INTRODUCTION — Hypertension is common among dialysis patients [1]. This topic reviews the epidemiology, pathogenesis, and treatment of hypertension in dialysis patients.
Hypertension among patients with acute or chronic kidney disease who are not on dialysis is discussed elsewhere.
●(See "Overview of hypertension in acute and chronic kidney disease".)
●(See "Antihypertensive therapy and progression of nondiabetic chronic kidney disease in adults".)
Hypertension in the general adult population is discussed elsewhere.
●(See "Overview of hypertension in adults".)
●(See "Choice of drug therapy in primary (essential) hypertension".)
●(See "Goal blood pressure in adults with hypertension".)
EPIDEMIOLOGY — Hypertension is a common finding in dialysis patients. Prevalence estimates vary widely among studies because of differences in the definition of hypertension and in methods of measuring blood pressure (BP; ie, either before and after dialysis or using ambulatory BP recordings). Based upon multiple studies, over 50 to 60 percent of hemodialysis patients (up to 85 percent in some reports) and nearly 30 percent of peritoneal dialysis patients are hypertensive [2-6]. In one multicenter trial that included 2535 adult hemodialysis patients, the prevalence of hypertension, defined as one-week average predialysis systolic BP measurements 150 mmHg or diastolic BP 85 mmHg or the use of antihypertensive medications, was 86 percent [5,6].
Hypertension is more common among patients who are just initiating dialysis (greater than 80 percent) because almost all such patients are volume overloaded [7]. Persistent hypertension often reflects inadequate volume control despite the initiation of dialysis [4,8]. (See 'Pathogenesis' below.)
PATHOGENESIS — Volume expansion is the major cause of hypertension in dialysis patients [9,10]. Volume overload leads to an elevation in blood pressure (BP) via the combination of a rise in cardiac output and high systemic vascular resistance [7,11]. The role of volume expansion is supported by studies that have shown improvement in BP with volume reduction [12-14].
The removal of the excess sodium and reduction in target dry weight can result in the normalization of BP in >60 percent of hemodialysis patients and in many peritoneal dialysis patients [7,12,15-20].
Sympathetic overactivity, activation of the renin-angiotensin system, and arteriosclerosis also contribute to hypertension in hemodialysis patients [21-23].
Other potential contributors include changes in endothelium-derived vasoactive peptides [24-27], increases in intracellular calcium [28,29], and decreases in renalase [30]. Renalase is a catecholamine-metabolizing enzyme released by the kidney in response to catecholamine surge.
Elevated BP may also be associated with use of erythropoiesis-stimulating agents (ESAs), over-the counter drugs such as nasal decongestants and nonsteroidal antiinflammatory drugs (NSAIDs), illicit drugs such as cocaine, and herbal remedies such as ma-huang and St. John's wort [7,11,31,32]. (See "Overview of hypertension in adults", section on 'Primary hypertension'.)
MONITORING AND DIAGNOSIS — Ambulatory blood pressure monitoring (ABPM) is considered the gold standard for the diagnosis of hypertension [33]. (See "Goal blood pressure in adults with hypertension", section on 'Importance of how blood pressure is measured'.)
Among hemodialysis patients, ABPM provides reproducible readings and correlates with outcomes but is generally not used clinically, as it is cumbersome and poorly suited to day-to-day management of hypertension [34-36].
We use self-recorded home blood pressure (BP) monitoring to monitor BP and diagnose hypertension. Self-recorded home BP readings are efficient, accurate, and correlate with ABPM [34,37-39] and with outcomes [40-43]. We instruct patients to check home BP readings twice daily for four days after the mid-week dialysis treatment and to provide them for review. The optimal frequency of monitoring is not known. We suggest home BP monitoring at monthly intervals [37,44,45].
We do not use pre- and postdialysis BP measurements to diagnose hypertension or titrate antihypertensive therapy, although BP is closely monitored throughout the dialysis treatment to assess the hemodynamic stability of the patient during the treatment. The pre- or postdialysis BP readings correlate only weakly with ABPM. They associate inversely with clinical outcomes, which is counterintuitive [46,47]. Predialysis BP readings tend to overestimate and postdialysis readings underestimate BP readings obtained by ABPM, and the degree of bias is variable. In one systematic review of studies, compared with 44-hour ABPM, predialysis systolic BP was variably 42 mmHg higher or 25 mmHg lower, and postdialysis systolic BP was 33 mmHg higher to 36 mmHg lower [48].
By contrast to pre- and postdialysis readings, BP readings obtained outside the dialysis unit (either by ABPM or self-recorded home measurement) are directly related to all-cause mortality [40-43]. As an example, a 2015 study showed that a single recording of systolic BP measured outside the dialysis unit was directly related to mortality (hazard ratio [HR] 1.26, 95% CI 1.14-1.40) for every 10 mmHg increase [43].
If ABPM is used to confirm home-recorded BP readings, it is best performed over 44 hours during the interdialytic period to account for volume-related increases in BP [34,38]. ABPM generally shows a linear increase in BP as volume accrues.
If home BP monitoring is not possible or is unavailable, as a last resort, we use median intradialytic systolic BP to make diagnostic decisions. As an example, in a patient who dialyzes Monday-Wednesday-Friday, if the systolic BP is 146 mmHg on Wednesday, the patient is very likely to be hypertensive. In one study, the midweek median intradialytic BP of 140 mmHg was approximately 80 percent sensitive and approximately 80 percent specific in diagnosing hypertension among dialysis patients. For median diastolic BP of 80 mmHg, the sensitivity and specificity for diagnosing hypertension in the interdialytic period was approximately 75 percent each [49]. Furthermore, median intradialytic BP can track changes evoked by probing dry weight in these patients [50]. Nonetheless, median intradialytic systolic BP has wide limits of agreement with 44-hour ambulatory systolic BP ranging from 16 to 20 mmHg.
BENEFITS OF TREATING HYPERTENSION — Multiple studies and meta-analyses of randomized, controlled trials in dialysis patients have suggested a benefit of using antihypertensive agents to lower blood pressure (BP) on cardiovascular events and cardiovascular mortality [51-56]. The best data are from two meta-analyses:
●A 2009 systematic review and meta-analysis of eight randomized, controlled trials that enrolled 1679 dialysis patients found that lowering BP with antihypertensive therapy was associated with decreased risks of cardiovascular events (relative risk [RR] 0.71, 95% CI 0.55-0.92), all-cause mortality (RR 0.80, 95% CI 0.66-0.96), and cardiovascular mortality (RR 0.71, 95% CI 0.50-0.99) [55].
●A second 2009 meta-analysis including five randomized trials with 1202 hemodialysis patients showed that, compared with placebo or control therapy, BP lowering with antihypertensive therapy resulted in a 31 percent reduction in the risk of cardiovascular events (pooled hazard ratio [HR] 0.69, 95% CI 0.56-0.84) [56].
TREATMENT — The optimal blood pressure (BP) goal and the interventions that are available to treat hypertension in dialysis patients are discussed here.
Blood pressure target — The threshold BP that should be treated is not known with certainty. BP target ranges for dialysis patients have been extrapolated from studies in the nondialysis patient population. We target an interdialytic self-measured home BP of <140/80 mmHg.
If interdialytic self-measured home BP is not available, targeting a median midweek BP of <140/80 mmHg appears to be a reasonable alternative strategy. We calculate the median midweek BP from all the BPs measured during a midweek dialysis session (eg, on Wednesday for a patient receiving dialysis on Mondays, Wednesdays, and Fridays). We do not use a predialysis BP target to control hypertension. (See "Goal blood pressure in adults with hypertension".)
There are no large-scale trials that define optimal self-measured home BP targets among dialysis patients. Our assessment of the best target BP is based upon findings reported in observational studies combined with our clinical experience managing dialysis patients.
In an observational study of 150 hemodialysis patients, BP was recorded by three methods: pre- and post-dialysis BP by routine automated oscillometric recordings; 44-hour ambulatory BP by monitoring during the midweek interdialytic interval; and home BP by self-measurement over one week [40]. Patients were followed for a median period of two years. The BPs obtained by home and ambulatory monitoring (as opposed to those obtained pre- and post-dialysis) were associated with mortality. In addition, home systolic BP of 125 to 145 mmHg and ambulatory systolic BP of 115 to 125 mmHg appeared to be associated with the lowest risk of mortality. Similar findings were noted in another observational study in which home systolic BP of 120 to 130 mmHg and ambulatory systolic BP of 110 to 120 mmHg were associated with the lowest mortality [41].
Multiple large observational studies have demonstrated a U-shaped relationship between predialysis and postdialysis BP and mortality among dialysis patients [40,41,46,47,51,57-63]. This U-shaped relationship suggests that both low and high predialysis and postdialysis BPs are associated with a higher mortality compared with mid-range BPs. However, BPs recorded on an interdialytic day are monotonically associated with mortality [43].
Targeting predialysis BPs is not helpful. As an example, one pilot trial evaluated the target predialysis BP in dialysis patients [64]. The trial randomly assigned 126 long-term hemodialysis patients to one of two BP goals: an intensive arm (predialysis systolic BP of 110 to 140 mmHg) and a standard arm (predialysis systolic BP of 155 to 165 mmHg). Compared with patients in the standard arm, those in the intensive arm had a higher risk of recurrent hospitalization, vascular access thrombosis, and intradialytic hypotension. Thus, until trial data becomes available, targeting a BP of <140/80 among dialysis patients is reasonable. We preferably use self-measured home BP to achieve this target for reasons discussed above. (See 'Monitoring and diagnosis' above.)
Interventions — Treatment interventions include reducing the target dry weight in an effort to achieve euvolemia and antihypertensive medications. If possible, the target dry weight should be adjusted before antihypertensive agents are added. However, patients are often on multiple antihypertensive agents when they start maintenance dialysis. Among such patients, the approach will vary depending on severity of hypertension and hemodynamic stability during dialysis. As an example, in some patients, ultrafiltration is limited because of intradialytic hypotension; such patients may benefit from tapering antihypertensive agents. In other patients who have severe hypertension, antihypertensive agents may need to be continued while the target dry weight is gradually reduced.
Achieving optimal dry weight — Reducing the target dry weight gradually can normalize the BP or make the hypertension easier to control in a vast majority of dialysis patients [18,65]. The exact definition of target dry weight remains uncertain, but multiple definitions have been suggested [66-68]. We believe that the best definition of dry weight is the lowest tolerated postdialysis weight at which there are minimal signs or symptoms of either hypovolemia or hypervolemia [69].
Assessment of volume status — Patient history and physical examination are generally used to assess the optimal target dry weight. The patient should be questioned about interdialytic symptoms that suggest orthostatic hypotension (such as lightheadedness) and intradialytic symptoms such as muscle cramps that might indicate that the dry weight is below desired. However, muscle cramps may not be a reliable indicator of hypovolemia, especially when they do not improve despite an increase in dry weight.
A physical examination is generally performed at the beginning of dialysis and includes an assessment for presence of increased jugular venous pulse, peripheral or pulmonary edema, and ascites (suggesting volume overload) at a given weight and BP. Unfortunately, one problem with a reliance upon a clinical assessment of volume status is that volume expansion may persist even among those thought to have attained euvolemia.
Other methods to assess dry weight include bioimpedance analysis [70,71], relative plasma volume (RPV) monitoring [72,73], measurement of the inferior cava diameter [74-76], and plasma natriuretic peptides (particularly atrial and B-type) concentrations [77,78]. These methods are not commonly used clinically, although studies have suggested utility, particularly of bioimpedance analysis and RPV monitoring [70,72,73]. When they are used, they should function as adjuncts, rather than as alternatives, to the clinical assessment of the patient.
An emerging strategy to assess volume excess is lung ultrasound, which can be used to measure lung water as a marker of lung congestion. One trial compared lung ultrasound-guided dry weight reduction versus usual care on BP improvement among 71 hemodialysis patients [79-81]. At 12 months, lung ultrasound-guided dry weight reduction was greater in the ultrasound group (-2 versus +0.5 kg), and accompanied by a greater decline in 44-hour ambulatory systolic (6 versus 0.5 mmHg) and diastolic (4 versus 1 mmHg) blood pressure, ultrasound B lines (metric of lung water; -5 lines versus +6 lines), and rate of intradialytic hypotension. However, this was a small trial and these findings need to be replicated in larger, more diverse populations before it can be introduced into routine clinical care.
Other methods for determining dry weight have not been compared with clinical assessment alone [73,77,82,83]. Until such methods are validated, the clinician must define the dry weight and goal BP for each dialysis patient based upon his or her best judgment.
How to reduce target dry weight — The reduction in dry weight is best done gradually. We reduce the target weight over days to weeks [7,12,15,16,53,84-88]. In a patient who is just starting maintenance hemodialysis who is either hypertensive (as defined above) or on antihypertensive agents, we reduce the target dry weight by 0.5 L per session. In patients who are unable to tolerate this, we attempt 0.2 L per session. (See 'Blood pressure target' above.)
Patients should avoid large interdialytic weight gain (ideally <2 to 3 L) in order to limit the amount of fluid that needs to be removed in an individual session; a patient who gains 5 liters in between dialysis sessions will have difficulty achieving the previous target dry weight, which generally precludes removing an additional 0.5 L to achieve a lower target dry weight.
The best way to limit interdialytic weight gain is to limit salt intake. Salt intake drives thirst. It is not helpful to restrict fluid without restricting salt.
All patients should adhere to a restricted salt diet (1500 to 2000 mg of sodium/day) [53,89,90]. However, patient adherence to a low-sodium diet is often suboptimal.
In some patients, it is difficult to reduce the target dry weight. In such patients, we use the following approach:
●Increase dialysis time – Increasing the length or frequency of sessions is often effective in reducing target dry weight [91].
The utility of lengthier dialysis sessions was demonstrated in a large dialysis center in Tassin, France, where a standard regimen is eight hours, three times per week [16,92-94]. This regimen was associated with the maintenance of normotension without medications in almost all patients [16,92-94]. The improved BP was largely attributed to optimal volume control, although other factors may contribute, such as decreased afferent renal nerve activity and efferent sympathetic activation [21]. However, this regimen is not widely used in in-center hemodialysis. (See "Patient survival and maintenance dialysis", section on 'Adequacy of dialysis'.)
The efficacy of more frequent dialysis in achieving BP control is demonstrated by nocturnal hemodialysis, in which dialysis is performed six or seven nights a week during sleep (usually 6 to 12 hours in total) [95]. Almost all patients become normotensive without medications. (See "Technical aspects of nocturnal hemodialysis".)
Short daily hemodialysis may also be associated with better BP control. (See "Short daily hemodialysis".)
●Reduce dialysate sodium – If increasing the dialysis time is ineffective, we reduce the dialysate sodium concentration.
The use of standard sodium prescriptions leads to decreased sodium loss during dialysis and mild increases in serum sodium values postdialysis [96]. This results in volume overload and increased thirst. A lower dialysate sodium concentration may result in lower antihypertensive medication requirements and decreased BP [97]. The dialysate sodium should be reduced gradually (ie, 1 mEq/L every three to four weeks) to approximately 136 mEq/L.
The dialysate sodium may be reduced in a fixed or variable fashion.
A variable reduction in dialysate sodium on BP was evaluated in one randomized, crossover study [98]. A programmed decrease in sodium dialysate concentration from 155 to 135 mEq/L was compared with the standard stable sodium dialysate concentration of 140 mEq/L [98]. Postdialysis BP and antihypertensive use were reduced when patients were dialyzed with a variable sodium prescription.
A fixed lower dialysate sodium concentration in combination with sodium restriction was evaluated in a small, uncontrolled study [99]. Eight hypertensive hemodialysis patients were dialyzed against a gradually lowered sodium dialysate concentration (140 to 135 mEq/L at a rate of 1 mEq/L every three to four weeks) and were encouraged to limit salt intake to <6 g/day [99]. At study end, the mean arterial pressure was lower, and antihypertensive medications were no longer required in four patients. However, adherence to the diet was difficult, and the frequency of muscle cramps during dialysis was increased. This regimen engenders the risk of episodic hypotension and should be instituted cautiously (ie, with close observation).
Antihypertensive medications — Most hemodialysis patients will require antihypertensive agents to control BP despite achieving optimal dry weight. The optimal antihypertensive regimen for hemodialysis patients is not known. Our approach to managing hypertension among dialysis patients who require medications after optimization of volume status (see 'Achieving optimal dry weight' above) is as follows:
●Our first-choice antihypertensive agent is a beta-blocker (BB), even among patients previously controlled with another agent. Among the available BBs, we prefer atenolol, but other BBs are acceptable alternatives. Dosing varies by modality of dialysis:
•Among patients receiving hemodialysis, we dose atenolol post-dialysis thrice weekly. We typically start it at 25 or 50 mg depending upon the severity of hypertension. The maximum dose that we use among hemodialysis patients is 100 mg thrice weekly.
•Among patients receiving peritoneal dialysis, we dose atenolol once daily. We typically start it at 25 or 50 mg once daily depending upon the severity of hypertension. The maximum daily dose that we use among peritoneal dialysis patients is 50 mg once daily.
A dose-limiting side effect of BBs is bradycardia. Among patients with symptomatic bradycardia from BBs (eg, lightheadedness, presyncope or syncope, exercise intolerance), we reduce the dose of the BB. Among patients with asymptomatic bradycardia, we avoid increasing the BB dose once the heart rate is 50 beats per minute or below and reduce the dose when the heart rate is 40 beats per minute or below. Side effects of BBs are discussed at length elsewhere. (See "Major side effects of beta blockers".)
●Our second-choice agent is a dihydropyridine calcium channel blocker (CCB), such as amlodipine 10 mg dosed daily. We add amlodipine among patients who have BPs that are not adequately controlled with the maximum dose BB or among patients who develop intolerable side effects (eg, bradycardia) to the BB. CCBs are not cleared by dialysis and, therefore, do not need to be supplemented or dosed postdialysis. Side effects of CCBs are discussed at length elsewhere. (See "Major side effects and safety of calcium channel blockers".)
●Our third-choice agent is an angiotensin-converting enzyme (ACE) inhibitor or angiotensin receptor blocker (ARB). We add an ACE inhibitor or ARB among patients with BPs that are inadequately controlled with a BB and a CCB and among patients who have inadequately controlled BP with one and intolerance to another. Side effects of ACE inhibitors and ARBs are discussed at length elsewhere. (See "Major side effects of angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers".)
The management of patients who remain hypertensive despite maximally tolerated doses of BB, CCB, and either ACE inhibitor or ARB is discussed below. (See 'Resistant hypertension' below.)
Our preference for BBs as the first-line agent is based upon findings from the Hypertension in Hemodialysis Patients Treated with Atenolol or Lisinopril (HDPAL) trial in which 200 patients were randomly assigned to receive either drug [38]. At 12 months, compared with lisinopril, atenolol led to a numerically greater reduction in BP using the 44-hour interdialytic ambulatory BP monitoring (mean reduction -21/-13 versus -18/-10 mmHg) and the self-measured home BPs (mean reduction -25/-12 versus -19/-10 mmHg); these differences were not statistically significant. Over the course of the trial, compared with patients in the lisinopril group, those in the atenolol group required fewer antihypertensive medications despite a lesser degree of reduction in their dry weight. Additionally, there were fewer serious cardiovascular (CV) events including cardiovascular death, myocardial infarction, stroke, and hospitalization for heart failure in the atenolol group compared with the lisinopril group (20 events among 16 patients versus 43 events among 28 patients), leading to early termination of the trial.
Our next preference for CCBs is based upon their efficacy and tolerance in addition to their beneficial effect on CV outcomes in dialysis patients [100-102]. In one trial, compared with patients randomly assigned to placebo, those assigned to amlodipine had a reduction in the composite of all-cause mortality and CV events (hazard ratio [HR] 0.53, 95% CI 0.31-0.93). Amlodipine led to a clinically meaningful but statistically nonsignificant reduction in all-cause mortality (12 percent with amlodipine and 17 percent with placebo) [102].
We do not use nondihydropyridine CCBs (such as verapamil or diltiazem) because drug interactions with these agents are common and bradycardia can occur if dosed concomitantly with a BB.
We offer ACE inhibitors and ARBs only to patients who have an elevated BP despite maximally tolerated doses of BBs and CCBs. This is because ACE inhibitors or ARBs lead to modest reduction in BPs and no reduction in fatal and nonfatal CV events. As examples, in a 2010 meta-analysis of trial data including 837 hemodialysis patients, there was no significant reduction in BP or fatal and nonfatal CV events among patients treated with ACE inhibitors or ARBs compared with those in the standard care group [103]. In a subsequent trial of 469 hemodialysis patients, compared with standard care, patients randomly assigned to olmesartan had no significant reduction in BP (mean difference in BP of 0.9 mmHg) or in the incidence of fatal and nonfatal CV events (HR 1.00, 95% CI 0.62-1.52) [104]. Another smaller trial reported similar findings [105].
In addition, ACE inhibitors and ARBs can cause hyperkalemia [38], hypotension [38,105], reduction in the effect of erythropoiesis-stimulating agents, and anaphylactoid reaction in patients dialyzed with an AN69 dialyzer [106], thereby lowering the overall appeal of these agents. (See "Major side effects of angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers".)
RESISTANT HYPERTENSION — Some dialysis patients are resistant to both volume control and initial antihypertensive medications. Factors that can contribute to resistant hypertension include (see "Definition, risk factors, and evaluation of resistant hypertension" and "Treatment of resistant hypertension"):
●Nonadherence to the antihypertensive regimen (see "Patient adherence and the treatment of hypertension")
●Concurrent use of a medication that can raise blood pressure (BP; such as nonsteroidal antiinflammatory drugs [NSAIDs] or erythropoietin-stimulating agents) (see 'Pathogenesis' above)
●Inadequate dialysis (less than four hours per session, thrice weekly) (see "Prescribing and assessing adequate hemodialysis")
●Renovascular hypertension (see "Establishing the diagnosis of renovascular hypertension")
●Expanding cyst size among patients with polycystic kidney disease (see "Autosomal dominant polycystic kidney disease (ADPKD): Evaluation and management of hypertension")
Nonadherence with medications is a common cause of resistant hypertension. Chronically nonadherent hypertensive patients who refuse to take medications at home may benefit from the administration of long-acting antihypertensive medications in the dialysis unit [107].
If a treatable cause cannot be found, minoxidil may be effective in reducing the BP. The central sympathetic agonists, such as methyldopa and clonidine, are used less frequently because of their adverse effects involving the central nervous system. Some clinicians have found clonidine patches to be effective and well tolerated, but this is not a universal finding [106,107]. Guanfacine, on the other hand, may be less sedating.
Mineralocorticoid receptor antagonists (eg, spironolactone) are commonly used in nondialysis patients with resistant hypertension. Two trials reported very large benefits on cardiovascular mortality from spironolactone in patients receiving dialysis [108,109]. Effects of this magnitude are rarely if ever observed in rigorous cardiovascular trials; in addition, the findings have not been independently confirmed. We generally do not use mineralocorticoid receptor antagonists in hemodialysis patients because of the potential risk of hyperkalemia [110].
Renal denervation is an experimental therapy in which sympathetic nerves innervating the kidney are ablated for BP control. This method was evaluated in a small nonrandomized trial of 24 hemodialysis patients who had resistant hypertension despite maximal medical therapy with confirmed adherence [111]. Over a follow-up period of one year, patients treated with renal denervation in addition to medical therapy had a substantial and sustained reduction in BP compared with patients on medical therapy alone (32/18 mmHg versus 7/3 mmHg). However, more data are needed before renal denervation can be recommended in hemodialysis patients. (See "Treatment of resistant hypertension", section on 'Renal denervation'.)
Bilateral nephrectomy is no longer performed ever since effective antihypertensive medications became available.
HYPERTENSION DURING HEMODIALYSIS — 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 is intermittent in a given patient with a widely variable frequency. The pathogenesis is unclear, although some evidence suggests that altered nitric oxide/endothelin-1 balance and/or endothelial dysfunction may contribute [112,113].
Limited observational evidence suggests that this increase in blood pressure (BP) is associated with adverse outcomes [114].
Although the exact mechanism of this relationship is unclear, studies suggest that intradialytic hypertension is associated with both volume excess and interdialytic hypertension [115,116].
The optimal approach to intradialytic hypertension is not known. However, given the association with volume overload, challenging the dry weight may be effective [72]. Carvedilol, which blocks endothelin-1 release, may also be effective. In a 12-week pilot study, the initiation of carvedilol titrated to 50 mg twice daily was associated with a decrease in the frequency of intradialytic hypertensive episodes from 77 to 28 percent of hemodialysis sessions.
Use of a dialysate sodium concentration that is lower than the patient’s serum sodium may decrease BP during dialysis. This was suggested by a three-week randomized, crossover trial that compared the effect of high- and low-dialysate sodium concentrations on systolic BP among 16 patients with intradialytic hypertension [117].
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Dialysis".)
SUMMARY AND RECOMMENDATIONS
●Hypertension is a common finding in dialysis patients, particularly at initiation. Volume expansion is the major cause of hypertension in dialysis patients, although sympathetic overactivity, activation of the renin-angiotensin system, and arteriosclerosis also contribute. (See 'Epidemiology' above and 'Pathogenesis' above.)
●We use self-recorded home blood pressure (BP) monitoring to screen for hypertension. Self-recorded home BP readings are efficient, accurate, and correlate with readings obtained by ambulatory blood pressure monitoring (ABPM). We do not use pre- and postdialysis BP measurements to diagnose hypertension and inform antihypertensive therapy, since these measurements do not correlate with ABPM or with clinical outcomes. The optimal frequency of screening is not known. We suggest home BP monitoring twice daily for four days after a mid-week dialysis session, performed at monthly intervals.
If home BP monitoring is not possible or feasible, we use median intradialytic BP of 140/80 mmHg to diagnose and treat hypertension. As an example, in a patient who dialyzes Monday-Wednesday-Friday, if the systolic BP is 146 mmHg on Wednesday, the patient is very likely to be hypertensive. (See 'Monitoring and diagnosis' above.)
●The threshold BP that should be treated is not known with certainty. We treat interdialytic self-recorded home BP that is >140/80 mmHg. If home BP is not available, we target midweek median intradialytic BP to <140/80 mmHg. We do not use a predialysis BP target to control hypertension. (See 'Blood pressure target' above.)
●The primary strategy to improve BP in a dialysis patient is by reducing volume. BP treatment consists of reduction in target dry weight in effort to achieve euvolemia and pharmacologic interventions. We use intra and interdialytic symptoms and clinical examination to assess volume status and individualize optimal target dry weight. (See 'Assessment of volume status' above.)
●The reduction in dry weight is best done gradually. We reduce the target weight over days to weeks. Patients should avoid large interdialytic weight gain. Some patients require an increase in frequency of dialysis to achieve optimal dry weight. If these measures failure to reduce BP, we reduce the dialysate sodium concentration. (See 'How to reduce target dry weight' above.)
●Many hemodialysis patients will require antihypertensive agents. The optimal agent is not known with certainty. Our approach is as follows (see 'Antihypertensive medications' above):
•Among dialysis patients who need antihypertensive therapy, we suggest treatment with a beta blocker (BB) rather than another antihypertensive agent (Grade 2B). Atenolol is our usual choice, but other BBs are acceptable alternatives. Among hemodialysis patients, we dose atenolol thrice weekly with a starting dose of 25 mg up to a maximum of 100 mg. Among peritoneal dialysis patients, we dose atenolol daily with a starting dose of 25 mg up to a maximum dose of 50 mg. We reduce the dose of the BB for symptomatic bradycardia and if the heart rate is at or below 40 beats per minute. We stop increasing the dose of the BB if the heart rate is at or below 50 beats per minute.
•Among patients who have BPs that are not adequately controlled with the maximum dose BB or who develop intolerable side effects (eg, bradycardia) to the BB, we add calcium channel blockers (CCBs), such as amlodipine 10 mg.
•Among patients who have BPs that are inadequately controlled with a BB and a CCB and among patients who have inadequately controlled BP with one and intolerance to another, we add an angiotensin converting enzyme (ACE) inhibitor or angiotensin receptor blocker (ARB).
●Patients who have BPs that are uncontrolled despite use of maximally tolerated doses of a BB, CCB, and an ACE or ARB have resistant hypertension. Such patients require an evaluation for possible underlying causes and possible treatment with additional antihypertensive agents such as minoxidil. (See 'Resistant hypertension' above.)
ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Lionel U Mailloux, MD, FACP, who contributed to an earlier version of this topic review.
