NEPHROLOGY 2000; 5, 237–241

INTRODUCTION

Hypertension is extremely prevalent in the chronic di-alysis population: results from a European study showedthat up to 83% of patients on renal replacement therapywere on antihypertensive treatment.1 In northernEurope, approximately 50% of the population on renalreplacement therapy die from cardiovascular (CV)related causes.1 Hypertension has been shown to be an

important, independent risk factor for the developmentof cardiovascular and cerebrovascular disease in patientswith essential hypertension.2 Hypertension has beenlinked to reduced survival on dialysis,3 and with cardio-vascular remodelling associated with a worse outcome.4

Hypertension in the dialysis population is thereforean important modifiable CV risk factor, which if con-trolled should reduce cardiovascular mortality, althoughno trial-derived data exist to support this firmly heldbelief. Studies of 24-h blood pressure (BP) profiles usingambulatory monitoring have shown that the prevalenceof abnormal 24-h blood pressure load and abnormalblood pressure diurnal rhythm (‘non-dipping’) is up to80%.5 There are many potential explanations for hyper-tension and abnormal blood pressure diurnal rhythm in

Original Article

Low-sodium haemodialysis without fluid removal improvesblood pressure control in chronic haemodialysis patients

CKT FARMER,1 P DONOHOE,1 P DALLYN,2 J COX2, JC KINGSWOOD2 AND DJA GOLDSMITH1

1Renal Unit, Guy’s Hospital, St. Thomas Street, London, United Kingdom and 2Trafford Department of RenalMedicine, Royal Sussex County Hospital, Eastern Road, Brighton, East Sussex

SUMMARY: Hypertension is an important and well-established risk factor for both cardiovascularand cerebrovascular disease. Hypertension is much more common in patients on renal replacementtherapy than in the general population. Up to 80% of patients on renal replacement therapy are hyper-tensive and about 50% of dialysis patients die from cardiovascular causes. Salt and water overloadare major factors exacerbating hypertension in the dialysis population. This was a prospectivecrossover study of 10 patients examining the effect of haemodialysis for 2 weeks using usual (Na+

138–140mmol/L) sodium dialysate with a 2-week period of low (reduced by an average of 5mmol/LNa+ to 133mmol/L on average) sodium dialysate on inter-dialytic ambulatory blood pressure (ABPM)and trans-thoracic bioimpedance (TTB). Ten patients, mean age 67 years, completed the study (twowomen and eight men). No patient became severely hyponatraemic during the study period. Mean48 h inter-dialytic blood pressure (BP) fell from 141/83 to 133/78 (P < 0.01). Mean arterial BP mea-sured immediately prior to TTB fell from 92.8 mmHg to 87.5 mmHg (P < 0.01) during the low-sodiumhaemodialysis period. Afterload (systemic vascular resistive index – SVRI) measured by TTB fell sig-nificantly during the low-sodium haemodialysis period (SVRI on Na+-140 = 3426 cf. Na+-134 = 2281;P = 0.01). Dialysate sodium reduction without extra fluid removal had a beneficial effect on inter-dia-lytic 48-h blood pressure in chronic stable haemodialysis patients. Lowering dialysate sodium reducedthe systemic vascular resistance index as measured by TTB. Reduction of dialysate sodium was welltolerated, although mild dizzines and cramps did occur. These data suggest that sodium overloadand water overload may have independent effects on BP and that simple-to-achieve and modestchanges in dialysate sodium could usefully augment the action of antihypertensives in dialysispatients.

KEY WORDS: ambulatory blood pressure, blood pressure, dialysate sodium, trans-thoracicbioimpedance.

Correspondence and present address: DJA Goldsmith, Renal Unit,4th Floor Thomas Guy House, Guy’s Hospital, St. Thomas Street,London SE1 9RT, UK.

Accepted for publication 31 January 2000.

study. Antihypertensives (drug class or dose) were in use in six of the10 subjects at the start of the study (doxazosin in 3, nifedipine in 4,amlodipine in 1, and atenolol in 2) and were not altered throughoutthe study period.

The study was divided into two phases.

Phase 1

Patients were dialysed according to their normal regime (conven-tional sodium dialysate) for 14 days (six dialysis sessions, each of 4 h delivered dialysis), on each occasion blood was drawn for plasmasodium, urea, creatinine and potassium pre- and post-dialysis. Twodialysate sodium samples were taken from the dialysis circuit anddialysate sodium was measured spectrophotometrically. Patients alsounderwent ABPM for 48 h in an inter-dialytic period between dialysesfive and six.

Ambulatory blood pressure monitoring

ABPM was performed using SPACELABS® (Spacelabs Inc, Redmond,USA) 90207 ambulatory blood pressure monitors. Monitors wereplaced on the patients by a single technician, five recordings were usedto calibrate the monitors with synchronous measurement using amercury sphygomanometer.5 Blood pressure was taken at 30-min inter-vals for the 48-h period. Day and night blood pressure were calculatedusing a sleep diary completed by all patients. All ambulatory monitor-ing was performed during the ‘short gap’ (2-day inter-dialytic period).Patients’ 48 h BP, daytime and night-time mean blood pressure werecalculated. Lack of normal diurnal rhythm (non-dipping) was definedas lack of normal 10% decline in both systolic and diastolic BP duringsleep compared with waking values.

All patients had trans-thoracic echocardiography to assess thediameter of the inferior vena cava after a dialysis session, and also theprevalence of left ventricular hypertrophy (LVH). All echocardiogramswere performed and interpreted (see13 for details) by a single operatorblind to patient details.

Trans-thoracic bioimpedance

Bioimpedance measurements were all performed in duplicate 30 minsafter the end of the mid-week haemodialysis session. Preload, afterload,cardic work and pump efficiency were measured using the non-invasive technique of trans-thoracic bioimpedence (TTB). TheBoMed® (Irvine, CA, USA) NCCOM3-R7 CDDP system was used tomeasure bioimpedance. This method of measurement has been previ-ously described and validated in both animal models14 and patients ina critical care setting.15

Pump efficiency (EF) = 0.84–0.64*STR, where STR = PEP/VET.Pre-ejection period (PEP) is defined as the time elapsed between theonset of Q waves in the ECG QRS complex and the opening of theaortic valve. Ventricular ejection time (VET) is defined as the timeelapsed between opening and closure of the aortic valve. The durationof electromechanical systole (Q-S2) is a function only of heart rate andis independent of heart disease.16

Phase 2

Patients underwent ‘low-sodium’ haemodialysis for a period of 2 weeks(six dialysis sessions also each of 4 h delivered dialysis), dialysate

patients with end-stage renal failure (ESRF).6 The extentto which it is necessary to invoke these over and above the almost invariable presence of significantly expand-ed extracellular volume and chronic salt overload is controversial.7,8

It was realized early in the modern dialysis era thataltering the sodium concentration of dialysis fluid couldaffect blood pressure in haemodialysis patients. With themore recent advent of short-hours, high-flux haemodi-alysis (and mandatory rapid ultrafiltration) the use oflow-sodium dialysate has been said to be associated with an increased incidence of adverse effects, particularlycramps and intra- or post-dialysis hypotension, in sus-ceptible patients.9 For these reasons, and the switch fromacetate to bicarbonate-buffered dialysate, the sodiumconcentration of dialysis baths has risen to unphysiol-ogically high levels, inducing higher inter-dialytic BP to reduce the ‘inconvenience’ and possible risks of intra-dialytic hypotension.10

Recently, a study has shown that it is possible toreduce blood pressure and reduce numbers of antihyper-tensives using low-sodium dialysate.11 Significant com-plexity can be involved in sodium-profiling patients,demanding much more sophisticated dialysis hardwareand software.12 We wanted to alter dialysis sodium in asimple fashion that could be achieved with virtually alldialysis facilities, and to see if this alteration would engi-neer a useful fall in systemic BP.

In this study, our aims were to examine the effect oflow-sodium dialysate on BP levels, BP diurnal rhythm,and trans-thoracic bioimpedance-derived systemic vas-cular resistance, and also the incidence of intra-dialyticand inter-dialytic side-effects.

SUBJECTS AND METHODS

In this prospective crossover interventional study, we studied 10 compliant haemodialysis (HD) patients recruited from our inpa-tient haemodialysis unit, all on thrice-weeky bicarbonate-buffered HD (running conductivities equivalent to dialysate sodium 138–140 mmol/L range) uninterrupted for more than 3 months and withstable urea-reduction ratios and controlled BP (pre-dialysis BP <160/90 mmHg) without the use of angiotensin-converting enzyme(ACE) inhibitors or angiotensin antagonists, and with dialysishypotension requiring intravenous bolus saline in fewer than 5% ofdialysis sessions in the preceding 3 months. These patients were onrenal diets comprising 1.2 g protein/kg body weight/day and estimatedsodium intake of 100 mmol. Local ethical approval was obtained. Typeone and type two diabetic patients were excluded from study becauseof the potential for diabetic autonomic neuropathy. Patients with documented hyponatraemia (<130 mmol/L) were also excluded from study. Because of the need for ambulatory blood pressure moni-toring (ABPM), patients with A-V fistulae in both arms were excluded.When considering patients, their ‘dry weight’ was assessed by a seniorphysician using standard clinical criteria; if patients were deemed to be at their dry weight, with no significant postural drop in BP (< 20 mmHg systolic and 10 mmHg diastolic) they were eligible for the

238 NEPHROLOGY CKT Farmer et al.

sodium was reduced by reducing dialysate conductivity to the samedegree (5 mS/cm) for the six consecutive dialysis sessions in this phase;reduction in dialysate sodium was confirmed by measuring dialysatesodium on two occasions during each of the six subsequent dialysis ses-sions. Although the extent of the alteration in dialysate sodium con-centration varied between patients, intra-patient variability for the sixlow-sodium dialysis sessions was negligible. Dry weight estimation,ABPM and TTB were repeated according to the same protocol as phase1. Patients were asked to complete a questionnaire outlining symptomsexperienced during the low-sodium dialysate period.

RESULTS

All 10 patients (two women and eight men) completedboth phases of the study. Their mean age at the time ofthe study was 67 years.

Over the 3-week period of this study, the target dryweight for these patients was constant. There was no dif-ference in the mean inter-dialytic weight gain (1.7 kg or2.6% of total body weight (range 0.9–2.4 kg) for phase 1vs 1.8 kg or 2.8% of total body weight (range 0.8–2.4 kg)for phase 2) and ultrafiltration volume (2.0 L (range1.0–2.5 L) for phase 1 vs 1.9 L (range 0.9–2.5 L) for phase2) (P = NS for both comparisons) between the twophases of this study. Mean dialysate sodium for the phase

1 period was 137.7 mmol/L and during phase 2 was 132.7 mmol/L (P < 0.001). Dialysate sodium was calcu-lated by taking the mean of all dialysate sodium collec-tions relating to phases 1 and 2. Dialysis dose, asestimated by urea reduction ratio (URR), was unchangedduring the trial period (phase 1 mean URR 57.4%, phase2 mean URR 56.2%; P > 0.1, paired t-test). No patientbecame severely hyopnatraemic during the study period;one patient developed a plasma sodium of 131 mmol/Lwithout ill-effects. Mean pre-dialysis plasma sodium priorto the low-sodium dialysis phase was 139 mmol/L; afterlow sodium dialysis it was 138 mmol/L (P > 0.1, paired t-test) (Table 1).

Mean 48-h inter-dialytic blood pressure fell from141/83 to 133/78 (P < 0.01, paired t-test); mean arterialmeasured immediately prior to TTB fell from 92.8 mmHgto 87.5 mmHg (P < 0.01) during low-sodium haemodi-alysis (Fig. 1). During the control period, there was one‘dipper’ and nine patients were ‘non-dippers’. During thelow-sodium dialysate period, there were five ‘dippers’ andfive ‘non-dippers’ (Table 2). There was a significant cor-relation between reduction in dialysate sodium and fallin systolic BP (r = 0.39, P < 0.05). No such relationshipwas found for diastolic BP.

By trans-thoracic echocardiography, all patients exhi-

Improved blood pressure in haemodialysis patients NEPHROLOGY 239

Table 1 Changes in plasma and dialysate sodium and haemocrit

Normal sodium dialysate Low-sodium dialysate

Mean (SD) Range Mean (SD) Range P (paired t-test)

Pre-dialysis dialysate sodium (mmol/L) 137.7 (2.6) 137–143 132.7 (2.7) 130–137 0.001Reduction in dialysate Na 5 (2.3) 3–8Urea reduction ratio 57.4 (3.6) 50.2–62.4 56.2 (3.5) 51.8–61.2 NS% change in body weight 2.6 (0.3) 0.9–3.5 2.8 (0.3) 1.2–3.5 NSPlasma haematocrit 0.29 (.03) 0.31 (.03) NSPlasma sodium (mmol/L) 139 (3.1) 136–143 138 (3.4) 131–140 NS

Table 2 Changes in ambulatory BP and bioimpedance parameters

Normal sodium dialysate Low sodium dialysate

Mean SD Mean SD P (paired t-test)

Twenty-four hour blood pressure (mmHg) 141/83 11.8/9.3 133/78 8.4/10.3 0.01Blood pressure variability1 13.5/10.4 12.4/9.5 0.06/0.05Daytime (awake) BP (mmHg) 142/85 11/8.5 135/80 13.0/5.0 0.02/0.01Night-time(asleep) BP (mmHg) 135/80 7.9/8.9 126/73 11.9/12.1 0.01/0.01Night–day SBP and DBP ratios 0.95; 0.94 0.93; 0.91 NSPreload2 77.7 32.7 82.2 34.0 NS(0.3)Afterload2 3425 1980 2281 1187 0.03Cardiac work2 2.8 1.2 3.4 1.5 0.02Pump efficency2 49.7 12.9 51.5 8.4 NS(0.3)Mean arterial pressure3 92.8 13.5 87.5 12.4 0.01

1The standard deviation of BP for the 48-h period.2Measured by TTB.3Mean arterial pressure at the time of performing TTB.

The pathogenesis of hypertension in ESRF patientson haemodialysis is thought to relate to chronic plasmavolume expansion. However, some patients may remainhypertensive despite attaining their ‘dry weight’; otherhypertensive mechanisms may have greater relevance tosome patients (e.g. excess sympathetic nerve activityfrom native kidneys,19 accumulation of dialysable (e.g.ADMA20) or non-dialysable (e.g. PTH21,22 and endothe-lin23) pressor substances, or administration of erythro-poietin.24 In the assessment of BP, the high prevalanceof blunted or absent diurnal BP rhythm in dialysispatients needs also to be accounted for.5,6

In this study, we aimed to assess the effect of low-sodium haemodialysis without altering dry weight instable chronic haemodialysis patients. Our aim was toassess the effect of lowering dialysate sodium in a simplefashion, and thus total body sodium, on BP. We alsoexamined the effect of low dialysate sodium on SVRIusing TTB. We were trying to garner evidence for thedissociation of BP effect from salt as opposed to wateroverload, and to see if an easily achieved change indialysate could usefully augment BP therapy in stablepatients. We were not trying to use alterations in dialy-sis sodium to impact on intra-dialytic BP variability orsymptoms.

We found that using lower sodium dialysate producedan inter-dialytic BP (measured by ambulatory monitor-ing) that was significantly reduced in all patients by anamount at least equivalent to an antihypertensive drug.25

Figure 1 shows the effect on systolic and diastolic BP. We also found that a 2-week period of low-sodiumhaemodialysis also reduced the proportion of patientswho had an abnormal blood pressure diurnal rhythmfrom 90% to 50%. The initial prevalence of abnormalblood pressure rhythm (90%) was similar to thatdescribed in a previous study.5 It is difficult to ascribe thisreduction in prevalence of ‘non-dippers’ simply torandom change in blood pressure rhythm, although aformal study of the reproducibility of diurnal BP changesin dialysis patients is long overdue.

Finally, we showed that the patients receiving low-sodium haemodialysis had a significant reduction in theirafterload as measured by TTB. This accords with thefindings of greater vascular reactivity with low-sodiumdialysis shown by van Kuijk et al. 26 We could not assessthe possible effects of fluid shifts across cell membranesas a result of the slightly lower plasma sodium (and henceplasma osmolality), but given the tight physiologicalcontrol of intracellular sodium exerted by the plasmamembrane sodium–potassium ATPase pump it is notlikely that this was a major factor.

This study clearly has some important limitations,namely small patient numbers, limited duration, and the use of stable compliant patients, with controlled BP. Also, assumptions about extracellular and bloodvolumes, and extracellular and total body sodiumcontent, have been made without either being measured

bited left ventricular hypertrophy (mean left ventricularmass index (LVMI) 164 ± 31 g/m2; range 113–224 g/m2),but the patients had a well-preserved ejection fraction(mean EF 42%). Mean post-dialysis IVC-diameter wasestimated in nine patients as 0.4 cm/m2 (range 0.1–0.7 cm/m2). Pump efficiency estimated by TTB was 51%.

Afterload (systemic vascular resistive index – SVRI),measured by TTB was reduced significantly during thelow-sodium haemodialysis period. Mean SVRI reducedfrom 3426 to 2281 (P = 0.01, paired t-test). These resultsare summarized in Table 2.

The symptoms questionnaire showed that fivepatients experienced no additional symptoms during thelow-sodium haemodialysis period. Five patients whoexperienced new mild symptoms, of which the com-monest were dizziness (three patients) or muscle cramps(two patients). The symptoms were not severe enoughto alter the dialysis schedule.

DISCUSSION

There have been many reports that have shown that theprevalence of hypertension in the ESRF patient isextremely high – typically 80–90% of patients are hyper-tensive and/or on antihypertensive therapy. Whetherthis has a detrimental effect on patient survival isunknown and awaits a formal prospective interventiontrial. Some centres, most notably Tassin-la-demi-Lune,have show that excellent blood pressure control can beachieved with long-hours haemodialysis,17,18 but moretypical dialysis regimens confers at best moderate BPcontrol.1,5 It is noteworthy that these patients have beenreported to be significantly vasodilated.

240 NEPHROLOGY CKT Farmer et al.

Fig. 1 Individual patients’ 48-h inter-dialytic blood pressurebefore and during low-sodium haemodialysis.

precisely. The technique of TTB is reproducible, i.e.precise, but not all studies have shown it to be accuratein determining cardiac output when compared withalternative measures. In this study we were interested inthe change in, not the absolute value of, SVR within thesame patient (i.e. patient acting as his own control overthe two dialysis periods).

Thus, reduction in SVR, i.e. vasodilatation, is thelikely mechanism for the BP reduction seen in this study.Dialysis patients are likely to be chronically vasocon-stricted because defects in NO-mediated vasodilatormechanisms, excess circulating plasma endothelin andangiotensin II, and from excess sympathetic nervoussystem activity. Chronic salt excess in blood vessel wallscould also adversely affect blood vessel function, and has been linked to a wide spectrum of disease.27 Usingadvanced methods such as pulse wave analysis andplethysmography28 may reveal more about how thissimple and well-tolerated antihypertensive manoeuvreworks. If the salutary effect on BP diurnal rhythm is con-firmed in larger studies, this would throw some light onthe pathogenesis of this abnormality, and also provide apotential intervention (long-acting antihypertensivesare ineffective at altering BP diurnal rhythm). It shouldalso not be forgotten that salt-restriction increases thepotency of many antihypertensives (e.g. beta-blockers,calcium-channel blockers and ACE inhibitors).

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