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Acute hemodialysis prescription

Author Section Editors Deputy Editor

Thomas A Golper, MD Jeffrey S Berns, MD Albert Q Lam, MD
Paul M Palevsky, MD
Richard H Sterns, MD

Disclosures

All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Dec 2021. | This topic last updated: Oct 07, 2020.
INTRODUCTION — Acute kidney injury (AKI), formerly called acute renal failure (ARF), is a major
cause of morbidity and mortality, particularly in the hospital setting. Despite improvements in kidney
replacement therapy (KRT) during the last several decades, the mortality rate associated with AKI in
critically ill patients remains high. (See "Kidney and patient outcomes after acute kidney injury in
adults".)

Acute KRT is commonly indicated for patients with AKI. Available modalities for acute KRT include
peritoneal dialysis, intermittent hemodialysis and variations of intermittent hemodialysis (such as
hemofiltration and slow equilibrium dialysis [SLED]), and continuous renal replacement therapy (CRRT).

This topic reviews the acute hemodialysis prescription for patients with AKI. The indications for acute
dialysis are discussed elsewhere.

●(See "Kidney replacement therapy (dialysis) in acute kidney injury in adults: Indications, timing, and
dialysis dose", section on 'Urgent indications'.)

Other dialysis modalities are discussed separately.

●(See "Kidney replacement therapy (dialysis) in acute kidney injury in adults: Indications, timing, and
dialysis dose", section on 'Optimal modality'.)

●(See "Continuous kidney replacement therapy in acute kidney injury".)

●(See "Use of peritoneal dialysis (PD) for the treatment of acute kidney injury (AKI) in adults".)

The optimal vascular access for hemodialysis is discussed elsewhere.

●(See "Central catheters for acute and chronic hemodialysis access and their management".)

●(See "Approach to the adult patient needing vascular access for chronic hemodialysis".)

COMPONENTS OF THE ACUTE HEMODIALYSIS PRESCRIPTION — The components of the acute

dialysis prescription include the choice of hemodialysis membrane, dialysis session length, dialysate
composition and temperature, blood flow rate, amount and rate of ultrafiltration (UF), choice of
anticoagulation, and dialysis dose.

Individual components of the prescription vary depending upon the indications for dialysis and on
patient-specific variables.

Hemodialyzer membranes — There are three types of membranes used to manufacture dialyzers:
cellulose, substituted cellulose, and noncellulose synthetic materials. The vast majority of dialyzers
contain synthetic membranes. We use dialyzers with noncellulose synthetic membranes for acute

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hemodialysis. Cellulose membranes and, to a lesser degree, substituted cellulose membranes, are
relatively bioincompatible, which means that they tend to initiate an inflammatory cascade and activate
complement resulting in the generation of the anaphylatoxins C3a and C5a. Synthetic membranes are
more biocompatible than the cellulose membranes and may be associated with fewer infectious
complications and an increased probability of improved restoration of kidney function. (See "Dialysis-
related factors that may influence recovery of kidney function in acute kidney injury (acute renal
failure)", section on 'Characteristics of the dialysis membrane'.)

There are a variety of noncellulose synthetic membranes available including polyacrylonitrile (PAN),
polysulfone, polycarbonate, polyamide, and polymethylmethacrylate (PMMA) membranes. Except for
PAN membranes, all are effective and safe. We do not use PAN membranes (which are not available in
the United States) for acute intermittent hemodialysis, although this membrane is used in some
continuous renal replacement systems. PAN membranes can activate the kallikrein-kinin cascade,
leading to the generation of bradykinin, which is a mediator of pulmonary vasoconstriction, and
systemic hypotension [1]. If patients are being dialyzed with a PAN membrane, they should not receive
angiotensin-converting enzyme (ACE) inhibitors. Anaphylactoid reactions have been described with
concomitant use of ACE inhibitors and PAN membranes [2,3]. Reactions may be related to increased
bradykinin levels. When ACE inhibitors (which are also kinase inhibitors) are used during dialysis with
PAN membranes, bradykinin levels are even further elevated [4,5]. By contrast, angiotensin receptor
blockers are not kinase inhibitors and have not been associated with anaphylaxis with PAN membranes.

ACE inhibitor-associated anaphylactoid reactions are far less common with surface-treated PAN/AN69
membranes but have been reported [6].

The synthetic membranes listed above are high-flux membranes. High-flux membranes have greater
permeability for larger molecules, which may enhance removal of toxins and improve outcome [7].
However, a benefit to high-flux membranes has not been demonstrated by clinical studies. (See
"Dialysis-related factors that may influence recovery of kidney function in acute kidney injury (acute
renal failure)", section on 'Characteristics of the dialysis membrane'.)

Low-flux cellulose dialyzers are either conventional (ie, low efficiency) or high efficiency. If
conventional-efficiency low-flux cellulose dialyzers are used, the dialysis time may need to be increased
beyond that which is commonly recommended. (See "Kidney replacement therapy (dialysis) in acute
kidney injury in adults: Indications, timing, and dialysis dose", section on 'Intermittent hemodialysis'.)

If a high-efficiency cellulose dialyzer is used, the urea clearance is similar to high-flux membranes,
providing blood flow is adequate. However, the increased clearance that is provided by the larger
surface area is not observed if blood flow is limited. Thus, among patients who have a poorly
functioning central venous catheter, high-efficiency membranes provide no additional benefit and should
not be used. (See 'Dialysis dose' below and 'Blood flow rate' below.)

Dialysis session length — The duration of each hemodialysis session affects clearance of uremic
toxins and correction of electrolyte abnormalities. A dialysis session of less than three hours duration is
considered short and that of greater than four hours duration is considered long. Sessions less than
three hours in length may not replace enough alkali or remove enough potassium, acid, or uremic
solutes. Thus, the dialysate composition and ultrafiltration goals should be modified, taking session
length, frequency, and intensity into account. (See 'Dialysate composition' below and 'Ultrafiltration'
below and 'Dialysis dose' below.)

Dialysate composition — The dialysate solution composition consists of potassium, sodium,

bicarbonate (or other buffer), calcium, magnesium, chloride, and glucose. Unlike chronic hemodialysis
(in which the dialysate composition is generally the same for every treatment), the dialysate
composition in acute hemodialysis is routinely altered each treatment to correct the metabolic
abnormalities that can rapidly develop during acute kidney injury (AKI). This is particularly true when
dialysis is initiated specifically for the treatment of potassium and/or acid-base derangements.

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Potassium — Patients with severe hyperkalemia are often treated medically prior to dialysis. This
issue is discussed separately. (See "Treatment and prevention of hyperkalemia in adults", section on
'Patients with a hyperkalemic emergency'.)

There are no rigorous outcomes data that inform the selection of dialysate potassium concentration.
Recommendations are based upon understanding of the physical principles underlying dialysis, clinical
observations, and on the limited studies performed in maintenance dialysis population [8-11].

The typical potassium concentration in the dialysate for acute hemodialysis ranges from 2 to 4 mEq/L.
The prescribed dialysate potassium concentration is based upon the predialysis serum potassium value,
session length, and frequency [12]. Among patients with acute kidney injury who are dialyzed in the
hospital setting, it is important to determine the predialysis serum potassium level at the start of the
hemodialysis session.

The rate of correction of serum potassium may be important. This will depend upon the serum to
dialysate potassium concentration gradient and the aggressiveness of other components of the dialysis
prescription, including flow rates, dialyzer surface area, alkali concentration, etc. (See 'Pre- and
post-hemodialysis laboratory value monitoring' below and 'Efficiency of potassium removal' below.)

Although there is no general consensus concerning the optimal strategy, the following is our approach
to adjusting the dialysate potassium concentration [12]. The serum potassium concentrations noted
below are rather arbitrary, and other approaches are likely to be equally effective and safe.

Patients with serum potassium <4.5 mEq/L — If the predialysis serum potassium level is
<4.5 mEq/L, we use a dialysate potassium concentration of 4 mEq/L [12]. This concentration prevents
the development of hypokalemia.

Some clinicians prefer a slightly lower net dialysate potassium concentration if the serum potassium is
4 to 4.5 mEq/L. However, we suggest not using a 3.5 mEq/L dialysate, since this requires adding
potassium to stock dialysate concentrate, which is not precise and introduces the risk of contamination.

Another approach that safely provides a lower dialysate concentration is to alternate dialysate
concentrations of 3 and 4 mEq/L on an evenly timed basis to achieve an effective total dialysate
concentration of 3.5 mEq/L. This approach requires intense attention to detail.

Patients with serum potassium between 4.5 and 5.5 mEq/L — If the predialysis serum
potassium level is between 4.5 and 5.5 mEq/L, we use a dialysate potassium of 3 mEq/L.

However, if the patient has an ongoing reason for hyperkalemia (eg, marked rhabdomyolysis), then we
may use a lower dialysate potassium of 2 mEq/L to decrease the risk of the patient developing
hyperkalemia prior to the next dialysis session. Among such patients, the serum potassium may be low
normal following dialysis, however, and we usually do not do this among patients who are at risk for
arrhythmias related to potassium removal [13-16]. For patients at increased risk of arrhythmias, some
nephrologists even avoid using a dialysate potassium <3 mEq/L. However, the increased safety of a 3
compared with a 2 mEq/L potassium dialysate in this situation has not been shown. Patients who have
ongoing risks of hyperkalemia and are at risk for arrhythmias may benefit from continuous renal
replacement therapy (CRRT) rather than intermittent hemodialysis. (See 'Telemetry' below.)

Patients with serum potassium between 5.5 and 8 mEq/L — For most patients with a
predialysis potassium level between 5.5 and 8 mEq/L, we use a 2 mEq/L dialysate potassium bath. As
noted above, some nephrologists do not use a dialysate potassium <3 mEq/L for patients who are at
risk for arrhythmias. Such patients include those with coronary artery disease, left ventricular
hypertrophy (LVH), digoxin use, hypertension, and advanced age. (See 'Telemetry' below.)

Patients with serum potassium >8 mEq/L — For patients with severe hyperkalemia (eg, >8
mEq/L), we use a dialysate potassium concentration of 1 mEq/L in order to rapidly decrease the serum
potassium to a safer level. However, for such patients, some nephrologists use a 2 mEq/L potassium

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dialysate, which is also effective.

As noted above, some nephrologists do not use a dialysate potassium <3 mEq/L for patients at risk for
arrhythmia, even with severe hyperkalemia. (See 'Telemetry' below.)

All patients who are being dialyzed with a dialysate potassium concentration of 1 mEq/L should be
monitored on telemetry for arrhythmias and have the serum potassium measured every 30 to 60
minutes during dialysis. Once the serum potassium is between 6 and 7 mEq/L, the dialysate potassium
concentration can be changed to 2 mEq/L for the remainder of the hemodialysis session; this is less
likely to cause hypokalemia and avoids a large blood-dialysate potassium difference, which may
contribute to the risk of arrhythmia [17].

We do not use a zero potassium bath, even for severe hyperkalemia, although it is most effective in
reducing the serum potassium in a short period of time [18,19]. A zero potassium bath has been
associated with an increased risk of hypokalemia and dialysis-induced arrhythmias, although rigorous
data are lacking [17,19].

Efficiency of potassium removal — The rate of potassium removal by dialysis is affected by

multiple variables. Potassium is transferred from serum into the dialysate during dialysis. Serum
potassium decreases quickly during the initial one to two hours of the treatment. Later during the
dialysis session and afterward, there is flux of potassium from the intracellular space to the serum.

The amount of potassium removal is equal to the amount removed by ultrafiltration (convection) and
the amount removed by diffusion. The rate of diffusion is proportional to the gradient between the
serum and dialysate concentrations. The administration of insulin, intravenous (IV) glucose, beta
agonists, or bicarbonate either concurrently or prior to hemodialysis all lower the rate of potassium
removal during dialysis because they cause intracellular translocation of potassium, which lowers the
serum potassium concentration. Such therapies, if used, should be stopped once dialysis is initiated.
The approach to hyperkalemia prior to dialysis is discussed elsewhere. (See "Treatment and prevention
of hyperkalemia in adults".)

The dialysate glucose concentration may modulate potassium removal since the glucose load enhances
insulin secretion, which drives potassium into the cells. In one study, dialysis against a standard
dialysate glucose concentration (ie, 200 mg/dL [11.1 mmol/L]) resulted in less potassium removal
compared with glucose-free dialysate solution [20]. Thus, in cases of severe hyperkalemia where
potassium removal is critical, a lower dialysate glucose concentration may theoretically be used to
facilitate potassium removal. However, this is usually not done in practice. (See 'Glucose' below.)

Metabolic acidosis also affects serum potassium levels. The correction of metabolic acidosis allows
extracellular potassium to enter cells and may speed the correction of hyperkalemia without net
potassium removal.

Sodium — The choice of dialysate sodium concentration for individual patients depends upon the
predialysis serum sodium concentration and the hemodynamic status of the patient.

The dialysate sodium may affect hemodynamic stability during acute hemodialysis. This is discussed
below. (See 'Ultrafiltration-related hypotension' below.)

Our approach is based upon the predialysis serum sodium concentration.

Patients with normal serum sodium — For patients with normal or near-normal serum sodium
levels, we use a dialysate sodium concentration of 137 mEq/L.

The dialysate sodium concentration that results in no net diffusive transfer of sodium is generally 0.1 to
3 mEq/L below that of the predialysis serum sodium concentration [21-24], although there may be
significant differences between prescribed and measured bath sodium concentrations [25].

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Chronic hyponatremia — Severe chronic hyponatremia may be safely corrected with

hemodialysis; however, rapid correction must be avoided [26]. Rapid correction of severe chronic
hyponatremia can lead to osmotic demyelination (pontine and extrapontine myelinolysis). Uremia may
provide some protection against osmotic demyelination. However, there is a case report of osmotic
demyelination following dialysis of severely hyponatremic patients [27].

Definitions of chronicity and the recommended rate of correction are the same as that in the nondialysis
general population. (See "Overview of the treatment of hyponatremia in adults".)

Among patients with severe chronic hyponatremia (ie, <120 mEq/L), we adjust the dialysate sodium to
prevent rapid correction [28]. We set the dialysate sodium to the lowest commercially available setting
(130 mEq/L), reduce the blood flow rate to 2 mL/kg/min, and reduce the hemodialysis session length
[29].

Because of the low blood flow rate, the sodium concentration of the blood returning to the patient rises
to equal the sodium concentration of the dialysate (130 mEq/L). The expected rate of rise of the serum
sodium concentration can be estimated from the rate of sodium infusion into the patient (which is the
product of the concentration gradient between blood and dialysate and the blood flow rate) divided by
total body water. However, hourly measurements of the serum sodium concentration during the course
of dialysis are mandatory, and administration of small amounts of 5 percent dextrose in water (D5W)
may still be required to assure that correction does not exceed 6 mEq/L during the dialysis treatment.

The goal is to correct the hyponatremia over the course of multiple hemodialysis sessions that are
performed over a period of several days.

CRRT may also be used to safely correct hyponatremia. CRRT is less efficient in the rate at which serum
sodium is changed and results in a more gradual correction over a longer time span [30-33]. (See
"Continuous kidney replacement therapy in acute kidney injury".)

Chronic hypernatremia — Among patients requiring acute dialysis, our approach to chronic
hypernatremia depends on its severity.

If the serum sodium concentration is only mildly elevated, we use a dialysate sodium concentration that
is within 2 mEq/L of the plasma sodium concentration for the first dialysis session. The use of dialysate
sodium concentrations more than 3 to 5 mEq/L below the plasma sodium concentration is associated
with hypotension, muscle cramps, and, most importantly, disequilibrium syndrome. Subsequently,
correction of the hypernatremia is performed with the administration of hypotonic solutions. (See
"Treatment of hypernatremia in adults".)

Rapid correction of severe chronic hypernatremia should be avoided as overcorrection may lead to
cerebral edema [26]. Patients with extremely high serum sodium concentrations are best treated with
CRRT [34,35]. (See "Continuous kidney replacement therapy in acute kidney injury".)

Acute hypo- or hypernatremia — Patients with hyperacute salt poisoning (eg, due to the
suicidal ingestion of sodium chloride or the inadvertent IV infusion of hypertonic saline during a
therapeutic abortion) or hyperacute water intoxication (eg, as a complication of marathon running or
use of the drug, "Ecstasy") should undergo aggressive correction of their serum sodium concentration.
Rapid correction is well tolerated in hyperacute disturbances. Conventional hemodialysis with a
standard sodium concentration can be used to correct the electrolyte disturbance rapidly. (See
"Overview of the treatment of hyponatremia in adults".)

Buffer solutions — The main dialysate buffer used in intermittent hemodialysis is bicarbonate.
Bicarbonate is inexpensive and generally well tolerated. Although acetate used to be the predominant
buffer used in hemodialysis, it is no longer routinely used, because it is associated with cardiac and
hemodynamic instability.

A disadvantage of bicarbonate is that it precipitates as an insoluble salt when stored with the divalent

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cations, calcium and magnesium [36]. As a result, the buffer and electrolytes are stored separately
prior to hemodialysis [36]. Possible side effects of bicarbonate are related to the increase in pH induced
by dialysis and include hypoxemia due to decreased respiratory drive and altered mental status,
weakness, cramping, and lethargy [37].

The dialysate bicarbonate concentration varies based upon the acid-base status of the patient. The
acid-base status should be assessed using both the serum bicarbonate and pH. (See "Simple and mixed
acid-base disorders".)

Our approach is based on our clinical experience, and we stress that there are no published data to
support these recommendations.

Metabolic acidosis — Our approach to metabolic acidosis depends upon its severity and cause.

For patients who have mild or moderate metabolic acidosis (ie, serum bicarbonate 10 to 23 mEq/L and
an acidemic pH) or who have no acid-base disorder, we generally use a standard dialysate bicarbonate
concentration of approximately 30 to 35 mEq/L.

For patients with severe metabolic acidosis (ie, serum bicarbonate <10 mEq/L and a severely acidemic
pH), we use a dialysate bicarbonate solution of approximately 35 to 40 mEq/L. For such patients, an
extended duration of hemodialysis may be necessary.

The use of this high dialysate bicarbonate concentration may result in the slower removal of potassium
due to its intracellular translocation [38]. In addition, among patients who are treated with opioids, use
of a high dialysate bicarbonate may increase opioid distribution into the central nervous system.

Alkalosis — The severity of the alkalemia and the process generating the alkalosis are the main
determinants of the dialysate bicarbonate concentration. In particular, the clinician should investigate
whether there is ongoing generation versus a one-time insult causing the alkalosis. A one-time insult
can be resolved with a single hemodialysis treatment, whereas ongoing generation of alkalosis may
require frequent and/or long hemodialysis sessions with a lower bicarbonate dialysate.

Both the blood pH and serum bicarbonate should be determined to appropriately assess the degree of
alkalosis.

If the predialysis serum bicarbonate level is >28 mEq/L or respiratory alkalosis is present, we use a
bicarbonate concentration 25 to 30 mEq/L [12]. We do not use a dialysate bicarbonate lower than 25
mEq/L.

If this dialysate does not address ongoing alkalosis, we administer 0.9 percent sodium chloride (NaCl)
while removing volume as necessary. Infusion of larger volumes of 0.9 percent NaCl may require
adjustments to the dialysate sodium concentration. The administration of chloride often corrects the
alkalosis, although the entire mechanism by which this occurs is not clear. One mechanism is that the
ultrafiltration of fluid containing a higher concentration of bicarbonate is replaced by infusion of a
bicarbonate-free solution (ie, NaCl).

Patients on mechanical ventilation — Among patients who are unable to increase their
ventilation, the administered bicarbonate with dialysis may result in higher CO2 values. The pCO2 of the
dialysate with bicarbonate dialysate can be as high as 100 Torr. If the patient’s pulmonary function is
intact, hyperventilation provoked by the increased pCO2 may decrease hypoxia. However, if the patient
is on ventilatory support, the ventilator settings may need to be adjusted to correct hypercapnia. In a
patient that is not completely dependent on the ventilator, the hypercapnia may serve as a stimulus for
improved ventilation and facilitate weaning and extubation.

In addition, in patients being mechanically ventilated using low-tidal volume ventilation, an increased
dialysate bicarbonate concentration may be required to increase the serum bicarbonate concentration to
compensate for the respiratory acidosis resulting from "permissive hypercapnia." In contrast, in patients

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being mechanically hyperventilated to compensate for metabolic acidosis, the minute ventilation
(respiratory rate and/or tidal volume) may need to be reduced to avoid severe alkalemia as the
metabolic acidosis is corrected with dialysis.

Calcium — The dialysate calcium ranges from 2 to 3.5 mEq/L and is adjusted based on the serum
calcium. The plasma ionized calcium should be measured prior to starting dialysis, but the total calcium
is usually the measure performed and used to decide the dialysate calcium. Since total plasma calcium
levels are poorly predictive of the ionized level (which is the clinically active value), the plasma ionized
calcium level should be measured prior to hemodialysis in patients with significant hypocalcemia or
hypercalcemia. If the ionized calcium cannot be obtained, the measured total plasma calcium level
should be corrected based upon the serum albumin level since the total plasma calcium concentration
will change in parallel to the albumin concentration; this correction, however, will not account for
changes in acid-base status. (See "Relation between total and ionized serum calcium concentrations".)

There are limited published literature to inform the selection of dialysate calcium. Most of the literature
is in the end-stage kidney disease (ESKD) setting and concerns the role of calcium in bone/mineral
metabolism or in cardiovascular disease. In patients with AKI, or hospitalized ESKD patients in whom
acute dialysis is required, immediate cardiac concerns predominate, and the outcomes data derived
from outpatients are less pertinent. The major concern in acute hemodialysis is that lower bath calcium
concentrations may prolong and increase the variability of the QTc interval, both risk factors for sudden
death [16]. The serum calcium can also influence potassium-induced arrhythmias [10].

Our approach is based on clinical experience:

●For patients with mild hypocalcemia, normocalcemia, or mild hypercalcemia (total plasma calcium level
between 8 to 12 mg/dL [2 to 3 mmol/L, corrected for hypoalbuminemia]), we use a dialysate calcium
concentration of 2.5 mEq/L.

●For patients with significant hypocalcemia (total plasma calcium level <8 mg/dL [<2 mmol/L],
corrected for hypoalbuminemia), particularly if the patient is symptomatic, we use a dialysate calcium
concentration of 3 to 3.5 mEq/L.

●For patients with severe hypercalcemia (total plasma calcium level >12 mg/dL [>3 mmol/L] corrected
for hypoalbuminemia), we use a dialysate calcium concentration of 2 to 2.5 mEq/L.

Magnesium — The usual dialysate magnesium concentration is 0.5 to 1 mEq/L. Either concentration
will address hypermagnesemia. Hypomagnesemia is usually corrected with IV or oral supplementation.
(See "Hypomagnesemia: Evaluation and treatment".)

Glucose — The standard dialysate glucose concentration is 100 to 200 mg/dL (5.5 to 11.1 mmol/L).
The relative benefits of using a lower as compared with a higher glucose concentration have not been
evaluated in the acute setting.

Blood flow rate — For the first dialysis session, we select the blood flow rate based on the degree of
azotemia prior to starting dialysis. There are no published data to guide an optimal approach.

If the blood urea nitrogen (BUN) is >100 mg/dL, we use a blood flow rate of 200 mL/min for the first
treatment or two (of 2 to 2.5 hours each). We gradually increase the blood flow and treatment time
over several consecutive days. Among patients with severe azotemia, the rapid reduction of BUN and
plasma osmolarity should be avoided in order to prevent dialysis dysequilibrium syndrome. The
incidence of dialysis dysequilibrium syndrome in AKI is not known and can be affected by other
concomitant disease processes. (See "Dialysis disequilibrium syndrome".)

If aggressive dialysis were needed for other reasons, such as severe hyperkalemia, we are not as
conservative in terms of modifying blood flow and treatment time. Additional details about dialysis
dosing are presented separately. (See "Kidney replacement therapy (dialysis) in acute kidney injury in
adults: Indications, timing, and dialysis dose", section on 'Optimal dosing'.)

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In addition, for severely azotemic patients, continuous renal replacement therapies (CRRTs) may be
used; compared with acute intermittent hemodialysis, lower blood flows are sufficient to achieve
adequate clearance using CRRT due to its continuous nature [7]. (See "Continuous kidney replacement
therapy in acute kidney injury".)

Ultrafiltration

Determining goal — Determining optimal ultrafiltration (UF) requirements in critically ill AKI
patients is challenging. Volume status and the desired UF requirement are determined in part by
physical examination and hemodynamic indices. In general, no one, specific test or parameter is
sufficient in isolation.

The following two overriding principles should be recognized:

●The approach to volume overload is different for chronic dialysis patients and for critically ill AKI
patients. The target weight of a chronic dialysis patient is usually determined empirically as the weight
at which clinical signs of extracellular fluid expansion are absent and below which clinical signs of
extracellular depletion arise. In contrast, among critically ill AKI patients, the volume expansion that is
frequently observed is often necessary to maintain optimal circulatory and oxygen transport status.

●The relationship between blood volume and hypotension is different in chronic dialysis patients and
critically ill AKI patients. Among critically ill AKI patients, the relationship between volume status and
hemodynamic stability is unpredictable. As an example, blood volume monitoring, which is a
biofeedback system that automatically adjusts UF rate and dialysate sodium content in response to a
fall in circulating intravascular volume, reduces the occurrence of intradialytic hypotension in end-stage
kidney disease (ESKD) patients [39] but is ineffective for preventing hypotension in critically ill AKI
patients [40]. This lack of a predictable relationship between volume status and hemodynamic stability
means that UF goals for a given patient should be assessed not only in terms of fluid mass balance or
the mandatory removal of obligatory fluid loads, but also in terms of the effect of intervention on the
patient's broader clinical condition and hemodynamic status.

In hemodynamically stable patients, the estimation of target intravascular volume can be made in the
usual fashion utilized for chronic dialysis patients. However, in hemodynamically unstable patients,
target intravascular volume should be titrated to invasive or noninvasive monitoring (such as
bioimpedance analysis, pulse contour analysis [PiCCO], echocardiography, or inferior vena cava
diameter measurement), which should guide the UF goals for a given intermittent hemodialysis session.

Ultrafiltration-related hypotension — UF during hemodialysis can result in significant intradialytic

hypotension. This can be treated by reducing or discontinuing UF.

In addition, measures that help prevent intradialytic hypotension during acute hemodialysis in AKI
include:

●Increasing the frequency and/or duration of treatments

●Cool-temperature dialysis (see "Intradialytic hypotension in an otherwise stable patient", section on

'Second-line approach')

●Sodium and UF modeling

●Higher dialysate calcium concentration if this can be done without rendering the patient hypercalcemic

●Midodrine (alpha-1 adrenergic agonist used in autonomic dysfunction), which may be administered in
the absence of more powerful, pharmacologic forms of pressor support

Any or all of these suggestions may be necessary in any given hemodialysis treatment. In addition to
these interventions, 0.9 percent NaCl intravenous (IV) boluses given during hemodialysis can
transiently increase blood pressure.

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We generally treat intradialytic hypotension using the following measures, recognizing that some may
be more appropriate than others under specific conditions:

●Increasing the frequency and/or duration of treatments – Increasing the frequency of

treatments decreases the required UF requirement per session. Increasing the duration of each session
decreases the UF rate required to meet UF goals per session. Such changes may depend upon nursing
availability.

●Sodium and UF modeling – Sodium modeling is a method by which a higher dialysate sodium
concentration is used at the beginning of hemodialysis and progressively decreased throughout the
session to avoid abruptly lowering the plasma osmolarity [37]. UF modeling is an automated method by
which the set UF rate is higher early in the hemodialysis procedure and lower later in the procedure or
some modification of this [41]. Combination sodium and UF modeling has been studied but has not been
conclusively shown to be beneficial [42]. It is usually used because of its ease of application. (See
"Intradialytic hypotension in an otherwise stable patient", section on 'Prevention of recurrent
episodes'.)

Sodium modeling may decrease hemodynamic instability during acute hemodialysis. This was
demonstrated in a randomized, crossover study of 10 AKI patients in the intensive care unit (ICU) [43].
The study used either a fixed dialysate sodium regimen (140 mEq/L) and fixed UF rate or a variable
sodium dialysate (160 to 140 mEq/L) and variable UF rate (such that half of the fluid was removed
during the first third of the treatment and the remaining half over the last two-thirds). Compared with
the fixed regimen, sodium and UF modeling was associated with greater hemodynamic stability and
fewer interventions involving nursing and volume replacement.

Multiple sodium modeling prescriptions are programmed in most hemodialysis machines, though the
availability of specific programs may differ in machines used in Europe versus the US. Patients may
respond to only one or all available prescriptions. Thus, trials are required to find the best sodium
modeling prescription in AKI patients on hemodialysis.

We prefer either of the following two specific strategies:

•With one high/low-sodium modeling prescription, a high-dialysate sodium (eg, 150 mEq/L) alternates
with a low-dialysate sodium (eg, 130 mEq/L), with each level set for an equal amount of time. The
average of the high/low-sodium levels (eg, 140 mEq/L) is the dialysate sodium usually prescribed in
hemodynamically stable patients with normal serum sodium levels. During the low-sodium period, the
UF rate is minimized or stopped. UF only occurs during the high-sodium period to draw out intracellular
water due to the extracellular hypernatremia. This program is widely available in Europe but not in
some machines in the US.

•Another sodium modeling prescription is to set the initial dialysate sodium at a high level (eg, 150 to
160 mEq/L). The dialysate sodium level is then decreased in stepwise, exponential, or linear
decrements (depending on clinical effect) to a final low level (eg, 140 mEq/L). To maintain isonatremia,
the time-average concentration of dialysate sodium should be the same or marginally lower than the
predialysis serum sodium concentration (approximately within 1 to 2 mEq/L). With a linear sodium
profile, for example, the duration (and degree) of dialysis spent below the isonatremic concentration
must be approximately equal to that spent above it [21].

Anecdotal experience has suggested that, in addition to the above approaches, using a slightly higher
sodium of 143 mEq/L or so throughout the entire dialysis rather than 137 to 138 mEq/L may be
effective in increasing hemodynamic stability. This will raise the plasma sodium concentration, at least
temporarily.

Although sodium modeling may be associated with improved hemodynamic stability acutely, if dialytic
support is prolonged, sodium modeling may be associated with a positive sodium balance due to
diffusion of sodium from dialysate to blood because of the higher sodium concentration in the dialysate

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used during sodium modelling. This may lead to difficulty in blood pressure and edema management.

●Cool-temperature dialysis – Cool-temperature dialysis may increase hemodynamic stability. Data in

support of this intervention are largely derived from the chronic hemodialysis setting. The method for
performing cool-temperature dialysis is the same as that among chronic dialysis patients and is
presented separately. (See "Intradialytic hypotension in an otherwise stable patient", section on
'Second-line approach'.)

However, cool-temperature dialysis typically can cause symptoms of hypothermia, and hypothermia may
have adverse effects upon myocardial function, end-organ perfusion, blood clotting, and, possibly, renal
recovery [44].

●Higher dialysate calcium concentration – Increasing the dialysate calcium may be used in
combination with sodium and UF modeling and a lower dialysate temperature to treat intradialytic
hypotension. However, we do not use a dialysate calcium concentration >3.5 mEq/L. (See 'Calcium'
above.)

In a prospective, crossover study that included patients who were also on midodrine, cool dialysate, or a
combination of these two therapies, compared with low-dialysate calcium, the use of high-dialysate
calcium increased post-hemodialysis mean arterial pressure (MAP) but was not associated with a
reduction in symptoms or interventions for intradialytic hypotension [45].

●Other measures – Despite the measures listed above, hemodynamic instability may still occur
because of the various dialysis-independent causes of intradialytic hypotension present in the acute
setting (eg, cardiogenic, vasodilatory, or hypovolemic shock). If measures to improve hemodynamic
stability during intermittent hemodialysis sessions are not successful, switching to prolonged
intermittent renal replacement therapy (PIRRT) or continuous renal replacement therapy (CRRT)
usually improves hemodynamics while maintaining an acceptable rate of UF and solute clearance. (See
"Prolonged intermittent renal replacement therapy" and "Continuous kidney replacement therapy in
acute kidney injury".)

Anticoagulation — Issues surrounding anticoagulation in patients undergoing acute hemodialysis are

presented separately. (See "Anticoagulation for the hemodialysis procedure".)

Dialysis dose — Dialysis dose in AKI is discussed elsewhere. (See "Kidney replacement therapy
(dialysis) in acute kidney injury in adults: Indications, timing, and dialysis dose", section on
'Intermittent hemodialysis'.)

TELEMETRY — We recommend that patients with underlying cardiac disorders who undergo acute
hemodialysis be placed on a cardiac rhythm monitor during the dialysis session. Dialysis-induced
reductions in the serum potassium can provoke ventricular arrhythmias. The risk is increased by the
presence of coronary artery disease, LVH, digoxin use, hypertension, and advanced age [13-17,46].

Other measures to reduce the risk of arrhythmias include close monitoring of the serum potassium and
avoidance of very low dialysate potassium, as noted above. (See 'Patients with serum potassium >8
mEq/L' above.)

PRE- AND POST-HEMODIALYSIS LABORATORY VALUE MONITORING — A basic metabolic profile

(electrolytes, glucose, urea, creatinine, phosphate, calcium, and magnesium) should be reviewed prior
to acute hemodialysis sessions since electrolyte and acid/base status can profoundly change between
treatments and require alterations in the dialysis prescription. In some patients, it may also be
appropriate to obtain a basic metabolic profile or other blood chemistries sometime after the end of
dialysis to monitor the response to the treatment. Postdialysis chemistry studies, if indicated, should
generally be done after the first one to two hours following completion of the session to allow for
equilibration between the plasma and intracellular compartments.

WATER — Water used for acute hemodialysis should meet the requirements of the International

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Organization for Standardization (ISO) 13959; 2009: Water for hemodialysis and related therapies
[47]. (See "Assuring water quality for hemodialysis".)

MANAGEMENT DURING RECOVERY OF KIDNEY FUNCTION — Most patients who survive acute
kidney injury (AKI) recover kidney function [48,49]. Patients should be monitored closely for recovery
and dialysis discontinued when acceptable kidney function is restored.

Continued hemodialysis may be detrimental to renal recovery. Hypotension associated with dialysis may
reduce kidney function [50,51], and morphologic studies in humans have shown fresh ischemic lesions
in kidney biopsy specimens from patients with AKI of over three weeks duration [52].

There are no accepted standards for discontinuation of dialysis [53-56].

In some cases, renal recovery is obvious, as indicated by rapidly increasing urine output and/or
decreasing levels of predialysis serum creatinine and/or blood urea nitrogen (BUN) values. In many
cases, however, renal recovery is both slow and sporadic.

For those AKI patients who are otherwise medically recovered from their acute illness, kidney function
alone is usually sufficient to guide dialysis requirements. Such patients rarely require dialysis when
their glomerular filtration rate (GFR) is >10 to 15 mL/min, particularly when their predialysis serum
creatinine and/or BUN values are decreasing, unless dialysis is needed for management of volume
overload [57,58]. In this setting, we generally use the serum creatinine, rather than the BUN, because
the creatinine is less confounded by the effects of metabolism.

For patients who are acutely ill, the decision to discontinue dialysis should not be made solely on the
presence or degree of renal recovery [53,56]. The decision should consider the patient’s overall
condition (including presence of increased catabolism, fluid overload, ongoing hemodynamic instability,
and ongoing requirement for nephrotoxic drugs or large volumes of fluid). It should be noted that the
recovery of electrolyte homeostasis does not always parallel the recovery of GFR, so electrolyte
abnormalities may also determine the need for dialytic support during the AKI recovery phase. As GFR
improves, water homeostasis may not have been restored, and an osmotic diuresis may result in
polyuria that must be managed.

Over half of AKI patients will be able to successfully stop dialysis on their first attempt, and others will
need reinitiation of treatment, albeit at lower doses [48,59,60]. Urine output and duration of the need
for dialysis have been reported to be important predictors of successful discontinuation of dialysis.
Stopping dialysis is less likely to be successful if urine output is less than 400 to 600 mL/day (without
diuretics) [48,60].

There are no studies that suggest an optimal approach to withdrawing dialytic support. We generally
tailor our approach to the individual patient and expected patient response. For those with clinically
obvious and rapid renal recovery, abrupt cessation of dialysis is appropriate and well tolerated, as long
as adequate monitoring is in place.

However, for those who are still acutely ill or who have had a very slow or sporadic recovery, we
generally wean dialysis by decreasing the frequency of treatments as tolerated, which is usually over
several weeks. This approach may also be optimal for those with pre-existing chronic kidney disease
(CKD) or those with other important comorbidities such as congestive heart failure, where renal
recovery might be compromised.

Patients with high interdialytic weight gains (despite improved GFR) may benefit from a trial of loop
diuretic therapy while the dialysis duration or frequency is being decreased.

The addition of diuretics does not enhance kidney function recovery or improve kidney function
[61,62], but may increase urine output and sodium excretion [63-65] and allow for a lower dose of
dialysis [66].

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Two clinical trials and one observational study have shown that the addition of high-dose diuretics in
patients with AKI does not improve weaning from kidney replacement therapy (KRT) in the hospital or
intensive care unit (ICU) setting [60,65,67]. Diuretic therapy should thus not be routinely used for this
purpose [54].

A key element to successful discontinuation of dialysis is monitoring for renal recovery. In the hospital,
predialysis laboratory tests should include serum potassium, bicarbonate, creatinine, and BUN. For
patients whose urine output is greater than 400 mL/day, some clinicians perform a timed urine
collection (on an interdialytic day) or interdialytic urine collection for creatinine and urea clearance to
guide decision making.

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.)

●Basics topic (see "Patient education: Hemodialysis (The Basics)")

●Beyond the Basics topic (see "Patient education: Hemodialysis (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

●Acute kidney injury (AKI), formerly called acute renal failure (ARF), is a major cause of morbidity and
mortality, particularly in the hospital setting. Acute kidney replacement therapy (KRT), including acute
intermittent hemodialysis, is commonly indicated for patients with AKI. (See 'Introduction' above.)

●The components of the acute dialysis prescription include the choice of hemodialysis membrane,
dialysate composition and temperature, blood flow rate, amount and rate of ultrafiltration (UF), choice
of anticoagulation, and total dialysis dose. (See 'Components of the acute hemodialysis prescription'
above.)

●We use biocompatible high-flux membranes for acute hemodialysis. (See 'Hemodialyzer membranes'
above.)

●Dialysate components include potassium, sodium, bicarbonate buffer, calcium, magnesium, chloride,
and glucose. The dialysate composition is routinely altered to correct the metabolic abnormalities that
can rapidly develop during AKI. Specific parameters are provided. (See 'Dialysate composition' above.)

●For the first dialysis treatment, the blood flow rate depends on the degree of azotemia. If the blood
urea nitrogen (BUN) is >100 mg/dL, we use a blood flow rate of ≤200 mL/min for the first treatment or
two (of 2 to 2.5 hours each). Otherwise, we use a dialysis blood flow rate of 400 mL per minute. (See
'Blood flow rate' above.)

●The UF requirement is determined by physical examination and hemodynamic indices. In

hemodynamically unstable patients, target intravascular volume should be titrated to invasive or
noninvasive monitoring. In general, no one specific test or parameter is sufficient in isolation. (See

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'Determining goal' above.)

●UF may cause intradialytic hypotension. Intradialytic hypotension can be treated by reducing or
discontinuing UF and/or reducing the blood flow rate. Other measures that may reduce intradialytic
hypotension and help deliver effective hemodialysis include increasing the frequency and/or duration of
treatments, sodium and UF modeling, cool-temperature dialysis, and higher dialysate calcium
concentration. (See 'Ultrafiltration-related hypotension' above.)

●Most patients who survive AKI recover kidney function. Dialysis should not be continued for longer
than is necessary. For patients who are still acutely ill, the decision to discontinue dialysis should be
determined by the degree of recovery of kidney function and by the patient's overall condition
(including presence of increased catabolism, fluid overload, ongoing hemodynamic instability, and
ongoing requirement for nephrotoxic drugs or large volumes of fluid). (See 'Management during
recovery of kidney function' above.)

ACKNOWLEDGMENT — The editorial staff at UpToDate would like to acknowledge Mark R Marshall,
MD, and Phillip Ramos, MD, MSCI, who contributed to earlier versions of this topic review.

The editorial staff would also like to acknowledge Gerald Schulman, MD, FASN, now deceased, who
contributed to an earlier version of this topic.

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