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Intradialytic hypotension in an otherwise stable patient

Intradialytic hypotension in an otherwise stable patient
Literature review current through: Jan 2024.
This topic last updated: Oct 02, 2023.

INTRODUCTION — Hypotension during hemodialysis is common. In some patients, the development of hypotension necessitates intravenous fluid replacement before patients are able to safely leave the dialysis unit. Intradialytic hypotension may reduce the efficacy of the dialysis procedure and contributes to the excessive morbidity and mortality that is associated with hemodialysis.

This topic reviews the etiology, evaluation, treatment, and prevention of intradialytic hypotension in an otherwise stable patient. Other complications of hemodialysis are discussed elsewhere:

(See "Acute complications during hemodialysis".)

(See "Evaluation of sudden cardiac arrest and sudden cardiac death in patients on dialysis".)

Hypertension during dialysis is discussed elsewhere:

(See "Hypertension in patients on dialysis", section on 'Hypertension during hemodialysis'.)

DEFINITION OF INTRADIALYTIC HYPOTENSION — There is no generally accepted definition of intradialytic hypotension. Kidney Disease Outcomes Quality Initiative (KDOQI) and European Best Practice Guidelines define intradialytic hypotension as the presence of a decrease in systolic blood pressure ≥20 mmHg or a decrease in mean arterial pressure by 10 mmHg, provided that the decrease in blood pressure is associated with clinical events and need for nursing interventions [1]. An observational study examined the association between various definitions of intradialytic hypotension and mortality and found only the intradialytic hypotension definition of a nadir intradialytic systolic blood pressure <90 mmHg in 30 percent of treatments to associate with higher mortality [2].

EPIDEMIOLOGY AND RISK FACTORS — Hypotension during (or immediately following) hemodialysis complicates 5 to 30 percent of all dialysis treatments, depending on the definition used [3-5]. In one study that included 44,801 dialysis treatments in 1137 patients, 75 percent of patients had at least one episode of intradialytic hypotension [3]. In some patients, more than 50 percent of treatments are complicated by intradialytic hypotension [6].

Demographic risk factors that have been associated with intradialytic hypotension include older age, longer dialysis vintage, diabetes, lower predialysis blood pressure, lower albumin, female sex, Hispanic ethnicity, and higher body mass index [3]. The odds of hypotension occurrence decrease throughout dialysis sessions of the week [7].

ETIOLOGY

Overview — Occasionally, patients with dialysis-induced hypotension have serious medical conditions requiring immediate attention. These conditions include systemic infection, arrhythmias, pericardial tamponade, valvular disorders, myocardial infarction, hemolysis, hemorrhage, air embolism, and a reaction to the dialyzer membrane or machine tubing [4,8,9]. It is important to recognize such conditions. (See 'Acute management' below and "Acute complications during hemodialysis" and "Reactions to the hemodialysis membrane".)

More commonly, intradialytic hypotension occurs in the absence of serious medical conditions. Major factors that contribute to intradialytic hypotension include rapid or excessive ultrafiltration, a rapid reduction in plasma osmolality, incorrectly low prescribed target weight, autonomic neuropathy, and diminished cardiac reserve (figure 1 and figure 2) [3,4,10-12].

Other contributors to intradialytic hypotension include the intake of antihypertensive medications or the ingestion of a meal immediately before or during dialysis.

The composition and temperature of the dialysate fluid may contribute to intradialytic hypotension. Hypotension has been associated with the use of dialysate acetate, low sodium, high magnesium, and low calcium [9,13,14]. Dialysate temperature that is higher than body temperature has also been associated with hypotension.

Other suggested contributors include the release of adenosine during organ ischemia, the increased synthesis of endogenous vasodilators (such as nitric oxide), and inappropriately low plasma vasopressin levels [9,15-20].

Major factors are discussed below.

Ultrafiltration, erroneous target weight, and reduction in osmolality — Intradialytic hypotension commonly occurs when the ultrafiltration rate (ie, the rate at which fluid is removed) is high. In this setting, hypotension results from intravascular volume depletion beyond the level at which blood pressure can be sustained by hemodynamic compensatory mechanisms. Intravascular volume depletion may occur when the rate of fluid removal by ultrafiltration (which is from the vascular space) is significantly faster than the rate of refill of the intravascular space from the interstitial space.

Rapid ultrafiltration may be performed to attain the prescribed target weight (frequently called "dry weight," which is a poorly defined and controversial term) within the prescribed duration of the dialysis session, which is typically three to five hours. This cause of intradialytic hypotension is especially common among patients who have large interdialytic weight gains [21,22].

Even in the absence of large interdialytic weight gain, excessive ultrafiltration may be performed to attain an inappropriately low prescribed target weight. This is generally due to the inaccurate determination of fluid status [23].

A rapid reduction in plasma osmolality during hemodialysis may also contribute to intravascular volume depletion. The reduction in plasma osmolality causes extracellular water to move into the cells, which decreases the extracellular volume (figure 3). In one study, higher calculated predialysis serum osmolarity, largely due to increased urea or glucose, but not to increased sodium, was associated with an increased risk of intradialytic hypotension [24]. (See "Kidney replacement therapy (dialysis) in acute kidney injury: Metabolic and hemodynamic considerations".)

Autonomic dysfunction — Autonomic dysfunction (dysautonomia) occurs in over 50 percent of patients on maintenance dialysis [25]. Patients with longstanding diabetes mellitus are at particularly elevated risk for autonomic neuropathy [25].

Autonomic dysfunction impairs the ability to mount a sufficient sympathetic response to maintain the systemic blood pressure during ultrafiltration. Normally (ie, in healthy individuals), a decline in blood volume leads to a decline in blood pressure, activation of the baroreceptors, and a subsequent increase in efferent sympathetic activity [26]. The ensuing rise in systemic vascular resistance and cardiac output minimizes the reduction in blood pressure.

These homeostatic responses do not occur appropriately in patients with autonomic dysfunction [27-31]. Mechanisms that prevent the homeostatic responses include:

Downregulation of alpha-adrenergic receptors, which diminishes the hemodynamic response to endogenous catecholamines [29]

Endothelial dysfunction, which impairs sympathetic activity, decreases the reuptake of norepinephrine [32], and enhances inflammatory responses that further augment autonomic dysfunction [33,34]

A paradoxical decrease in sympathetic and increased parasympathetic nervous system activity during ultrafiltration [30,31]

Decreased cardiac reserve — The risk of intradialytic hypotension is greatly increased in patients with a prior history of heart failure, cardiomegaly, or ischemic heart disease [35]. These conditions lead to poor left ventricular performance and a diminished cardiac reserve in the setting of a hemodynamic challenge. The role of diminished cardiac reserve is suggested by a study in which dobutamine stress echocardiography was performed among 18 patients with dialysis instability and 18 without such instability [36]. The baseline cardiac index was similar in the two groups. However, cardiac reserve, as determined by the increase in cardiac index with dobutamine, was significantly lower among patients who were prone to hypotension during dialysis. Another study indicated that patients prone to intradialytic hypotension had low cardiac index and increased vascular peripheral resistance in the first 30 minutes on hemodialysis [37]. (See "Overview of screening and diagnosis of heart disease in patients on dialysis".)

CLINICAL PRESENTATION — Although occasionally asymptomatic, patients with hypotension usually have lightheadedness, muscle cramps, nausea, vomiting, and dyspnea. Vagal symptoms, including yawning, sighing, and hoarseness, may be observed before the drop in blood pressure is detected [4].

ACUTE MANAGEMENT — The acute management of intradialytic hypotension includes the following:

Ultrafiltration rate should be decreased or stopped, depending upon the severity of hypotension.

The patient should be placed in the Trendelenburg position, where the body is laid flat on the back (supine position), with the feet higher than the head by 15 to 30 degrees.

Intravascular volume should be replaced in cases when blood pressure is not restored after stopping ultrafiltration and repositioning the patient. We give an intravenous fluid bolus of 250 to 500 mL. Intravenous fluid is effective in restoring blood pressure [38,39]. The optimal replacement fluid is not known. Common replacement fluids include isotonic saline, hypertonic glucose, 5 percent dextrose, or albumin solutions. Most clinicians use isotonic saline as first-line therapy for hypotension since saline is effective, inexpensive, and widely available [38,40]. A randomized, controlled trial has suggested that isotonic saline and albumin are comparable in restoration of blood pressure [38], although a small trial has suggested that hypertonic glucose (20 percent) may have the most pronounced effects on blood volume [39].

Oxygen should be administered. There is evidence that intradialytic blood oxygen saturation and its variability are associated with intradialytic hypotension [41,42]. A decrease in central venous oxygen saturation most likely indicates a decline in cardiac output (figure 4).

Patients with persistent hypotension despite measures above should be evaluated for evidence of an underlying serious cause. This assessment primarily includes a physical examination, including auscultation of heart and lungs, palpation of the abdomen, and examination of the hemodialysis access for evidence of infection [4,43]. An electrocardiogram should be performed. Particular concerns include occult sepsis, previously unrecognized cardiac and/or pericardial disease, and gastrointestinal bleeding [43].

Rare, serious causes of hypotension on dialysis include hemolysis, reaction to dialyzer, or air embolus. Hemolysis may be suggested by the simultaneous occurrence of symptoms in multiple patients and occasionally port-wine appearance of blood in the venous line. Air embolus may be accompanied by distinctive clinical findings, including characteristic heart sounds. (See "Air embolism", section on 'Clinical features'.)

Reactions to the dialyzer or machine tubing may be manifested by chest and back pain and by signs of allergic reaction (urticaria, flushing, coughing, sneezing), in addition to hypotension. (See "Reactions to the hemodialysis membrane", section on 'Type A reactions' and "Reactions to the hemodialysis membrane", section on 'Type B reactions'.)

Hypotension that does not respond to saline bolus or is accompanied by symptoms such as fever, chills, chest and/or abdominal pain, or dyspnea suggests a serious cause. Such patients are generally referred to a hospital for more extensive evaluation.

Once serious causes have been excluded, further evaluation is directed to the prevention of future episodes. (See 'Prevention of recurrent episodes' below.)

PREVENTION OF RECURRENT EPISODES — Patients who have recurrent episodes of intradialytic hypotension should be carefully evaluated and preventive strategies put in place. We use a stepped approach that starts with simple interventions. Subsequent evaluation and intervention depend upon patient response to initial measures. This approach is approximately similar to that suggested by the European Best Practices Guideline [1].

First-line approach — The first-line approach includes reassessing the target weight, avoiding food intake during dialysis, withholding antihypertensive agents prior to dialysis, and limiting interdialytic sodium intake to reduce ultrafiltration requirements.

Reassess target weight – We reassess the prescription target weight. The optimal target weight is often determined empirically by trial and error ("probing"). Using a trial-and-error approach, the target weight is set just above the weight at which unacceptable symptoms, such as cramping, nausea, and vomiting, or hypotension occur. Future episodes of intradialytic hypotension may be prevented in some patients by increasing the target weight. The target weight is highly variable in many patients and can fluctuate with intercurrent illnesses (such as diarrhea or infection).

A large number of modalities other than the clinical examination have been evaluated in an effort to more objectively estimate target weight [21,44-47]. These include blood volume monitoring, ultrasound assessment of the inferior vena cava or lungs, natriuretic peptide measurements, extravascular lung water indices, and bioimpedance methods [47].

Among patients with intradialytic hypotension, it is reasonable to use blood volume monitoring, lung ultrasound, and bioimpedance when these technologies are available. The best studies have favored methods that use bioimpedance measurements of extracellular and total body water [48-51]. A randomized, controlled trial including 126 patients indicated that fluid management with bioimpedance spectroscopy improved blood pressure control, left ventricular mass, and pulse wave velocity [51].

Automatic regulation of the ultrafiltration rate combined with adjustment of dialysate sodium based upon sensor-detected changes in relative blood volume may decrease hypotension [52]. In a multicenter, randomized, controlled trial that included 36 hypotension-prone hemodialysis patients, the use of blood volume monitoring to adjust the ultrafiltration rate and the dialysate sodium resulted in a 30 percent reduction in intradialytic hypotension [53]. However, this technology is not widely available.

Feedback regulation of the ultrafiltration rate without adjustment of the dialysate sodium may not be as effective in reducing intradialytic hypotension. This was shown in a randomized crossover trial that included 26 hemodialysis patients with recurrent intradialytic hypotension [54]. The target weight was established by clinical exam during a four-week run-in period. Patients were then assigned to an intervention group (best practice plus blood volume-guided ultrafiltration) or control (best practice alone). After eight weeks and a two-week wash-out phase, participants crossed over for a second eight-week phase.

There was no difference between groups in the rate of symptomatic intradialytic hypotension (0.1/hour in the intervention group versus 0.07/hour in the control group) or in the proportion of sessions with episodes of asymptomatic hypotension or in symptoms alone.

Avoid food during dialysis – We ask patients who are prone to intradialytic hypotension to avoid food during dialysis. Peripheral vascular resistance generally drops 20 to 120 minutes after the ingestion of food, which may cause a decrease in blood pressure [4,16,55-57].

Withhold antihypertensive agents – Patients who are prone to intradialytic hypotension should withhold antihypertensive agents prior to dialysis. Among such patients, we avoid prescribing blood pressure medications that need to be taken twice (or more) daily. Whenever possible, we prefer medications that can be given once daily and then ask patients to take the dose at night.

Limit interdialytic sodium intake – We ask patients who are prone to intradialytic hypotension to limit sodium (salt) intake, which results in a reduction in fluid intake. Sodium intake in between dialysis sessions directly correlates with the amount of volume that needs to be removed during each dialysis session. Excessive sodium intake results in thirst and larger extracellular volume gain that must be removed by ultrafiltration. Since the dialysis time for each session is generally fixed, the ultrafiltration rate must be increased to attain target weight by the end of the individual session. The optimal sodium intake is not known. We generally ask patients to limit sodium intake to 1 to 2 grams per day; this amount of sodium is equivalent to 2.5 and 5 grams of salt, respectively, or roughly one-half and one teaspoon of salt, respectively.

Review dialysate composition – We generally make sure that dialysate calcium and magnesium are ≥2.25 mEq/L and ≥1.0 mEq/L, respectively. Low-dialysate calcium and magnesium have been associated with intradialytic hypotension. (See 'Etiology' above.)

We also assess the dialysate sodium concentration. Sodium balance, thirst, and interdialytic weight gain are influenced by dialysate sodium. While lower dialysate sodium concentrations are associated with lower interdialytic weight gains and ambulatory blood pressures, some studies suggest that they are also associated with a greater risk of intradialytic hypotension [58-61]. However, we do not use a high fixed-dialysate sodium concentration (ie, >140 mEq/L) or sodium modeling (which is a method whereby the sodium concentration is set high at the beginning of the dialysis session and gradually decreased during the session), as higher concentrations of dialysate sodium (fixed or modeled) have been associated with higher weight gain and blood pressure in both controlled and observational studies [62-67]. Clinicians who choose to use modestly increased dialysate sodium (eg, 140 to 143 mEq/L) or sodium-modeling programs for selected patients with intradialytic hypotension must be aware of the counterproductive risk of increased interdialytic weight gain.

Acetate is also associated with hypotension [68] (see 'Etiology' above). Since acetate dialysis has been replaced by bicarbonate dialysis in most facilities, this issue has been largely solved.

Increase urine output – Among patients with residual urine output, we attempt to augment urine output with oral diuretic administration. Use of loop diuretics has been associated with lower interdialytic weight gain and lower rates of intradialytic hypotension among hemodialysis patients [69-71].

Second-line approach — The second-line approach includes a cardiac evaluation, the use of cool dialysate, and an increase in dialysis time and/or frequency.

Assess primary cardiac factors – We perform a careful assessment for primary cardiac factors that may promote the development of intradialytic hypotension. As noted above, the risk of intradialytic hypotension is increased in patients with heart failure, cardiomegaly, or ischemic heart disease [35] (see "Overview of screening and diagnosis of heart disease in patients on dialysis", section on 'Screening and diagnosis of heart disease'). A pericardial effusion should be excluded with an echocardiogram. (See "Pericardial effusion: Approach to diagnosis", section on 'Cardiac imaging'.)

Use of cool dialysate – If primary cardiac factors are not present on evaluation, we use cool-temperature dialysis. Cool-temperature dialysis may increase hemodynamic stability [72-88].

There are two ways to perform cool-temperature hemodialysis:

Empiric fixed reductions of dialysate temperature

Isothermic dialysis

If employing a fixed reduction, we reduce the dialysate temperature to 0.5 to 1°C below the patient’s body temperature (as monitored by tympanic thermometer). This may lower the body temperature up to approximately 1°C. This change is generally well tolerated, although some patients develop unacceptable side effects such as chilling or cramping [89].

In isothermic dialysis, the increase in body core temperature (which normally occurs during hemodialysis [90]) is sensed by a feedback temperature-controlled device that cools the dialysate temperature [89]. This prevents further increases in the patient’s core temperature.

The benefit of cool-temperature dialysis was assessed in a 2016 systematic review of 26 trials with a total of 484 patients [86]. Eleven of these trials (120 patients, total of 552 hemodialysis sessions, average 4.6 sessions per patient) provided sufficient information to allow calculation of the pooled effect. This analysis showed that, compared with standard dialysis, cool-temperature dialysate reduced the risk of intradialytic hypotension by 68 percent (95% CI 44-82 percent). Analysis of nine trials (2548 dialysis sessions) showed that uncomfortable symptoms on dialysis (including feeling cold, shivering, or cramps) were 2.95 times more common with cool-temperature dialysis (95% CI 0.88-9.82). Cool-temperature dialysis had no effect on dialysis adequacy or overall quality of life as assessed by the 36-question health survey assessment form.

A 2019 Cochrane review of 25 studies (712 participants) yielded similar findings that reduction of dialysate temperature improved intradialytic hypotension rates but appeared to increase patient discomfort [91]. However, the quality of the data was rated as weak, and most studies were determined to be of unclear or high-risk bias. In a subsequent pragmatic cluster-randomized trial with a median follow-up of 1.8 years, 8000 patients dialyzed in 42 outpatient hemodialysis units with cooler dialysate (0.5 to 0.9°C below predialysis body temperature; mean dialysate temperature 35.8°C) were compared with approximately 7400 patients dialyzed in 42 outpatient hemodialysis units with a standard dialysate temperature of 36.5°C [92]. The composite outcome of cardiovascular mortality and hospitalization for cardiovascular events was similar in the cooler and standard dialysate groups (21.4 and 22.4 percent, respectively), as was the mean decrease in intradialytic systolic blood pressure (26.6 and 27.1 mmHg, respectively), though blood pressure data only were analyzed for approximately 1 percent of dialysis treatments. The standard dialysis temperature in this trial was cooler than the 37°C used as a control group in many prior studies of cool dialysate, and the trial did not compare cooler with standard dialysate in subgroups of patients with frequent intradialytic hypotension. In a substudy of the trial, patients in the cooler dialysate group were more likely to report feeling uncomfortably cold during dialysis compared with patients in the standard dialysate group.  

Overall, data do not show a clear benefit of cool-temperature dialysate for all patients. However, it is possible that cool-temperature dialysis in selected patients may reduce hemodynamic instability without any negative effect on dialysis adequacy but with an increase in feeling uncomfortably cold during dialysis.

The mechanisms by which cool-temperature dialysis may improve vascular stability are not completely understood. Both increased systemic vascular resistance and enhanced cardiac contractility have been observed, changes that may be mediated at least in part by cold-induced activation of the sympathetic nervous system and decreased silent ischemia [52,53,78,89,93-97].

The 2005 Kidney Disease Outcomes Quality Initiative (KDOQI) guidelines and 2007 European Best Practice Guidelines in hemodialysis recommend the use of cool-dialysate temperature dialysis in patients with frequent episodes of intradialytic hypotension [98,99]. These guidelines also suggested that dialysate temperatures below 35°C should not be used. The 2019 United Kingdom Renal Association Clinical Practice Guidelines recommend a dialysate temperature no greater than 36°C.

Increasing dialysis time – If the above measures fail to sufficiently decrease the frequency of intradialytic hypotension, we increase the dialysis time. This may be done by increasing the time per session or by adding an additional treatment per week. Increasing the time and/or frequency of hemodialysis may be effective in preventing or reducing intradialytic hypotension [99].

Third-line approach — If other treatment options fail to prevent intradialytic hypotension, we use a third-line approach, which includes giving midodrine and/or switching the patient to other forms of dialysis.

Midodrine – If all other measures fail to decrease the frequency of intradialytic hypotension, we use the selective alpha-1 adrenergic agonist, midodrine. Among patients with autonomic neuropathy and possibly other patients with severe hemodialysis hypotension not responsive to the above measures, midodrine may be effective and well tolerated [80,100-104]. The optimal dose is not known with certainty. We generally give 2.5 to 5 mg, 15 to 30 minutes prior to dialysis. In cases where hypotension occurs later in the hemodialysis treatment, we utilize split dosing, with an initial dose given 30 minutes prior to dialysis and a second dose given halfway through treatment (at least three hours after the first dose).

Studies that have evaluated the use of midodrine for treatment of intradialytic hypotension have yielded mixed results. A 2004 systematic review of 10 studies representing a total of 117 patients found that the use of midodrine, compared with controls, was associated with increases in the postdialysis systolic and diastolic blood pressure (of 12.4 and 7.3 mmHg, respectively) [103]. The nadir systolic and diastolic blood pressures were also higher with midodrine (by 13.3 and 5.9 mmHg, respectively). However, these data did not examine any hard clinical outcomes such as cardiovascular events or death. A 2018 retrospective study compared clinical and hemodynamic outcomes between adult, in-center hemodialysis patients who were prescribed midodrine (n = 1046) and matched controls who did not receive midodrine (n = 2037) [105]. Compared with nonuse, midodrine use was associated with higher rates of death (adjusted incidence rate ratio 1.37, 95% CI 1.15-1.62), all-cause hospitalization (1.31, 95% CI 1.19-1.43), and cardiovascular hospitalization (1.41, 95% CI 1.17-1.71). Midodrine use tended to be associated with lower predialysis systolic blood pressure, lower nadir systolic blood pressure, greater fall in systolic blood pressure during dialysis, and a greater proportion of treatments affected by intradialytic hypotension. While these findings question the clinical benefit of midodrine, this study was limited by its observational nature and potential for residual confounding.

The major side effects of midodrine include piloerection, urinary retention, supine hypertension (which can be relieved by elevating the head of the bed), paresthesia, and pruritus [100,103,104].

Change to other modes of dialysis – Changing from standard, thrice-weekly, in-center hemodialysis to other modes of dialysis, such as peritoneal dialysis, daily dialysis, hemodiafiltration (HDF; if available), or nocturnal hemodialysis, may be an option for patients who have chronic, debilitating intradialytic hypotension. HDF may mitigate intradialytic hypotension. A meta-analysis including five trials with 1259 patients and an average follow-up of 24 months showed that HDF reduced symptomatic hypotension (relative risk [RR] 0.49, 95% CI 0.28-0.86) [106] (see "Chronic intermittent high-volume hemodiafiltration", section on 'Outcomes'). The gradual volume changes associated with peritoneal dialysis or nocturnal hemodialysis may be better tolerated among such patients [99,107]. (See "Technical aspects of nocturnal hemodialysis".)

Other treatments — In addition to the measures listed above, the correction of anemia to target levels with erythropoiesis-stimulating agents may decrease the frequency of intradialytic hypotension by improving cardiac function. This is discussed elsewhere. (See "Cardiovascular and renal effects of anemia in chronic kidney disease", section on 'Effect of treatment of anemia on heart failure'.)

Methods that have or are being studied, but have not been conclusively shown to be beneficial, include combination sodium and ultrafiltration modeling [108] and the administration of sertraline [109], vasopressin [110], an adenosine receptor antagonist [110], and carnitine [111,112].

OUTCOMES — Patients with intradialytic hypotension have increased morbidity and mortality [2,113-117].

Dialysis treatment is less effective when complicated by hypotension since treatments may be stopped early, and the target weight may not be achieved. Moreover, some patients require administration of saline prior to leaving the dialysis unit.

With severe intradialytic hypotension, bowel ischemia, stroke, loss of white matter, or myocardial infarction may occur [4,118]. Recurrent regional ischemia could lead to increased endotoxin translocation from the gut [119]. The frequency with which these events occur as a result of intradialytic hypotension is not known.

Patients with frequent intradialytic hypotension are at increased risk of fistula thrombosis [114]. This was shown in a secondary analysis of the HEMO study in which 1426 subjects were stratified by the percentage of dialysis treatments that were complicated by hypotensive episodes requiring saline infusion or reduction of either the ultrafiltration rate or blood flow. At three years of follow-up, there were 2005 episodes of vascular thrombosis. As has been shown before, the overall rate of thrombosis was much higher among patients with grafts compared with fistulas (see "Approach to the adult patient needing vascular access for chronic hemodialysis"). However, among patients with fistulas, the risk of thrombosis was doubled among those who had more than 30 percent of dialysis treatments complicated by hypotension compared with those who had stable treatments (relative risk [RR] 2.02, 95% CI 1.22-3.35). This association was not observed for patients who had prosthetic arteriovenous grafts. This study also demonstrated a correlation of both fistula and graft thrombosis with lower pre- and postdialysis blood pressures. These data and the primary results of the HEMO trial are discussed elsewhere. (See "Prescribing and assessing adequate hemodialysis", section on 'Target Kt/V'.)

Intradialytic hypotension has been associated with increased mortality [2,113-117]. In one study of 631,922 patients, high versus low variability in intradialytic systolic blood pressure was associated with increased all-cause mortality (adjusted hazard ratio [HR] 1.26, 95% CI 1.08-1.47) [116]. The timing of intradialytic hypotension in a given hemodialysis session may be relevant to mortality risk. In one study of 3000 patients, patients with intradialytic hypotension in the first half of the hemodialysis session had poorer survival than patients with intradialytic hypotension in the second half of the session (all-cause mortality HR 1.4, 95% CI 1.2-1.7 and cardiovascular mortality HR 1.6, 95% CI 1.2-2.2) [120].

High ultrafiltration rates (defined as an ultrafiltration volume >5.7 percent of postdialysis weight [121] or >13 mL/hour/kg [122,123]) have also been associated with increased cardiovascular mortality risk in hemodialysis patients [121-123]. Additional observational studies suggest that the ultrafiltration rate-related mortality risk may begin at rates as low as 6 mL/hour/kg [124,125]. (See "Evaluation of sudden cardiac arrest and sudden cardiac death in patients on dialysis" and "Patient survival and maintenance dialysis", section on 'Control of fluid balance and hypertension'.)

Based on these studies, many dialysis units are now prescribing ultrafiltration rates of no greater than 13 mL/hour/kg. This practice will likely complicate the treatment of patients who gain excessive fluid between treatments but may result in fewer episodes of intradialytic hypotension. Additional prospective, randomized studies of the association of ultrafiltration rate with cardiovascular mortality are needed.

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".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Beyond the Basics topics (see "Patient education: Dialysis or kidney transplantation — which is right for me? (Beyond the Basics)" and "Patient education: Hemodialysis (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

Symptomatic hypotension during (or immediately following) hemodialysis complicates 5 to 30 percent of all dialysis treatments and is associated with increased morbidity and mortality. Demographic risk factors that have been associated with intradialytic hypotension include older age, longer dialysis vintage, diabetes, lower predialysis blood pressure, low albumin, female sex, Hispanic ethnicity, and higher body mass index. (See 'Epidemiology and risk factors' above and 'Outcomes' above.)

Common causes of intradialytic hypotension include rapid or excessive ultrafiltration, rapid reduction in plasma osmolality, incorrectly low prescribed target weight, autonomic neuropathy, and diminished cardiac reserve. Other contributors to intradialytic hypotension include the intake of antihypertensive medications or the ingestion of a meal immediately before or during dialysis. Occasionally, patients with dialysis-induced hypotension have serious medical conditions requiring immediate attention. These conditions include systemic infection, arrhythmias, pericardial tamponade, valvular disorders, myocardial infarction, hemolysis, hemorrhage, air embolism, and a reaction to the dialyzer membrane or machine tubing. (See 'Etiology' above.)

Intradialytic hypotension can be asymptomatic, but patients usually have lightheadedness, muscle cramps, nausea, vomiting, and dyspnea. Vagal symptoms, including yawning, sighing, and hoarseness, may be observed before the drop in blood pressure is detected. (See 'Clinical presentation' above.)

Ultrafiltration should be stopped in patients who become hypotensive during dialysis. Initial management includes placing the patient in the Trendelenburg position, administering oxygen, and, if blood pressure is unresponsive to these measures, giving a bolus of intravenous fluid. We give isotonic saline since it is effective, inexpensive, and widely available. A bolus of 250 to 500 mL is usually effective in restoring blood pressure. Patients should be simultaneously evaluated for serious causes of hypotension. (See 'Acute management' above.)

Patients with recurrent intradialytic hypotension should be carefully evaluated and preventive strategies initiated. Our stepped approach starts with simple interventions. Further evaluation and intervention depends upon patient response to initial measures (see 'Prevention of recurrent episodes' above):

First-line approach (see 'First-line approach' above):

-Reassess and, if necessary, increase the target weight.

-Ask patient to avoid food intake during dialysis.

-Modify timing of antihypertensive agents to avoid intake prior to dialysis.

-Ask patient to limit interdialytic sodium (salt) intake.

-Make sure dialysate calcium and magnesium are ≥2.25 mEq/L and ≥1.0 mEq/L, respectively, and reassess the dialysate sodium prescription.

Second-line approach (see 'Second-line approach' above):

-Evaluate cardiac function.

-Use cool-temperature dialysate.

-Increase the dialysis treatment time.

Third-line approach (see 'Third-line approach' above):

-For patients who continue to have intradialytic hypotension despite the measures listed above, we suggest using midodrine (Grade 2C). We generally give 2.5 to 5 mg 15 to 30 minutes prior to dialysis. The major side effects of midodrine include piloerection, urinary retention, supine hypertension (which can be relieved by elevating the head of the bed), paresthesia, and pruritus. (See 'Third-line approach' above.)

-Change to other modes of dialysis, such as hemodiafiltration or peritoneal dialysis.

In addition to the measures listed above, the correction of anemia to target levels with erythropoiesis-stimulating agents may decrease the frequency of intradialytic hypotension by improving cardiac function. (See 'Other treatments' above.)

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Peter Kotanko, MD and William Henrich, MD, MACP, who contributed to earlier versions of this topic review.

  1. Kooman J, Basci A, Pizzarelli F, et al. EBPG guideline on haemodynamic instability. Nephrol Dial Transplant 2007; 22 Suppl 2:ii22.
  2. Flythe JE, Xue H, Lynch KE, et al. Association of mortality risk with various definitions of intradialytic hypotension. J Am Soc Nephrol 2015; 26:724.
  3. Sands JJ, Usvyat LA, Sullivan T, et al. Intradialytic hypotension: frequency, sources of variation and correlation with clinical outcome. Hemodial Int 2014; 18:415.
  4. Reilly RF. Attending rounds: A patient with intradialytic hypotension. Clin J Am Soc Nephrol 2014; 9:798.
  5. Assimon MM, Flythe JE. Definitions of intradialytic hypotension. Semin Dial 2017; 30:464.
  6. Santos SF, Peixoto AJ, Perazella MA. How should we manage adverse intradialytic blood pressure changes? Adv Chronic Kidney Dis 2012; 19:158.
  7. Rocha A, Sousa C, Teles P, et al. Effect of Dialysis Day on Intradialytic Hypotension Risk. Kidney Blood Press Res 2016; 41:168.
  8. Masani NN, Miyawaki N, Maesaka JK. A patient with an uncommon etiology of intradialytic hypotension. Semin Dial 2005; 18:435.
  9. Roy PN, Danziger RS. Dialysate magnesium concentration predicts the occurrence of intradialytic hypotension (abstract). J Am Soc Nephrol 1996; 7:1496.
  10. Henrich WL. Hemodynamic instability during hemodialysis. Kidney Int 1986; 30:605.
  11. van der Sande FM, Kooman JP, Leunissen KM. Intradialytic hypotension--new concepts on an old problem. Nephrol Dial Transplant 2000; 15:1746.
  12. Flythe JE, Kunaparaju S, Dinesh K, et al. Factors associated with intradialytic systolic blood pressure variability. Am J Kidney Dis 2012; 59:409.
  13. van der Sande FM, Cheriex EC, van Kuijk WH, Leunissen KM. Effect of dialysate calcium concentrations on intradialytic blood pressure course in cardiac-compromised patients. Am J Kidney Dis 1998; 32:125.
  14. Alappan R, Cruz D, Abu-Alfa AK, et al. Treatment of Severe Intradialytic Hypotension With the Addition of High Dialysate Calcium Concentration to Midodrine and/or Cool Dialysate. Am J Kidney Dis 2001; 37:294.
  15. Shinzato T, Miwa M, Nakai S, et al. Role of adenosine in dialysis-induced hypotension. J Am Soc Nephrol 1994; 4:1987.
  16. Barakat MM, Nawab ZM, Yu AW, et al. Hemodynamic effects of intradialytic food ingestion and the effects of caffeine. J Am Soc Nephrol 1993; 3:1813.
  17. Noris M, Benigni A, Boccardo P, et al. Enhanced nitric oxide synthesis in uremia: implications for platelet dysfunction and dialysis hypotension. Kidney Int 1993; 44:445.
  18. Yokokawa K, Mankus R, Saklayen MG, et al. Increased nitric oxide production in patients with hypotension during hemodialysis. Ann Intern Med 1995; 123:35.
  19. van der Zee S, Thompson A, Zimmerman R, et al. Vasopressin administration facilitates fluid removal during hemodialysis. Kidney Int 2007; 71:318.
  20. Ettema EM, Zittema D, Kuipers J, et al. Dialysis hypotension: a role for inadequate increase in arginine vasopressin levels? A systematic literature review and meta-analysis. Am J Nephrol 2014; 39:100.
  21. Kouw PM, Kooman JP, Cheriex EC, et al. Assessment of postdialysis dry weight: a comparison of techniques. J Am Soc Nephrol 1993; 4:98.
  22. Bégin V, Déziel C, Madore F. Biofeedback regulation of ultrafiltration and dialysate conductivity for the prevention of hypotension during hemodialysis. ASAIO J 2002; 48:312.
  23. Brennan JM, Ronan A, Goonewardena S, et al. Handcarried ultrasound measurement of the inferior vena cava for assessment of intravascular volume status in the outpatient hemodialysis clinic. Clin J Am Soc Nephrol 2006; 1:749.
  24. Mc Causland FR, Waikar SS. Association of Predialysis Calculated Plasma Osmolarity With Intradialytic Blood Pressure Decline. Am J Kidney Dis 2015; 66:499.
  25. Ewing DJ, Winney R. Autonomic function in patients with chronic renal failure on intermittent haemodialysis. Nephron 1975; 15:424.
  26. Kong CH, Thompson FD. Hemodynamic responses to head-up tilt in uremic patients. Clin Nephrol 1990; 33:283.
  27. Lilley JJ, Golden J, Stone RA. Adrenergic regulation of blood pressure in chronic renal failure. J Clin Invest 1976; 57:1190.
  28. Friess U, Rascher W, Ritz E, Gross P. Failure of arginine-vasopressin and other pressor hormones to increase in severe recurrent dialysis hypotension. Nephrol Dial Transplant 1995; 10:1421.
  29. Daul AE, Wang XL, Michel MC, Brodde OE. Arterial hypotension in chronic hemodialyzed patients. Kidney Int 1987; 32:728.
  30. Converse RL Jr, Jacobsen TN, Jost CM, et al. Paradoxical withdrawal of reflex vasoconstriction as a cause of hemodialysis-induced hypotension. J Clin Invest 1992; 90:1657.
  31. Barnas MG, Boer WH, Koomans HA. Hemodynamic patterns and spectral analysis of heart rate variability during dialysis hypotension. J Am Soc Nephrol 1999; 10:2577.
  32. Sobey CG, Sozzi V, Woodman OL. Ischaemia/reperfusion enhances phenylephrine-induced contraction of rabbit aorta due to impairment of neuronal uptake. J Cardiovasc Pharmacol 1994; 23:562.
  33. Kishi T. Regulation of the sympathetic nervous system by nitric oxide and oxidative stress in the rostral ventrolateral medulla: 2012 Academic Conference Award from the Japanese Society of Hypertension. Hypertens Res 2013; 36:845.
  34. Conti FF, Brito Jde O, Bernardes N, et al. Cardiovascular autonomic dysfunction and oxidative stress induced by fructose overload in an experimental model of hypertension and menopause. BMC Cardiovasc Disord 2014; 14:185.
  35. Nette RW, van den Dorpel MA, Krepel HP, et al. Hypotension during hemodialysis results from an impairment of arteriolar tone and left ventricular function. Clin Nephrol 2005; 63:276.
  36. Poldermans D, Man in 't Veld AJ, Rambaldi R, et al. Cardiac evaluation in hypotension-prone and hypotension-resistant hemodialysis patients. Kidney Int 1999; 56:1905.
  37. Kolb J, Kitzler TM, Tauber T, et al. Proto-dialytic cardiac function relates to intra-dialytic morbid events. Nephrol Dial Transplant 2011; 26:1645.
  38. Knoll GA, Grabowski JA, Dervin GF, O'Rourke K. A randomized, controlled trial of albumin versus saline for the treatment of intradialytic hypotension. J Am Soc Nephrol 2004; 15:487.
  39. Nette RW, Krepel HP, van den Meiracker AH, et al. Specific effect of the infusion of glucose on blood volume during haemodialysis. Nephrol Dial Transplant 2002; 17:1275.
  40. Emili S, Black NA, Paul RV, et al. A protocol-based treatment for intradialytic hypotension in hospitalized hemodialysis patients. Am J Kidney Dis 1999; 33:1107.
  41. Mancini E, Perazzini C, Gesualdo L, et al. Intra-dialytic blood oxygen saturation (SO2): association with dialysis hypotension (the SOGLIA Study). J Nephrol 2016.
  42. Campos I, Chan L, Zhang H, et al. Intradialytic Hypoxemia in Chronic Hemodialysis Patients. Blood Purif 2016; 41:177.
  43. Letteri JM. Symptomatic hypotension during hemodialysis. Semin Dial 1998; 11:253.
  44. Donauer J, Kölblin D, Bek M, et al. Ultrafiltration profiling and measurement of relative blood volume as strategies to reduce hemodialysis-related side effects. Am J Kidney Dis 2000; 36:115.
  45. Déziel C, Bouchard J, Zellweger M, Madore F. Impact of hemocontrol on hypertension, nursing interventions, and quality of life: a randomized, controlled trial. Clin J Am Soc Nephrol 2007; 2:661.
  46. Basile C, Vernaglione L, Di Iorio B, et al. Development and validation of bioimpedance analysis prediction equations for dry weight in hemodialysis patients. Clin J Am Soc Nephrol 2007; 2:675.
  47. Palmer BF, Henrich WL. Recent advances in the prevention and management of intradialytic hypotension. J Am Soc Nephrol 2008; 19:8.
  48. Kraemer M, Rode C, Wizemann V. Detection limit of methods to assess fluid status changes in dialysis patients. Kidney Int 2006; 69:1609.
  49. van de Pol AC, Frenken LA, Moret K, et al. An evaluation of blood volume changes during ultrafiltration pulses and natriuretic peptides in the assessment of dry weight in hemodialysis patients. Hemodial Int 2007; 11:51.
  50. Moissl U, Arias-Guillén M, Wabel P, et al. Bioimpedance-guided fluid management in hemodialysis patients. Clin J Am Soc Nephrol 2013; 8:1575.
  51. Hur E, Usta M, Toz H, et al. Effect of fluid management guided by bioimpedance spectroscopy on cardiovascular parameters in hemodialysis patients: a randomized controlled trial. Am J Kidney Dis 2013; 61:957.
  52. Santoro A, Mancini E, Paolini F, et al. Blood volume regulation during hemodialysis. Am J Kidney Dis 1998; 32:739.
  53. Santoro A, Mancini E, Basile C, et al. Blood volume controlled hemodialysis in hypotension-prone patients: a randomized, multicenter controlled trial. Kidney Int 2002; 62:1034.
  54. Leung KCW, Quinn RR, Ravani P, et al. Randomized Crossover Trial of Blood Volume Monitoring-Guided Ultrafiltration Biofeedback to Reduce Intradialytic Hypotensive Episodes with Hemodialysis. Clin J Am Soc Nephrol 2017; 12:1831.
  55. Sherman RA, Torres F, Cody RP. Postprandial blood pressure changes during hemodialysis. Am J Kidney Dis 1988; 12:37.
  56. Kearney MT, Cowley AJ, Stubbs TA, et al. Depressor action of insulin on skeletal muscle vasculature: a novel mechanism for postprandial hypotension in the elderly. J Am Coll Cardiol 1998; 31:209.
  57. Avci M, Arikan F. The effect of food intake during hemodialysis on blood pressure: A nonrandomized experimental trial. Ther Apher Dial 2023; 27:661.
  58. Aybal Kutlugün A, Erdem Y, Okutucu S, et al. Effects of lowering dialysate sodium on flow-mediated dilatation in patients with chronic kidney disease. Nephrol Dial Transplant 2011; 26:3678.
  59. Mc Causland FR, Brunelli SM, Waikar SS. Dialysate sodium, serum sodium and mortality in maintenance hemodialysis. Nephrol Dial Transplant 2012; 27:1613.
  60. Basile C, Pisano A, Lisi P, et al. High versus low dialysate sodium concentration in chronic haemodialysis patients: a systematic review of 23 studies. Nephrol Dial Transplant 2016; 31:548.
  61. Marshall MR, Vandal AC, de Zoysa JR, et al. Effect of Low-Sodium versus Conventional Sodium Dialysate on Left Ventricular Mass in Home and Self-Care Satellite Facility Hemodialysis Patients: A Randomized Clinical Trial. J Am Soc Nephrol 2020; 31:1078.
  62. de Paula FM, Peixoto AJ, Pinto LV, et al. Clinical consequences of an individualized dialysate sodium prescription in hemodialysis patients. Kidney Int 2004; 66:1232.
  63. Penne EL, Sergeyeva O. Sodium gradient: a tool to individualize dialysate sodium prescription in chronic hemodialysis patients? Blood Purif 2011; 31:86.
  64. Keen ML, Gotch FA. The association of the sodium "setpoint" to interdialytic weight gain and blood pressure in hemodialysis patients. Int J Artif Organs 2007; 30:971.
  65. Sang GL, Kovithavongs C, Ulan R, Kjellstrand CM. Sodium ramping in hemodialysis: a study of beneficial and adverse effects. Am J Kidney Dis 1997; 29:669.
  66. Song JH, Lee SW, Suh CK, Kim MJ. Time-averaged concentration of dialysate sodium relates with sodium load and interdialytic weight gain during sodium-profiling hemodialysis. Am J Kidney Dis 2002; 40:291.
  67. Davenport A, Cox C, Thuraisingham R, PanThames Renal Audit Group. The importance of dialysate sodium concentration in determining interdialytic weight gains in chronic hemodialysis patients: the PanThames Renal Audit. Int J Artif Organs 2008; 31:411.
  68. Jacob AD, Elkins N, Reiss OK, et al. Effects of acetate on energy metabolism and function in the isolated perfused rat heart. Kidney Int 1997; 52:755.
  69. Bragg-Gresham JL, Fissell RB, Mason NA, et al. Diuretic use, residual renal function, and mortality among hemodialysis patients in the Dialysis Outcomes and Practice Pattern Study (DOPPS). Am J Kidney Dis 2007; 49:426.
  70. Sibbel S, Walker AG, Colson C, et al. Association of Continuation of Loop Diuretics at Hemodialysis Initiation with Clinical Outcomes. Clin J Am Soc Nephrol 2019; 14:95.
  71. Tang X, Chen L, Chen W, et al. Effects of diuretics on intradialytic hypotension in maintenance dialysis patients: a systematic review and meta-analysis. Int Urol Nephrol 2021; 53:1911.
  72. Jindal K, Chan CT, Deziel C, et al. Hemodialysis clinical practice guidelines for the Canadian Society of Nephrology. J Am Soc Nephrol 2006; 17:S1.
  73. Maggiore Q, Pizzarelli F, Zoccali C, et al. Effect of extracorporeal blood cooling on dialytic arterial hypotension. Proc Eur Dial Transplant Assoc 1981; 18:597.
  74. Lindholm T, Thysell H, Yamamoto Y, et al. Temperature and vascular stability in hemodialysis. Nephron 1985; 39:130.
  75. Sherman RA, Rubin MP, Cody RP, Eisinger RP. Amelioration of hemodialysis-associated hypotension by the use of cool dialysate. Am J Kidney Dis 1985; 5:124.
  76. Quereda C, Orofino L, Marcen R, et al. Influence of dialysate and membrane biocompatibility on hemodynamic stability in hemodialysis. Int J Artif Organs 1988; 11:259.
  77. Orofino L, Marcén R, Quereda C, et al. Epidemiology of symptomatic hypotension in hemodialysis: is cool dialysate beneficial for all patients? Am J Nephrol 1990; 10:177.
  78. Jost CM, Agarwal R, Khair-el-Din T, et al. Effects of cooler temperature dialysate on hemodynamic stability in "problem" dialysis patients. Kidney Int 1993; 44:606.
  79. Schneditz D, Martin K, Krämer M, et al. Effect of controlled extracorporeal blood cooling on ultrafiltration-induced blood volume changes during hemodialysis. J Am Soc Nephrol 1997; 8:956.
  80. Cruz DN, Mahnensmith RL, Brickel HM, Perazella MA. Midodrine and cool dialysate are effective therapies for symptomatic intradialytic hypotension. Am J Kidney Dis 1999; 33:920.
  81. Yu AW, Ing TS, Zabaneh RI, Daugirdas JT. Effect of dialysate temperature on central hemodynamics and urea kinetics. Kidney Int 1995; 48:237.
  82. Maggiore Q, Pizzarelli F, Santoro A, et al. The effects of control of thermal balance on vascular stability in hemodialysis patients: results of the European randomized clinical trial. Am J Kidney Dis 2002; 40:280.
  83. Schneditz D, Ronco C, Levin N. Temperature control by the blood temperature monitor. Semin Dial 2003; 16:477.
  84. Pérgola PE, Habiba NM, Johnson JM. Body temperature regulation during hemodialysis in long-term patients: is it time to change dialysate temperature prescription? Am J Kidney Dis 2004; 44:155.
  85. Pizzarelli F. From cold dialysis to isothermic dialysis: a twenty-five year voyage. Nephrol Dial Transplant 2007; 22:1007.
  86. Mustafa RA, Bdair F, Akl EA, et al. Effect of Lowering the Dialysate Temperature in Chronic Hemodialysis: A Systematic Review and Meta-Analysis. Clin J Am Soc Nephrol 2016; 11:442.
  87. Zoccali C, Tripepi G, Neri L, et al. Effectiveness of cold HD for the prevention of HD hypotension and mortality in the general HD population. Nephrol Dial Transplant 2023; 38:1700.
  88. Elemshaty A, Sayed-Ahmed N, Mesbah A, Nassar MK. Could cooling dialysate improve inflammatory and nutritional status of hemodialysis patients? BMC Nephrol 2023; 24:255.
  89. Selby NM, McIntyre CW. A systematic review of the clinical effects of reducing dialysate fluid temperature. Nephrol Dial Transplant 2006; 21:1883.
  90. van der Sande FM, Rosales LM, Brener Z, et al. Effect of ultrafiltration on thermal variables, skin temperature, skin blood flow, and energy expenditure during ultrapure hemodialysis. J Am Soc Nephrol 2005; 16:1824.
  91. Tsujimoto Y, Tsujimoto H, Nakata Y, et al. Dialysate temperature reduction for intradialytic hypotension for people with chronic kidney disease requiring haemodialysis. Cochrane Database Syst Rev 2019; 7:CD012598.
  92. MyTEMP writing committee. Personalised cooler dialysate for patients receiving maintenance haemodialysis (MyTEMP): a pragmatic, cluster-randomised trial. Lancet 2022; 400:1693.
  93. Levy FL, Grayburn PA, Foulks CJ, et al. Improved left ventricular contractility with cool temperature hemodialysis. Kidney Int 1992; 41:961.
  94. Coli U, Landini S, Lucatello S, et al. Cold as cardiovascular stabilizing factor in hemodialysis: hemodynamic evaluation. Trans Am Soc Artif Intern Organs 1983; 29:71.
  95. Mahida BH, Dumler F, Zasuwa G, et al. Effect of cooled dialysate on serum catecholamines and blood pressure stability. Trans Am Soc Artif Intern Organs 1983; 29:384.
  96. Selby NM, Burton JO, Chesterton LJ, McIntyre CW. Dialysis-induced regional left ventricular dysfunction is ameliorated by cooling the dialysate. Clin J Am Soc Nephrol 2006; 1:1216.
  97. van der Sande FM, Wystrychowski G, Kooman JP, et al. Control of core temperature and blood pressure stability during hemodialysis. Clin J Am Soc Nephrol 2009; 4:93.
  98. K/DOQI Workgroup. K/DOQI clinical practice guidelines for cardiovascular disease in dialysis patients. Am J Kidney Dis 2005; 45:S1.
  99. Tattersall J, Martin-Malo A, Pedrini L, et al. EBPG guideline on dialysis strategies. Nephrol Dial Transplant 2007; 22 Suppl 2:ii5.
  100. Flynn JJ 3rd, Mitchell MC, Caruso FS, McElligott MA. Midodrine treatment for patients with hemodialysis hypotension. Clin Nephrol 1996; 45:261.
  101. Montagnac R, Clavel P, Delhotal-Landes B, et al. Use of midodrine (Gutron) to treat permanent hypotension in a chronic hemodialysis patient. Clin Nephrol 2001; 56:162.
  102. Perazella MA. Pharmacologic options available to treat symptomatic intradialytic hypotension. Am J Kidney Dis 2001; 38:S26.
  103. Prakash S, Garg AX, Heidenheim AP, House AA. Midodrine appears to be safe and effective for dialysis-induced hypotension: a systematic review. Nephrol Dial Transplant 2004; 19:2553.
  104. Low PA, Gilden JL, Freeman R, et al. Efficacy of midodrine vs placebo in neurogenic orthostatic hypotension. A randomized, double-blind multicenter study. Midodrine Study Group. JAMA 1997; 277:1046.
  105. Brunelli SM, Cohen DE, Marlowe G, Van Wyck D. The Impact of Midodrine on Outcomes in Patients with Intradialytic Hypotension. Am J Nephrol 2018; 48:381.
  106. Wang AY, Ninomiya T, Al-Kahwa A, et al. Effect of hemodiafiltration or hemofiltration compared with hemodialysis on mortality and cardiovascular disease in chronic kidney failure: a systematic review and meta-analysis of randomized trials. Am J Kidney Dis 2014; 63:968.
  107. Merino JL, Rivera M, Teruel JL, et al. CAPD as treatment of chronic debilitating hemodialysis hypotension. Perit Dial Int 2002; 22:429.
  108. Song JH, Park GH, Lee SY, et al. Effect of sodium balance and the combination of ultrafiltration profile during sodium profiling hemodialysis on the maintenance of the quality of dialysis and sodium and fluid balances. J Am Soc Nephrol 2005; 16:237.
  109. Dheenan S, Venkatesan J, Grubb BP, Henrich WL. Effect of sertraline hydrochloride on dialysis hypotension. Am J Kidney Dis 1998; 31:624.
  110. Imai E, Fujii M, Kohno Y, et al. Adenosine A1 receptor antagonist improves intradialytic hypotension. Kidney Int 2006; 69:877.
  111. Lynch KE, Feldman HI, Berlin JA, et al. Effects of L-carnitine on dialysis-related hypotension and muscle cramps: a meta-analysis. Am J Kidney Dis 2008; 52:962.
  112. Ibarra-Sifuentes HR, Del Cueto-Aguilera Á, Gallegos-Arguijo DA, et al. Levocarnitine Decreases Intradialytic Hypotension Episodes: A Randomized Controlled Trial. Ther Apher Dial 2017; 21:459.
  113. Shoji T, Tsubakihara Y, Fujii M, Imai E. Hemodialysis-associated hypotension as an independent risk factor for two-year mortality in hemodialysis patients. Kidney Int 2004; 66:1212.
  114. Chang TI, Paik J, Greene T, et al. Intradialytic hypotension and vascular access thrombosis. J Am Soc Nephrol 2011; 22:1526.
  115. McIntyre CW. Recurrent circulatory stress: the dark side of dialysis. Semin Dial 2010; 23:449.
  116. Flythe JE, Inrig JK, Shafi T, et al. Association of intradialytic blood pressure variability with increased all-cause and cardiovascular mortality in patients treated with long-term hemodialysis. Am J Kidney Dis 2013; 61:966.
  117. Tislér A, Akócsi K, Borbás B, et al. The effect of frequent or occasional dialysis-associated hypotension on survival of patients on maintenance haemodialysis. Nephrol Dial Transplant 2003; 18:2601.
  118. Cedeño S, Desco M, Aleman Y, et al. Intradialytic hypotension and relationship with cognitive function and brain morphometry. Clin Kidney J 2021; 14:1156.
  119. McIntyre CW, Harrison LE, Eldehni MT, et al. Circulating endotoxemia: a novel factor in systemic inflammation and cardiovascular disease in chronic kidney disease. Clin J Am Soc Nephrol 2011; 6:133.
  120. Keane DF, Raimann JG, Zhang H, et al. The time of onset of intradialytic hypotension during a hemodialysis session associates with clinical parameters and mortality. Kidney Int 2021; 99:1408.
  121. Jadoul M, Thumma J, Fuller DS, et al. Modifiable practices associated with sudden death among hemodialysis patients in the Dialysis Outcomes and Practice Patterns Study. Clin J Am Soc Nephrol 2012; 7:765.
  122. Movilli E, Gaggia P, Zubani R, et al. Association between high ultrafiltration rates and mortality in uraemic patients on regular haemodialysis. A 5-year prospective observational multicentre study. Nephrol Dial Transplant 2007; 22:3547.
  123. Flythe JE, Kimmel SE, Brunelli SM. Rapid fluid removal during dialysis is associated with cardiovascular morbidity and mortality. Kidney Int 2011; 79:250.
  124. Assimon MM, Wenger JB, Wang L, Flythe JE. Ultrafiltration Rate and Mortality in Maintenance Hemodialysis Patients. Am J Kidney Dis 2016; 68:911.
  125. Chazot C, Vo-Van C, Lorriaux C, et al. Even a Moderate Fluid Removal Rate during Individualised Haemodialysis Session Times Is Associated with Decreased Patient Survival. Blood Purif 2017; 44:89.
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