Acute hemodialysis prescription

Author:
Thomas A Golper, MD
Section Editors:
Jeffrey S Berns, MD
Paul M Palevsky, MD
Richard H Sterns, MD
Deputy Editor:
Shveta Motwani, MD, MMSc, FASN
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Apr 2020. | This topic last updated: Oct 12, 2018.

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

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

●(See "Renal 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 "Renal replacement therapy (dialysis) in acute kidney injury in adults:

Indications, timing, and dialysis dose", section on 'Optimal modality'.)
●(See "Continuous renal 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 "Centralcatheters for acute and chronic hemodialysis access".)

●(See "Approach to the 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, 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 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 renal function. (See "Dialysis-related factors that may influence
recovery of renal 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 renal 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 "Renal
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.)
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.

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".)

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 [12]. It is important to determine the predialysis
serum potassium level at the start of the hemodialysis session. (See 'Pre- and post-
hemodialysis laboratory value monitoring' 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 dialysate, which is generally 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 we check the serum potassium
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 in 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 the data are not very good [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.)

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].

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 dialysis time [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 renal 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 renal 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 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 on severity.

For patients with mild or moderate metabolic acidosis (ie, serum bicarbonate 10 to 23
mEq/L and an acidemic pH) or with 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 [38] and may also 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 NaCl
while removing volume as necessary. The administration of chloride often corrects the
alkalosis, although the mechanism by which this occurs is not completely clear.

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 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 would be confounded by other illnesses; if
aggressive dialysis were needed for other reasons, we would not be so conservative.
(See "Dialysis disequilibrium syndrome".)

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 renal 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.

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 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.
With cool-temperature dialysis, the patient's blood temperature is maintained
precisely at a target value by a series of feedback loops controlling thermal transfer
to and from the dialysate [44,45]. (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 [46].
●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 [47].
●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 renal 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 "Renal

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 [13-17,48].

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 Organization for Standardization (ISO) 13959; 2009: Water for

hemodialysis and related therapies [49]. (See "Water purification systems in
hemodialysis", section on 'Water treatment for hospital bedside dialysis machines'.)

MANAGEMENT DURING RECOVERY OF RENAL

FUNCTION Most patients who survive acute kidney injury (AKI) recover renal

function [50,51]. Patients should be monitored closely for recovery and dialysis
discontinued when acceptable renal function is restored.

Continued hemodialysis may be detrimental to renal recovery. Hypotension associated

with dialysis may reduce renal function [52,53], and morphologic studies in humans
have shown fresh ischemic lesions in kidney biopsy specimens from patients with AKI of
over three weeks duration [54].

There are no accepted standards for discontinuation of dialysis [55-58].

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,
renal 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 [59,60]. 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 [55,58]. 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 [50,61,62]. 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) [50,62].

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 renal
function [63,64], but may increase urine output and sodium excretion [65-67] and allow
for a lower dose of dialysis [68].

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 renal replacement
therapy (RRT) in the hospital or intensive care unit (ICU) setting [62,67,69]. Diuretic
therapy should thus not be routinely used for this purpose [56].

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 5 th 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 10 th 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 renal
replacement therapy (RRT), 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 '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 renal 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
renal 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 renal 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.

Use of UpToDate is subject to the Subscription and License Agreement.

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