Hypertension in Dialysis Patients

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Hypertension in dialysis patients

Last literature review version 18.2: May 2010 | This topic last updated: June 14, 2010

INTRODUCTION — There are several major issues to consider when approaching hypertensionin dialysis patients [ 1 ]:

What is the pathogenesis of the elevation in blood pressure (BP)?How is hypertension best defined?What are the target blood pressure goals?How should the hypertension be treated?

The possibility of bilateral renal artery stenosis should also be considered in patients withend-stage renal disease of uncertain cause. (See "Chronic kidney disease associated withatherosclerotic renovascular disease" .)

This topic review will present the epidemiology, pathogenesis, and treatment of hypertension indialysis patients, with an emphasis on hypertension in patients undergoing hemodialysis. Mostpatients undergoing peritoneal dialysis can become normotensive with strict adherence to volumecontrol, unless there are difficulties attaining effective ultrafiltration. This problem is reviewedseparately. (See "Problems with solute clearance and ultrafiltration in continuous peritoneal

dialysis" .)

EPIDEMIOLOGY — Hypertension is a common finding in dialysis patients. Based upon multiplestudies, over 50 to 60 percent of hemodialysis patients (up to 85 percent in some reports) andnearly 30 percent peritoneal dialysis patients are hypertensive [ 2-5 ]. These values are lower thanthe 80 percent incidence of hypertension at the initiation of dialysis, due largely to better volumecontrol in most patients [ 6 ].

Clinicians should strive for an even better blood pressure control rate [ 1 ]. Since poorly controlledhypertensive hemodialysis patients are more likely to have large interdialytic and excessiveweight gains, persistent hypertension often reflects volume control that remains imperfect despitethe initiation of dialysis [ 4,7 ].

Poor blood pressure control has also been reported in children undergoing dialysis. In one study,approximately one-half of children had uncontrolled hypertension after one year of dialysistherapy [ 8 ].

Cardiovascular risk — The relationship between hypertension and cardiovascular mortality inpatients with end-stage renal disease is complicated because of the high prevalence of comorbidconditions and underlying vascular pathology. Although a positive correlation has been found insome studies [ 9-11 ], a few reports in which patient outcomes were assessed for only one to twoyears have found little or no relationship between hypertension and mortality [ 12 ].

Enhanced mortality has also been reported among prevalent dialysis patients with the lowestblood pressures who were followed for short periods [ 12-16 ]. This was shown in the followingreports:

In a cohort study of 40,933 hemodialysis patients followed for a 15 month period, the hazard

Official reprint from UpToDate ®

www.uptodate.com ©2010 UpToDate ®

AuthorsWilliam L Henrich, MD, MACPLionel U Mailloux, MD, FACP

Section EditorsSteve J Schwab, MDGeorge L Bakris, MD

Deputy EditorTheodore W Post, MD


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ratio for all cause death for a predialysis systolic blood pressure


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evidence, for example, suggests that patients on chronic ambulatory peritoneal dialysis maybecome hypertensive after many years, possibly because of the loss in part of ultrafiltratingcapacity by the peritoneal membrane [ 30-35 ]. A decrease in dialysate sodium may also beassociated with a decrease in blood pressure [ 36 ].

Activation of the renin-angiotensin-aldosterone system due to primary vascular disease or toregional ischemia induced by scarring.

Increased activity of the sympathetic nervous system.

An increase in endothelium-derived vasoconstrictors (such as endothelin) or a reduction inendothelium-derived vasodilators (such as nitric oxide ).

The administration of erythropoietin .

An increase in intracellular calcium induced by parathyroid hormone excess [ 37 ]. Theobservation that correction of hyperparathyroidism via either vitamin D administration orparathyroidectomy lowers the blood pressure is compatible with this hypothesis [ 37,38 ]. In onereport, the mean systolic pressure fell over a period of months by a mean of 9 mmHg afterparathyroidectomy [ 38 ].

Calcification of the arterial tree.

Preexistent essential hypertension.

Volume overload — Volume expansion is perhaps the major factor in the development of hypertension in dialyzed patients [ 39 ]. It leads to an elevation in BP via the combination of a risein cardiac output and an inappropriately high systemic vascular resistance [ 6,28 ]. The latterfinding may result from activation of the renin-angiotensin system or from the secretion ofouabain-like inhibitors of Na-K-ATPase, leading to elevations in intracellular sodium and calcium.The rise in cell calcium in vascular smooth muscle cells can then induce vasoconstriction. (See"Natriuretic hormones: Atrial peptides and ouabain-like hormone" , for a discussion of thisphenomenon).

Regardless of the mechanism, removal of the excess sodium and attainment of "dry weight" (seebelow) can result in the normalization of BP in more than 60 percent of hemodialysis-dependentpatients and nearly all patients undergoing peritoneal dialysis [ 6,40-45 ]. The degree ofextracellular volume expansion may be insufficient to induce edema; thus, the absence of edemadoes not exclude hypervolemia.

Increased sympathetic activity — Sympathetic overactivity is a common finding in end-stagerenal disease, correlating with the increase in both vascular resistance and systemic BP [ 46 ]. Themechanism by which this occurs is unclear, but the afferent signal may arise within the kidney,

since sympathetic activation is not seen in anephric patients [ 46 ]. It has therefore been proposedthat activation of chemoreceptors within the kidney by uremic metabolites may play an importantrole. Activation of these chemoreceptors leads to a neural reflex that traverses afferent pathwaysto the central nervous system, resulting in increased efferent sympathetic tone.

Altered endothelial cell function — An intriguing concept regarding the pathogenesis of hypertension in end-stage renal disease is abnormal endothelial release of hemodynamicallyactive compounds. As an example, elevated plasma levels of the potent vasoconstrictorendothelin-1 have been found in uremic subjects [ 47,48 ]. The concentration of other endothelinisoforms also may be increased, but only endothelin-1 has been linked to high BP [ 49 ].

It should be appreciated, however, that these observations do not prove a cause and effectrelationship. The development of a method to inhibit the activity of endothelin (such as a receptorblocker) will be necessary to determine the physiologic importance of endothelin in thesepatients.

The endothelium also produces vasodilators, such as prostacyclin and nitric oxide (NO or


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endothelium-derived relaxing factor). NO is a synthetic product of L-arginine in endothelial cellsand is a potent vasodilator. There is evidence that uremic plasma contains a higher level of anendogenous compound — asymmetrical dimethylarginine — that is an inhibitor of NO synthesis[50 ]. This observations raises the possibility that NO deficiency may contribute to thedevelopment of hypertension in end-stage renal disease.

Erythropoietin — An increase in BP of 10 mmHg or more may occur in patients with renal failurewho are treated with erythropoietin . The risk is greatest in those with rapid correction of severe

anemia and with preexistent hypertension. (See "Hypertension following erythropoietin in chronickidney disease" .)

METHOD OF BLOOD PRESSURE MEASUREMENT — A reliance upon immediate predialysisand/or postdialysis BP measurements alone to detect hypertension in patients undergoinghemodialysis may be misleading. The predialysis systolic BP may overestimate the meaninterdialytic SBP by 10 mmHg, while the postdialysis systolic BP may underestimate the meansystolic BP by 7 mmHg [ 51 ]. Some studies, however, have suggested that the postdialysis BPmay be more reflective of interdialytic BP [ 52,53 ].

Continuous monitoring is therefore warranted in patients suspected of poor control (such as thosewith large interdialytic weight gain) [ 25,54-57 ]. The results with ambulatory blood pressuremonitoring appear to be relatively reproducible [ 56,58 ].

Ambulatory BP monitoring may also be useful in determining the "systolic load," which is theamount of time the systolic pressure exceeds 140 mmHg during the day [ 25,59-61 ]. This loadmay be an important factor in the development of left ventricular hypertrophy. The ambulatoryBP is also associated with significant prognostic value [ 59 ]. Interdialytic hypertension does notappear to be a problem with the Tassin and nocturnal hemodialysis regimens of long, slow dialysis[62 ].

Home blood pressure monitoring may also improve hypertension detection and prognostic value[60,63 ]:

In one study, the finding of an average systolic BP greater than 150 mmHg at home was moreaccurate than conventional blood pressure monitoring in helping diagnose hypertension (asdetermined by ambulatory BP) [ 63 ].

The best prognosis was observed with a home measurement of a systolic blood pressure of125 to 145 mmHg [ 60 ].

Uremic patients have an additional problem in that they lose the usual diurnal variation in bloodpressure, possibly leading to nocturnal hypertension [ 25 ]. Thus, even patients thought to be wellcontrolled with daytime BP measurements may still be at risk for hypertension-induced

cardiovascular morbidity [ 64 ]. This problem should be suspected if, for example, left ventricularmass increases (on echocardiography) despite seemingly adequate control of hypertension andanemia. (See "Myocardial dysfunction in end-stage renal disease" .)

OPTIMAL BLOOD PRESSURE — Current blood pressure target ranges for dialysis patients havebeen extrapolated from those suggested for the non-dialysis patient population. There have beenno randomized prospective studies evaluating the target blood pressure in dialysis patients. Ingeneral, the targeting of exact blood pressure goals (whether to a specific level or below a certainvalue) should ideally be set individually based upon the patient's cardiac and neurologic status,comorbid conditions, age, and other clinical factors [ 1 ].

For some dialysis patients, we suggest that goal BP levels be a predialysis value of below 140/90mmHg and a postdialysis value of below 130/80 mmHg [ 19,41,65-68 ]. If clinical characteristicspermit and ambulatory pressures are measured, a "normal" BP, defined as a mean ambulatory BPless than 135/85 mmHg during the day and less than120/80 mmHg by night, is a reasonabletarget goal.


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However, controversy exists over the blood pressure target; some investigators have postulatedthat excessively low systemic pressures lead to enhanced mortality (a so-called J- or U-shapedcurve) [ 13,69-72 ]:

A report of nearly 4500 hemodialysis patients found a significantly increased adjustedmortality risk among patients with a low predialysis systolic pressure (110 mmHg) and systolic pressures(>180 mmHg) [ 13 ].

In an observational study of 56,338 and 69,590 incident and prevalent hemodialysis patients,respectively, a markedly increased risk of death was noted among those with systolic bloodpressures less than 120 mmHg versus those with systolic blood pressures between 160 and 180mmHg (hazard ratio of 2.63 to 3.68 based upon different statistical adjustments) [ 71 ].

A retrospective analysis of 13,792 incident hemodialysis patients evaluated the correlationbetween survival and achieving K/DOQI clinical practice guidelines for multiple parameters [ 72 ].An increased mortality was associated with achieving the goal predialysis blood pressure of lessthan 140/90 mmHg (1.90, 95% CI 1.73-2.10).

Whether these results are due to a direct effect of a relatively low blood pressure or to anassociated comorbid condition is unclear.

In summary, the target goals should generally be realized based upon individual patientcharacteristics [ 1 ]. In some younger patients, the target BP may even be set as low as 120/80mmHg.

TREATMENT

Control of volume status — Control of volume status can either normalize the BP or make thehypertension easier to control in the great majority of dialysis patients. Nearly all peritonealdialysis patients, for example, can become normotensive with strict adherence to volume control

[43,73 ].

Avoidance of large weight gains in the interdialytic period is clearly desirable. To achieve thisgoal, patients should adhere to a restricted salt diet (750 to 1000 mg of sodium/day), which alsohelps decrease thirst [ 19,74,75 ]. However, patient compliance is often suboptimal. (See "Patientinformation: Low sodium diet" .)

As a result, heavy reliance is placed on the dialysis procedure to gradually remove fluid over aperiod of days to weeks until a stable "dry weight" is achieved [ 6,19,40,41,66,68,76-78 ]. Theexact definition of dry weight remains uncertain, but multiple definitions have been advanced. Asexamples, dry weight has been defined clinically as that weight at which:

Either the BP has normalized or symptoms of hypovolemia appear, not merely the absence ofedema.

The seated BP is optimized, and symptomatic orthostatic hypotension and clinical fluidoverload are not present postdialysis [ 79 ].

At the end of dialysis, the patient remains normotensive until the next dialysis withoutantihypertensive medication [ 80 ].

Numerous attempts have been made to utilize alternative methods to more accurately assess dryweight. These include bioimpedance plethysmography, and measurement of the inferior cava

diameter, plasma natriuretic peptide (particularly atrial and brain) concentrations, blood volume,and other parameters. However, these methods are frequently impractical, are not necessarilyaccurate, and a large prospective study has not yet been performed that compares these methodsto clinical assessment alone [ 81-84 ]. The clinician must therefore define the dry weight and goalblood pressure for each dialysis patient based upon his or her best judgment.


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Unfortunately, one problem with a reliance upon a clinical assessment of volume status is thatvolume expansion may persist even among those thought to have attained dry weight. Thispossibility was illustrated in a report in which the blood volume, inferior vena cava diameter, andposthemodialysis dry weight were evaluated in 35 stable hemodialysis patients (17 with and 18without hypertension, respectively) [ 85 ]. Despite the attainment of dry weight as determined bytraditional clinical standards, the blood volume of hypertensive patients was significantly higherthan in normotensive patients both before (3.53 versus 2.82 L/m2) and after (2.88 and 2.49L/m2) dialysis. In this study, the timing of the postdialysis inferior vena cava measurement wascritical, since many hours are required to reconstitute the plasma volume and intravascularcompartment. By comparison, other studies are flawed by too early a determination [ 86 ].

The view that volume expansion underlies the inability to control blood pressure in manyhemodialysis patients is also supported by studies that rely upon plasma atrial natriuretic peptide(ANP) concentrations to help assess the extracellular volume [ 87,88 ]. One study, for example,measured predialysis and postdialysis ANP values [ 87 ]. Predialysis levels were markedly elevatedin the hypertensive patients compared to those who were normotensive; in addition, thepostdialysis ANP concentrations normalized in those with dialysis-sensitive hypertension but wereunchanged in those with dialysis-resistant hypertension. In general, although predialysis ANPvalues may correlate with volume overload, postdialysis levels are unreliable in determining dryweight [ 81 ].

Two other factors may limit the degree of fluid removal by predisposing to episodes ofhypotension (and therefore the need for volume replacement) during the hemodialysis procedure:antihypertensive drugs; and rapid fluid removal required by shorter dialysis times. Thus, taperingdrug therapy and gradual fluid removal may be beneficial in patients in whom hypotension duringdialysis prevents the attainment of dry weight and a normal BP.

Chronic volume overload also may be due to the chronic dialysate sodium prescription. Dialysatesodium prescriptions are relatively higher than that observed in most dialysis patients, leading todecreased sodium loss during dialysis and mild increases in serum sodium values post-dialysis

[89 ]. This results in volume overload and increased thirst, thereby increased blood pressure. Tohelp avoid these, some advocate an individualized approach to the dialysate sodium prescription.

Among patients initiated on dialysis, a period of time must ensue between the attainment of dryweight and adequate control of blood pressure, a property termed the lag phenomenon [ 90 ]. Thisreflects the time required to convert the patient from a catabolic to an anabolic state, a period inwhich the extracellular fluid space slowly stabilizes [ 90 ]. A similar phenomenon has beenobserved with the use of diuretics for the treatment of hypertension in the patient without renalfailure [ 91 ].

Prolonged and/or more frequent hemodialysis — Patients in a large dialysis center in Tassin,France and some home hemodialysis patients undergo long, slow hemodialysis in which thestandard regimen is eight hours, three times per week. This regimen is associated with themaintenance of normotension without medications in almost all patients [ 41,62,92,93 ]. Althoughthese results have been largely attributed to optimal volume control, other factors may alsocontribute, such as more complete control of uremia [ 62 ] which, as noted above, may decreaseafferent renal nerve activity and efferent sympathetic activation [ 46 ]. A subset of these patients,for example, are normotensive despite the presence of increased extracellular fluid volume whilehaving achieved clinical dry weight [ 94 ]. The reason for this observation is unclear. This regimen,which is not widely used, is also associated with a high patient survival rate [ 41 ]. (See "Patientsurvival and maintenance dialysis", section on 'Adequacy of dialysis' .)

Nocturnal hemodialysis, a procedure in which dialysis is performed six or seven nights a weekduring sleep for a variable amount of time based upon the length of sleep desired (usually 6 to 12hours in total), is also associated with excellent blood pressure control [ 95 ]. Almost all patientsbecome normotensive without medications. To achieve this, the "target weight" is progressivelydecreased until all antihypertensive agents are discontinued. (See "Technical aspects of nocturnal


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hemodialysis" .)

Some studies also suggest that more frequent hemodialysis treatments, via short dailyhemodialysis, may also be associated with normotension without medications and with regressionof left ventricular hypertrophy. (See "Short daily hemodialysis" , for a detailed review of thisissue).

The 2007 European Best Practice Guidelines recommend that the treatment time and/orfrequency of dialysis should be increased in patients with hypertension despite optimal volumeremoval [ 96 ].

Antihypertensive medications — Therapy with antihypertensive drugs is primarily indicated inthe 25 to 30 percent of dialysis patients in whom hypertension persists despite seeminglyadequate volume control. Some evidence suggests that the administration of such agents mayprovide significant clinical benefits, including improved mortality.

A 2009 systematic review and meta-analysis of eight randomised controlled trials (three with andfive without hypertensive patients) that enrolled 1679 dialysis patients found that lowering bloodpressure with antihypertensive therapy was associated with decreased risks of cardiovascularevents (RR of 0.71, 95% CI 0.55-0.92), all cause mortality (RR 0.80, 0.66-0.96) and

cardiovascular mortality (0.71, 0.50-0.99) [ 97 ]. Although there was significant variation inattained blood pressure, the overall mean decrease in systolic and diastolic blood pressure withactive therapy was 4 to 5 mmHg and 2 to 3 mmHg, respectively. There were no studies thatcompared the efficacy of different antihypertensive agents; the relative effects of ARBs, ACEinhibitors, beta blockers, and calcium blockers were largely compared with placebo orconventional therapy. Additional limitations included the low number of patients (including thosewith hypertension), lack of information concerning volume control, and marked variations in bloodpressure reduction (due in part to absence of firm criteria for measurement) [ 98 ].

Despite these limitations, it generally appears that renin-angiotensin-system blockers, betablockers, and calcium-channel blockers provide similar efficacy in dialysis patients. Thus, the type

of antihypertensive therapy chosen is dictated in part by coexistent diseases [ 66 ].

In addition, several points about specific classes of antihypertensive drugs deserve emphasis, asdiscussed in the following sections [ 66,99 ]:

Calcium channel blockers — Calcium channel blockers are both effective and well toleratedin dialysis patients, even in those who are volume expanded [ 64 ]. The only randomizedprospective study found that amlodipine , compared with placebo, improved overall mortalityamong hypertensive dialysis patients [ 100 ].

Calcium channel blockers are particularly useful in patients with left ventricular hypertrophy anddiastolic dysfunction. Calcium channel blockers do not require supplementary postdialysis dosing.

ACE inhibitors — ACE inhibitors are well tolerated and are particularly effective in patientswith heart failure due to systolic dysfunction and in many patients after an acute myocardialinfarction. The 2006 K/DOQI guidelines also suggest that these agents and/or angiotensin IIreceptor blockers are preferred in dialysis patients with significant residual renal function [ 101 ].These agents may help preserve native kidney function. (See "Overview of the therapy of heartfailure due to systolic dysfunction" and "Angiotensin converting enzyme inhibitors and receptorblockers in acute myocardial infarction: Recommendations for use" .)

ACE inhibitors (and angiotensin II receptor blockers [ARBs], see next section) are associated witha decrease in left ventricular mass among hemodialysis patients [ 102,103 ]. There are conflictingdata concerning the effect of ACE inhibitors on mortality among hypertensive patients undergoingmaintenance dialysis.

A randomized prospective study found no survival benefit with fosinopril among hemodialysispatients with left ventricular hypertrophy [ 104 ].


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A possible mortality benefit was shown in an observational study in which hypertensivedialysis patients were administered antihypertensive regimens with or without ACE inhibitors (60and 66 patients, respectively) at the discretion of the physician [ 105 ].

ACE inhibitors have unique side effects in end-stage renal disease: they can interfere with theaction of erythropoietin ; and they can trigger an anaphylactoid reaction (possibly mediated bykinins) in patients dialyzed with an AN69 dialyzer. (See "Major side effects of angiotensin

converting enzyme inhibitors and angiotensin II receptor blockers", section on 'Angioedema andanaphylactoid reactions' and "Reactions to the hemodialysis membrane" .)

The effect of ACE inhibitors on erythropoiesis has been best described in renal transplantrecipients with erythrocytosis. In this setting, an ACE inhibitor can lower the hematocrit towardnormal in almost all patients. This can occur by reducing the secretion or interfering with theaction of EPO, including those receiving EPO supplementation [ 106,107 ]. (See "Erythrocytosisfollowing renal transplantation" .)

There are less consistent data concerning the effect of ACE inhibitors on erythropoietin doses indialysis patients. Increased dose requirements and no effects have been reported [ 108 ]. There isalso an increased risk of hyperkalemia among chronic hemodialysis patients treated with an ACEinhibitor [ 108 ]. (See "Major side effects of angiotensin converting enzyme inhibitors andangiotensin II receptor blockers" .)

ARBs — A number of angiotensin II receptor blockers (ARBs) are currently available. Amonghemodialysis patients, ARBs (and ACE inhibitors) are associated with a decrease in left ventricularmass [ 103 ]. (See "Renin-angiotensin system inhibition in the treatment of hypertension" .)

There is limited experience with ARBs in patients with hypertension and end-stage renal disease[108,109 ]. In one open-label trial, 360 hypertensive dialysis patients were randomly assigned toan ARB or no ARB [ 109 ]. After multivariate adjustment, ARBs significantly reduced fatal andnonfatal cardiovascular disease events (hazard ratio 0.5, 95% CI 0.33-0.79). The most common

adverse event was heart failure (fatal and nonfatal), with ARBs lowering the rate by one-half.The 2006 K/DOQI guidelines suggest that these agents and/or ACE inhibitors are preferred indialysis patients with hypertension and significant residual renal function [ 101 ]. These agentsmay help preserve native kidney function.

ARBS and ACE inhibitors have similar issues in terms of adverse effects, including hyperkalemiaand possible dampened erythropoiesis [ 108 ]. In addition, although ARBs do not affect bradykininlevels, anaphylactoid reactions have been reported among patients receiving ARBS duringhemodialysis with AN69 membranes [ 110,111 ]. (See "Reactions to the hemodialysis membrane" .)

Beta blockers — Beta blockers are particularly indicated in patients who have had a recent

myocardial infarction. As in nonuremic subjects, patients with end-stage renal disease who haveheart failure due to systolic dysfunction may also benefit from therapy with a beta blocker. Suchtherapy should be initiated at very low doses to minimize the risk of hemodynamic deterioration.(See "Myocardial dysfunction in end-stage renal disease" and "Use of beta blockers in heartfailure due to systolic dysfunction" .)

Potential side effects include central nervous system depression (an effect that may be moreprominent with lipid-soluble drugs that cross the blood-brain barrier), hyperkalemia (particularlywith non-selective beta blockers), bradycardia, and possible exacerbation of heart failure [ 108 ].In addition, beta blockers should be used cautiously in patients also taking a calcium channelblocker, since there are often additive negative chronotropic and inotropic actions.

Central sympathetic agonists — The central sympathetic agonists, such as methyldopa andclonidine , are used less frequently because of their adverse effects involving the central nervoussystem. Some physicians have found clonidine patches to be effective and well tolerated, but thisis not a universal finding [ 108,112 ].


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Bilateral nephrectomy may be considered in the rare noncompliant individual with life-threateninghypertension unable to be controlled with any dialysis modality. In one study, a significantdecrease in blood pressure was observed three to six months after nephrectomy with six patientshaving a diastolic pressure of less than 90 mmHg [ 118 ]. One patient had persistent increases inblood pressure due largely to excess fluid intake between dialysis treatments, thereby furthersupporting the hypothesis that hypervolemia is highly significant in the pathogenesis ofhypertension among dialysis patients. Bilateral nephrectomy is now largely abandoned, but wasinfrequently used for blood pressure control when potent antihypertensive agents were not yetwidely available.

HYPERTENSION DURING HEMODIALYSIS — Although hypotension during hemodialysis is afrequent complication, some patients develop paradoxical hypertension in the later stages of dialysis, a time at which most of the excess fluid has already been removed. This problem isintermittent in a given patient with a widely variable frequency. The pathogenesis is unclear,although some evidence suggests that altered nitric oxide /endothelin-1 balance may contribute[119 ].

The optimal therapy of this problem is not known. In our experience, various medical modalities(such as the administration of an angiotensin converting enzyme inhibitor or an alpha-blocker at

the time of hypertension, or pretreatment with antihypertensive medications to lower the bloodpressure before dialysis) have not been predictably effective. We have had some success with theadministration of isotonic saline to presumably treat hypovolemia-induced but excessive reflexsympathetic activation. Limited observational evidence suggests that this increase in bloodpressure is associated with adverse outcomes [ 120 ]. (See "Hemodynamic instability duringhemodialysis: Overview" .)

SUMMARY AND RECOMMENDATIONS — Despite a paucity of data concerning many aspects of the evaluation and treatment of hypertension in hemodialysis patients, certain generalrecommendations are appropriate [ 1 ]. All dialysis patients benefit by a comprehensive evaluationof their cardiovascular status, such as the assessment for traditional risk factors associated with

adverse outcomes. Appropriate modalities may include ambulatory blood pressure monitoring andcardiac echocardiography.

The target goals should generally be realized based upon individual patient characteristics, withthe lowest target BP values being consistent with patient well-being and the absence ofintradialytic hypotension [ 19 ]. For some patients on dialysis, the goal BP is a predialysis value ofless than 140/90 mmHg and a post-dialysis value of less than 130/80 mmHg [ 66 ]. If clinicalcharacteristics permit and ambulatory pressures are measured, a "normal" BP, defined as a meanambulatory BP less than 135/85 mmHg during the day and less than 120/80 mmHg at night, isalso a reasonable target goal.

To attain this level of control, the following measures may be utilized [ 1 ]:

Other than those drugs required for any underlying cardiac disease, antihypertensivemedications should be slowly withdrawn while uncovering the patient's true dry weight. Thisprocess should be undertaken over 3 to 6 weeks among younger patients, and up to 12 to 14weeks for older individuals and those with vascular pathology.

If the blood pressure remains elevated despite the attainment of dry weight, antihypertensivemedications should be administered. The choice of drug is based upon the benefits and adverseeffects previously delineated, but an antihypertensive agent is preferably administered during theevening with a once per day dosing schedule. The K/DOQI guidelines suggest that ACE inhibitorsor angiotensin II receptor blockers are preferred because they may provide greater benefits, suchas relatively more LVH regression [ 66 ].

Patients should be adequately dialyzed. (See "Kt/V and the adequacy of hemodialysis" and"Adequacy of peritoneal dialysis" .)


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Large interdialytic weight gains must be discouraged. As delineated in the K/DOQI guidelines,management of increased fluid accumulation should be accomplished by consultation withdieticians, low sodium intake, increased ultrafiltration, and/or increased dialysis treatments [ 66 ].

Low initial doses of subcutaneous erythropoietin should be administered, and the targethematocrit should be slowly obtained. (See "Erythropoietin for the anemia of chronic kidneydisease among predialysis and peritoneal dialysis patients" and "Erythropoietin for the anemia ofchronic kidney disease in hemodialysis patients" .)

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