thirst requires, as long as their salt intake is restricted. Visits are scheduled according to their clinical and laboratory data; monthly during the first 6 months and thereafter every 2 months. If necessary, more frequent visits are performed. At every visit, patient is questioned about salt intake and physical examination was performed to assess volume status. If necessary, hypertonic PD solutions (2.27% or 3.86% glucose) were used to remove excess volume. When in doubt, a ‘’captopril test’’ is performed as previously described [7,8]. In hypervolemic patients furosemide is added. Those not responding to diuretics or having a positive captopril test are treated with appropriate antihypertensive drugs.


Echocardiographic Measurements

At baseline, patients underwent echocardiography at the time of arterial stiffness investigation by the same operator. All echocardiographical measurements were performed according to American Society of Echocardiography recommendations (14). The following assessments were recorded: left atrium diameter (LAD), left ventricular end-diastolic (LVEDD) and end-systolic diameters (LVESD), right ventricular end-diastolic diameter, thickness of the posterior wall and the interventricular septum. Left ventricular mass (LVM) was calculated using the equation described by Devereux [14]. Left ventricular mass index (LVMI) was calculated by dividing LVM by body surface area. Intra-operator variability was less than % 8.


Carotid İntima Media Thickness Measurement

Common carotid artery intima-media thickness (CA-IMT) was assessed by high-resolution color Doppler ultrasound (HDI 5000, Philips, Bothell, WA, USA) with 5–12-MHz broadband electronic linear-array transducer. The intra-observer variability of measurement was 4% (mean difference, 0.02).


Bioimpedance Analysis

Volume status was determined by bioimpedance analysis (Bodystat Quadscan 4000 (Isle of Man, British Isles). Extracellular water corrected for height was assessed.


Arterial Stiffness Measurements

Arterial stiffness was assessed by carotid-femoral PWV with the SphygmoCor device (Atcor Medical, Sydney, Australia). Assessments were done by sequential recordings of the arterial pressure wave at the carotid and femoral arteries, and by measurement of the distance from the carotid sampling site to the suprasternal notch and from the suprasternal notch to the femoral sampling site [15]. With a simultaneous ECG recording of the R-wave as reference, the integral software calculated the pulse wave transit time. Measurements were performed in fasting status with an empty abdomen after 5-10 minutes of resting. If used, antihypertensive medications were stopped at least 24 hours prior to evaluation. Arterial stiffness was measured by the same operator at both time-points. Intra-operator variability was less than %5. Progression of arterial stiffness was defined as an increase in the cf-PWV> 5% (to rule out possible intra-observer effect) in the second measurement at the end of the follow-up. Patients were grouped as progressors and non-progressors on the basis of having a change of cf-PWV higher or equal lower than 5%, respectively.


Statistical analysis

All parameters were expressed as mean ± SD. A P value less than 0.05 was considered statistically significant. Comparisons between two groups were assessed by independent t-test analysis. Pearson’s rank correlation was used to assess correlations of arterial stiffness and other variables. Multivariate logistic regression analysis was used to study the predictive factors for arterial stiffness progression. Data of patients who did not undergo the second examination due to transfer to another dialysis center, switch of dialysis modality or transplantation were included in all analyses in order to minimize selection bias. Time-averaged data were used to evaluate the relation between laboratory data and changes in arterial stiffness. Calculations were performed using SPSS 15.0 (Chicago, IL, USA). In linear regression analysis for predictors of arterial stiffness 2 models were used: in model 1: Age, sex, body mass index, diabetes, history of CVD, mean blood pressure, PD modality, LVMI and ECW/height was included in the model. In model 2, CA-IMT was added to model 1.


Results

Baseline data

Demographical characteristics of the patients are listed on Table 1. Mean age was 51 ± 13 years and the preceeding time on PD was 40 ± 34 months (median 37 months). Fifty seven percent were women and 9% were diabetic. Eighteen percent of the patients were on APD. CVD history was present in 7% of the cases and 16% were on antihypertensive drugs. Thirty six percent of the patients were anuric. 4 patients were on 3.86 (or 4.25) % glucose PD solution and the remaining patients were on 2.27 (or 2.5) % or 1.36 (or 1.5) % glucose PD solution. A comparison with 50 healthy controls of similar age and sex distribution (mean age 51±9 years and 58% were women) showed that despite similar blood pressure levels (mean systolic and diastolic blood pressures were 128±18 mmHg and 78±9 mmHg, respectively), cf-PWV was higher in the PD patients (8.7±2.7 vs. 7.5±1.4 m/s; p=0.003).

At baseline, cf-PWV was positively correlated with age, blood glucose, history of CVD and diabetes, MAP, pulse pressure (PP), waist-hip ratio, CA-IMT, LAD, LVMI and extracellular water corrected for height (ECW/height). There was no correlation between arterial stiffness and dialysis duration in our study (r=0.107, p=0.317). Diabetic patients (11.9±4.6 & 8.2±2.2 m/s, p=0.01) and patients on APD (10.9±3.7 & 8.0±2.1 m/s, p= 0.01) had higher cf-PWV values compared to those who were not. We performed multiple linear regression analysis predicting cf-PWV with variables selected from univariate analysis. Age, diabetes, MAP, being on APD and LVMI were predictors for cf-PWV in model 1. CA-IMT, MAP and APD modality were predictors in model 2, which included model 1 and CA-IMT (Table 2).


Follow-up Data

All patients were invited to undergo a second examination 9 months on average after baseline determinations. Twenty nine patients did not undergo a second measurement due to the following reasons: 4 patients were transferred to other institutions, 3 patients died, 6 patients received kidney transplantation and 14 were switched to hemodialysis due to ultrafiltration failure and/or hypervolemia. Of the sixty-two patients, two patients were excluded a posteriori due to new onset arrhythmia which disabled cf-PWV measurements. Second arterial stiffness evaluation could be performed in 60 PD patients.

Of these patients, mean percentage change in cf-PWV from baseline was 1.6%. This would be not considered to be clinically significant and to rule out possible intra-observer effect (less than 5%), patients were grouped as progressors and non-progressors on the basis of having a change of cf-PWV higher or equal lower than 5%, respectively. According to this definition, 22 patients had progression (81 % of them having a change of cf-PWV higher than 10%) of cf-PWV and 38 had no progression. Δ cf-PWV (2.08±1.89 m/s and -1.25 ± 1.43 m/s p<0.01, respectively) and ΔMAP (10.8±13.6 and -6.7±16.4 mmHg, p<0.01, respectively) were significantly higher in progressors than non-progressors (Figure 1). In univariate analysis, Δ cf-PWV was correlated with change in MAP and pulse pressure (PP) (Figure 2, 3).

Baseline mean PTH was 422±373 pg/ml, CaxP=45±13 mg2/dl2, CRP=1.09±1.39 mg/dl and final mean PTH was 424±366 pg/ml, CaxP was 43±12 mg2/dl2, CRP=0.84±1.18 mg/dl.

When baseline and time-averaged characteristics were compared, there were no significant differences in time-averaged serum levels of blood glucose, albumin, hs-CRP, CaXP product, parathyroid hormone, cholesterol, and triglyceride. In addition, time averaged values of weekly total creatinine clearance, ultrafiltration volume and residual urine volume were not different between progressors and non-progressors. However, progressors had higher use of anti-hyperlipidemic agents than non-progressors. Comparisons of baseline vs 9-month data (paired t-test) showed that progressors showed an increase in blood glucose, systolic and diastolic blood pressure and decrease in residual diuresis, whereas non-progressors showed an increase in serum triglyceride levels and decrease in serum calcium level, systolic and diastolic blood pressure (Table 3). Whereas the use of low-calcium dialysate did not differ between groups at baseline (p=0.578; data not shown), it was significantly increased in non-progressors during the follow-up (from 66% to 82%, p=0.012) and there was no significant difference in progressors (from 73% to 86%, p=0.08). In a stepwise forward exclusion logistic regression analysis, only delta MAP was associated with the progression of arterial stiffness in PD patients (Table 4).


Discussion

Our study shows that PD patients have stiffer arteries than age- and sex-matched controls. Both cross-sectionally and longitudinally, MAP significantly contributes to the variance of arterial stiffness in PD patients under a strict blood pressure control regime. The contribution of MAP to the changes in arterial stiffness could be explained in part by functional changes of artery resulting from high blood pressure (the load on the vessel) in our study. Additionally, in the presence of disease-induced structural changes, the stiffening is less dependent on lowering blood pressure. In the study by Guerin et al. [16], it was shown that survival of end-stage renal failure patients was significantly worse in whose aortic PWV did not decline in response to blood pressure lowering. In accordance with this, when we divided patients according to ΔMAP, (ΔMAP<0, n=23,and ΔMAP≥0 n=37), only two out of 23 patients within the ΔMAP<0 group had stiffness progression (8.7%). Although these findings may support the existence of disease-induced structural changes of the arteries, the numbers of the patients who had progressed according to this definition are inadequate to reached definitive conclusion. It is also possible that longer follow-up may be needed to denote such changes. Altogether, these results may allow us to speculate that blood pressure control could be helpful to therapeutically reduce arterial stiffness in this population.

Hypertension is a major risk factor for the increased cardiovascular mortality rates of PD patients [17-20]. Increases in systolic blood pressure cause elevations in end-systolic stress subsequently leading to cardiac hypertrophy and higher myocardial oxygen requirement. On the other hand, a decrease in diastolic blood pressure alters coronary perfusion and causes myocardial ischemia [21]. In our study, which included patients with a good control of blood pressure (mean SBP and DBP of 121±24 and 77±14 mm/Hg, respectively), we found that per 1mmHg increment in MAP, the risk of progression of AS increases by 12.4 %. This result emphasizes the important effect of blood pressure changes on AS even in patients without evident hypertension, and goes in line with recent data showing MAP as the main determinant of IMT levels in pre-dialysis patients [22]. In our study, PP and changes in PP (Δ PP) were significantly correlated with baseline f-c PWV and Δf-c PWV, respectively. However, in multivariate analysis when ΔPP was added to the model for prediction of arterial stiffness progression, ΔMAP was the only significant predictor. This last observation disagrees with Kim. et al. [23], who reported that PP had the strongest correlation with PWV among a variety of BP parameters.

In our study, the rate of progression of arterial stiffness was 1.6% and this rate was lower than the recent study by Jung JY. et al. In this study, despite no exact data on progression of arterial stiffness is given, derived from a progression of 44±209 cm/s from the baseline value of 1022±276 cm/s, approximately 4.3% change over a 1 year period was observed. They also reported that “some” patients had a progression rate of more than 15%, which was the median of annual increasing change in cf-PWV. The reason for this difference between these 2 studies may be due to higher baseline mean arterial blood pressure (106.6±16.8 vs. 93±17 mmHg, respectively), left ventricular mass (127.4 ± 41.3 vs. 112±41 g/m2, respectively) and antihypertensive drug use (76.1% vs. 16%, respectively) in the study of Jung JY. et al. compared to our study; showing a population with a not so good volume control.

Cardiovascular disease is the leading cause of death for patients with end-stage renal disease (ESRD). The increased risk of cardiovascular mortality may be attributable to advanced atherosclerotic vascular changes and left ventricular hypertrophy [24]. We also found that, increased carotid IMT and LVMI along with older age and presences of diabetes were associated with increase in cf-PWV in our patients. One of the most important factors commonly contributing to atherosclerosis and LVH in dialysis patients may be increased end systolic stress, which has been shown to result from increased stiffness of large arteries and augmentation of systolic pressure in central arteries by wave reflection [25]. A raised pulse pressure due to increased vascular stiffness may induce arterial remodeling, increasing wall thickness, and the development of plaques. These mechanisms may also explain the association between cf-PWV and LVMI and CA-IMT in our patients.

A recent study recently identified age, fetuin-A, MAP and TG as factors associated with progression of AS in a cohort of 67 PD patients [26]. The fact that we didn’t observe any association between TG and arterial stiffness progression may be the consequence of a short follow-up. We found nevertheless that serum triglyceride levels increased during follow-up in non-progressors, but time-averaged TG levels were not different between groups. Two studies have reported that residual renal function is associated with all-cause and cardiovascular mortality in both hemodialysis and PD patients [27, 28]. Also, RRF related cross-sectionally to blood pressure control, left ventricular hypertrophy, increased sodium removal, improved fluid status and arterial stiffness [29]. However, despite a decrease in residual diuresis in progressors by time, we did not find in our study any predictivity of residual diuresis for progression of AS.

Increased arterial stiffness may be related to a high peritoneal permeability resulting in fluid overload in PD patients [30]. In this study, we found that APD modality was associated with increased arterial stiffness. Its explanation may be the use of more glucose and lower clearance of glomerulotoxic middle molecules. In some reports it has been suggested that the preservation of RRF was worse in APD patients. Patients having high/high-average transport characteristics were treated with APD modality in our study and their residual urine volume were significantly lower than on CAPD patients (data not shown). These factors may have indirectly contributed to development of arterial stiffness

In our previous study [31] we showed that dialysis with high dialysate Ca (1.75 mmol/L) was associated with increased arterial stiffness in PD patients. In this study, despite non-significance in multivariate analysis, we found that decreases in serum calcium level during follow-up in non-progressor group accompanied increased use of low-calcium dialysate. On the basis of this observation, we suggest that it may be a contributor to slowing down of progression of arterial stiffness together with control of blood pressure.

Major limitations of our study are that we enrolled prevalent HD patients who have been on peritoneal dialysis for an average of over 40 months and some of them for many more months that we have a short follow-up of only 9 months, that we are lacking a control group of patients who are having stage 5 CKD and that we have not studied all other possible factors (oxidative stress, arterial calcification, activation of the renin-angiotensin and sympathetic nervous system etc.) that may affect the arterial stiffness. However, we should emphasize that we did not find any association between PWV and inflammation marker (hs-CRP) and dialysis duration. Since we found an association between PWV and volume parameters (ECW/height, LAD and anti-hypertensive use), these results could support the relationship between arterial stiffness and hypervolemia. We did not find association between arterial stiffness and dialysis duration in our study.

Although our results should be interpreted with caution due to a relatively low number of patients enrolled, this observational study shows that MAP was the main determinant of AS and there was an association between MAP and AS and AS progression in PD patients with strict volume control. Altogether, this may suggest that efficient control of blood pressure could lead to reduced arterial stiffness, particularly in PD patients.



Acknowledgments

J.J.C. obtained support from the Loo and Hans Osterman’s Foundation. We thank all patients and staff for their help and support.

Disclosures

The authors declare no conflict of interest.

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