Effects of Low Sodium Dialysate in Chronic Hemodialysis Patients: An Echocardiographic Study

Abstract

Background. Chronic kidney disease (CKD) and hemodialysis (HD) patients who cannot restrict sodium consumption in their diets sometimes develop significant saline excess and hypertension between dialyses. This study assessed the effect of relatively low sodium dialysate dialysis on changes of echocardiography in hemodialysis patients. Methods and Results. Eighteen patients with end stage renal failure on chronic HD were studied (8 females, 10 males) with a mean age 48.3 ± 14.6 (24–70) years. The mean time on HD was 30.8 ± 14.0 (12–60) months. Patients with hematocrit levels under 24% were excluded from the study. In all patients, echocardiography was performed thrice weekly before and after eight-week HD treatment with low sodium dialysate hemodialysis by the same operator (135 mEq/L for patients with sodium levels less than 137, 137 for patients with sodium levels over 137). Left atrium (LA) and left ventricle (LV) volumes and ejection fractions were measured, specifically: LV systolic diameter (LVSD), LV diastolic diameter (LVDD), interventricular septum (IVS), tricuspid regurgitation (TR), mitral regurgitation (MR), pulmonary artery pressure (PAP), and inferior vein cava diameter (IVCD). Results. In terms of echocardiographic parameters, LVSD, TR, PAP, and IVCD were statistically decreased after low-sodium dialysate treatments (p = 0.002, 0.04, 0.013, and 0.00, respectively). Predialysis systolic and diastolic blood pressure (BP), post-dialysis systolic blood pressure, and interdialytic weight gain was statistically decreased when compared to basal levels (p = 0.00, p = 0.011, p = 0.022, p = 0.001, respectively). Conclusion A reduction of the dialysate sodium concentration based on the predialysis sodium levels of the patients could reduce the systolic BP and decrease the volume load on the heart as assessed by echocardiography. Within this short period, postdialysis diastolic BP could not be lowered. The effect of this approach should be studied in broad and lengthy series.

Keywords:

• renal failure
• hemodiolysis
• low-sodium dialysate
• echocardiography

INTRODUCTION

In chronic renal failure (CRF), extra cellular volume (ECV) increases even if the overload is not such that edema is obvious. Patients with advanced CRF are particularly sensitive to sodium load. Hypertension appears even with a relatively low normal sodium intake. This peculiar sensitivity to sodium load increases as CRF progresses.[1] In renal failure and hemodialysis (HD), the patients who cannot restrict sodium in their diets develop a significant saline excess between dialyses. The dialysate sodium concentration is an important issue for sodium overload. If there is a diffusive removal of sodium, as occurs with low dialysate sodium concentrations, the excess sodium removal over water removal causes a decrease in extracellular sodium concentration. A high dialysate sodium concentration may improve hemodynamic instability during dialysis, though possibly at the cost of increased inter-dialytic weight gain (IDWG) and hypertension. In general, an optimal dialysate sodium concentration would find a balance between both an adequate blood volume preservation and sodium removal.[2] The accumulation of water and sodium is the predominant factor in the pathogenesis of hypertension and left ventricular hypertrophy in HD patients.[3] Thus, an adequate removal of sodium and water during HD is of prime importance in improving the cardiovascular risk profile of HD patients. Manipulating the sodium concentration of the dialysate is another way to improve water and sodium control in HD patients. Reducing the sodium concentration of the dialysate increases the diffusive removal of sodium, which may reduce thirst and IDWG.[2]

This study assessed the effect of low sodium dialysis on certain echocardiographic findings in hemodialysis patients.

METHOD

This study was approved by the ethics committee of the Yuzuncu Yil University. Subjects who gave informed consent were included in the study.

We studied 18 patients with ESRD on chronic HD, included 8 females and 10 males, with a mean age 48.3 ± 14.6 (24–70) years. The mean time on HD was 30.8 ± 14.0 (12–60) months. Only patients with hematocrit levels higher than 24% were admitted to study. We measured the dry weight of all patients. No patients had an active infection, ongoing inflammatory disease, diabetes mellitus, or immune disorders. First, the mean of the previous five predialysis sodium measurements was accepted as the sodium value of the individual patient. The hemodialysis machine set up for dialysate sodium was adjusted to 135 mEq/L for patients with sodium levels less than 137, and adjusted to 137 for patients with sodium levels over 137. In all patients, echocardiography was performed before and after eight-week low sodium dialysate hemodialysis treatment by same operator. Blood pressures were recorded during the study for each hemodialysis sessions in all patients. Echocardiography was conducted with a Vingmed CFM 725 echocardiograph (Horton, Norway) and a 3.25 MHz transducer. M-mode echocardiographic measurements were obtained from the left parasternal window, and measurements were made according to the recommendations of the American Society of Echocardiography.[4] Left atrium (LA) and left ventricle (LV) volumes and ejection fractions were measured, namely, LV systolic diameter (LVSD), LV diastolic diameter (LVDD), interventricular septum (IVS), tricuspid regurgitation (TR), mitral regurgitation (MR), pulmonary artery pressure (PAP), and inferior vein cava diameter (IVCD).

Results of the echocardiographic estimations of the patients are reported as mean ± standard deviation (SD). The total variation was analyzed by performing paired t test. A probability level of less than 0.05 was considered significant.

RESULTS

The echocardiographic parameters are presented in Table 1. In terms of echocardiographic parameters, LVSD, TR, PAP, and IVCD were statistically decreased after low-sodium dialysate treatments (p = 0.002, 0.04, 0.013, and 0.00, respectively). Predialysis systolic and diastolic blood pressure (BP), postdialysis systolic BP, and IDWG were statistically decreased when compared to basal levels (p = 0.00, 0.011, 0.022, and 0.00, respectively; see Table 2). LA, LVDD, LVSD, PW, and EF were unchanged after low-sodium dialysate treatments (p = 0.2, 0.3, 0.16, 0.19, and 0.08, respectively; see Table 1).

Table 1 Echocardiographic parameters

	LA (mm)	LVDD (mm)	LVSD (mm)	IVS (mm)	PW (mm)	EF (%)	PAP (mmHg)	IVCD (mm)
Baseline echo	38.7 ± 5.1	50.6 ± 5.6	34.3 ± 4.9	11.9 ± 1.4	10.9 ± 1.5	64.1 ± 8.1	29.7 ± 14.4	13.4 ± 1.9
Range	29–51	29–49	26–44	10–14	9–13	40–74	17–66	10–18
Second month echo	37.9 ± 5.2	51.2 ± 5.5	35.6 ± 5.8	11.3 ± 1.4	10.6 ± 1.5	62.9 ± 7.9	24.4 ± 12.1	11.7 ± 1.7
Range	29–49	42–61	26–46	9–14	8–13	40–74	13–64	9–16
p	0.2	0.3	0.16	0.002	0.19	0.08	0.01	0.00

Table 2 Predialysis systolic and diastolic, post-dialysis systolic BP, and interdialytic weight gain

	Predialysis SBP (mm Hg)	Predialysis DBP (mm Hg)	Post-dialysis SBP (mm Hg)	Post-dialysis DBP (mm Hg)	IDWG (kg)
Baseline	179.7 ± 24.8	100.6 ± 12.8	141.4 ± 28.8	83.6 ± 11.4	2.5 ± 1
Range	140–240	80–125	100–200	70–100	0–4
Second month	151.7 ± 17.7	93.1 ± 10.5	132.3 ± 16.4	81.1 ± 10.8	1.8 ± 0.6
Range	125–190	70–110	100–160	60–100	0–2.5
p	0.00	0.01	0.02	0.33	0.00

DISCUSSION

Water and sodium overload is the predominant factor in the pathogenesis of hypertension and left ventricular hypertrophy in dialysis patients. Hypertension is associated with an increased risk for left ventricular hypertrophy. In uremic patients, a marked increase in left ventricular mass is seen very early in the course of renal failure. Left ventricular disease is already present in 85% of patients starting dialysis.[5] Dialysis patients with LVH have higher mortality rates than those with normal ventricular mass.[6] This study revealed a significant reduction of LVSD, TR, PAP, and IVCD in terms of echocardiographic parameters with low-sodium dialysate. It was previously reported that blood pressure normalization and left ventricular mass reduction were proved by strict volume control.[7–9] In these studies, the general strategy of volume control consists of combining dietary salt restriction and ultrafiltration (UF). On the other hand, the more efficient control of hypertension by prolonged and frequent dialysis has been attributed to the normalization of extracellular volume. Chan et al. reported that a reduction in blood pressure with nocturnal hemodialysis is accompanied by regression of LVH.[10] On the contrary, these major independent risk factors are only marginally reduced by the initiation of standard thrice-weekly dialysis, and cardiovascular events still represent the most common cause of death in hemodialysis patients. Fagugli et al. showed that daily hemodialysis allows optimal control of BP, a reduction in the left ventricular mass, and withdrawal of antihypertensive treatment.[11] Krautzig et al. showed that reducing dialysate sodium without changes in dry weight resulted in a small but significant decline in predialytic systolic blood pressure.[12] The success of the Tassin group in improving blood pressure control has also been partly attributed to the prescription of a sodium-restricted diet and the application of a low dialysate sodium concentration during long treatment times. However, Koman et al. showed that lowering dialysate sodium concentration without special attention to dietary sodium intake may not be sufficient to improve blood pressure control.[14] On the other hand, in several previous studies it was demonstrated that a strict sodium-restricted diet without changing dialysate sodium improved blood pressure.[6–8],[15] The rationale behind the effect of lowering body sodium content without changes in total body water is not clear; it has been attributed to factors such as Na-K-ATPase inhibitors, the effect on the sympathetic nervous or renin angiotensin aldosterone system, or reduced sodium logging in the vascular wall.[16] The present study used partially individualized low sodium dialysate and did not change the dry weight in most of the patients. The reduction of the SBP was in accordance with a previous study.[12] The significant reduction of IVS diameter, TR, and PAP reflect the reduction of the volume load on heart. In the study by Ozkahya et al., such changes could be observed after six months of sodium restriction and UF.[8] De Paulo et al. showed that an individualized sodium dialysate based on predialysis plasma sodium levels decreased thirst, IDWG, HD-related symptoms, and pre-HD BP,[17] which is in accordance with the present study.

CONCLUSION

A reduction of the dialysate sodium concentration based on the predialysis sodium levels of the patients could reduce the SBP and decrease the volume load on heart. Within this short period, DBP could not be lowered. The effect of this approach should be studied in broad and lengthy series. A short follow-up period, lack of control group, and small sample size are the limitations of this study.

Notes

*For this manuscript, there is no conflict of interest.