Acute hemodialysis prescription

Authors

Phillip Ramos, MD, MSCI

Mark R Marshall, MD

Thomas A Golper, MD Section Editors

Jeffrey S Berns, MD

Paul M Palevsky, MD

Richard H Sterns, MD Deputy Editor

Theodore W Post, MD

Last literature review version 17.1: January 2009 | This topic last updated: June 10, 2008 (More)

INTRODUCTION — Acute renal failure (ARF) is a major cause of morbidity and mortality, particularly in the hospital setting. Despite improvements in renal replacement therapy

(RRT) techniques during the last several decades, the mortality rate associated with ARF in critically ill patients remains above 50 percent. (See "Renal and patient outcomes after acute

tubular necrosis").

RRT is ideally initiated in the acute setting prior to the dangerous accumulation of extravascular volume and/or uremic toxins that can result in further multi-organ damage

and failure. Once the decision to initiate RRT has been made, the specific modality of dialytic support must be chosen. This consists of peritoneal dialysis, intermittent hemodialysis and

its variations (eg, hemofiltration), and continuous renal replacement therapy. Once the selection is made, the acute dialysis prescription can be determined.

An acute hemodialysis treatment is defined as a hemodialysis session specifically performed for ARF (also known as acute kidney injury [AKI]) or in the setting of a hospitalized end stage renal disease (ESRD) patient. The choice of specific dialysis modality, particularly the choice

between continuous or intermittent dialysis, is discussed separately. (See "Continuous renal replacement therapy in acute kidney injury (acute renal failure)").

The various components of the acute hemodialysis prescription will be described here. The use of peritoneal dialysis in ARF is discussed separately (See "Use of peritoneal dialysis for

the treatment of acute kidney injury (acute renal failure)").

INDICATIONS — The urgent indications for RRT in patients with ARF generally include volume overload refractory to diuretics, hyperkalemia, metabolic acidosis, uremia, and toxic

overdose of a dialyzable drug. In an attempt to minimize morbidity, dialysis should be started prior to the onset of overt complications of renal failure, whenever possible. This is

discussed in detail separately. (See "Renal replacement therapy (dialysis) in acute kidney injury (acute renal failure): Indications, timing, and dialysis dose", section on Indications).

MODALITY — Once the decision to initiate RRT has been made, the specific modality of dialytic support must be chosen. The possibilities include peritoneal dialysis, intermittent

hemodialysis and its variations (eg, hemofiltration), and continuous renal replacement therapy. Once this selection is made, the acute dialysis prescription can be determined. The

determining factors of which modality is chosen include the catabolic state, hemodynamic stability, and whether the primary goal is solute removal (eg, uremia, hyperkalemia), fluid

removal, or both. This is reviewed elsewhere. (See "Renal replacement therapy (dialysis) in acute kidney injury (acute renal failure): Indications, timing, and dialysis dose").

VASCULAR ACCESS — When acute hemodialysis is chosen as the dialytic support modality, vascular access must be established prior to initiating treatment. Placement of the venous

dialysis catheter must be considered carefully, especially in the critically ill patient.

The location depends upon factors such as body habitus, whether the patient is ambulatory or bed-ridden, presence of vascular disease or atypical anatomy, and the avoidance of

specific complications in an at-risk patient (eg, risk of pneumothorax while placing a subclavian venous dialysis catheter in a patient with severe chronic obstructive pulmonary

disease or history of deep vein thrombosis or other venous disease).

For hospitalized ESRD patients, daily reassessment of the existing angioaccess (eg, arteriovenous graft or fistula) is appropriate. Many events during the hospitalization can

jeopardize the existing access (eg, hypotension). (See "Acute hemodialysis vascular access" for a more detailed discussion of this issue).

HEMODIALYZER MEMBRANES — In the setting of ARF, the choice of artificial membranes utilized may have a bearing on clinical outcome. Previously, it was postulated that non-

complement activating membranes may incur less inflammatory risk with resultant decrease in infectious complications and possibly an increased probability of improved restoration of renal function. However, there are inconsistent findings concerning the effect of membrane

biocompatibility on outcomes among patients with acute renal failure, with several meta-analyses reporting disparate results. (See "Renal replacement therapy (dialysis) in acute

renal failure: Recovery of renal function and effect of hemodialysis membrane", section on Complement activation, for a discussion relating to these issues).

Membranes can also be of low or high flux. High flux membranes contain large pores that allow for enhanced permeability of larger molecules [1] . Although this property can

enhance removal of putative toxins and improve outcome, it could also allow the back transport (from dialysate to blood) of potentially harmful water-borne molecules. This

property is a factor that confounds some of the conclusions from previously performed studies. Certainly, having the purest dialysate water possible should be a goal when using

these more porous membranes to utilize their positive attributes and to minimize their potential risks.

Overall, there are theoretical advantages to high flux biocompatible membranes that have not been consistently corroborated by often underpowered or flawed clinical studies.

However, the effect of membrane biocompatibility on outcomes (when present) is consistently beneficial. In addition, since such membranes can now be obtained cheaply,

cost has been eliminated as a deciding factor.

We therefore suggest the following approach: If the water system used is high quality, high flux biocompatible dialysis membranes should be used in the ARF setting. If the water

system is not of high quality, low flux biocompatible dialysis membranes should be used. Another option is the use of in-line membrane filtration devices on dialysis machines to

generate ultrapure dialysate .

(See "Renal replacement therapy (dialysis) in acute renal failure: Recovery of renal function and effect of hemodialysis membrane", sections on Complement activation and High versus

low flux membranes and see "Maintaining water quality for hemodialysis", for a discussion concerning water quality.)

DIALYSATE COMPOSITION — The dialysate solution composition consists of potassium, sodium, bicarbonate buffer, calcium, magnesium, chloride, and glucose. Unlike chronic hemodialysis, the dialysate composition in acute hemodialysis is routinely altered each

treatment to correct the metabolic abnormalities that can rapidly develop during ARF. This is particularly true in the treatment of potassium and/or acid/base derangements. Thus, the

dialysate potassium, sodium, bicarbonate, and calcium are routinely changed in this setting.

Issues surrounding magnesium, chloride, and glucose include the following: The usual dialysate magnesium concentration is 0.5 to 1.0 mEq/L, and is not usually different from that

in the chronic setting. The amount of dialysate chloride is dependent upon the dialysate sodium and bicarbonate concentrations. The standard dialysate glucose concentration is 200

mg/dL, but may be decreased to more efficiently lower the serum potassium during hemodialysis .

Potassium dialysate composition — There is no standard dialysate potassium concentration in the acute hemodialysis prescription because of wide variability in serum potassium prior to initiating the hemodialysis session. It is crucial to know the predialysis serum potassium

level at the start of the hemodialysis session to tailor the dialysate potassium so that normokalemia will be attained with avoidance of hypokalemia.

The goal of an acute hemodialysis treatment is not necessarily to lower the total body potassium burden for general nutritional purposes. Instead, the goals are often more short

term, such as normalizing the serum potassium level for the next 24 hours.

The typical potassium concentration in the dialysate for acute hemodialysis ranges from 2.0 to 4.0 meq/L. However, the dialysate potassium concentration should be varied based upon

the pre-dialysis value [2] . As described below, the dialysate glucose concentration can be another determinant of the rate of potassium removal.

The prescribed dialysate bath potassium is determined by both the absolute serum potassium and the rate of rise in the inter-dialytic period. A rapid rate of rise in serum

potassium may best be treated by daily hemodialysis rather than lowering the dialysate potassium bath concentration.

Some patients with acute and/or severe hyperkalemia have muscle weakness and cardiac conduction abnormalities, and should be treated with more rapidly acting medical therapies

prior to the initiation of dialysis. The first electrocardiographic changes with hyperkalemia are tall peaked T waves and shortened QT interval (show ECG 1). This is followed by

progressive lengthening of the PR interval and QRS duration, and then loss of the P wave with further prolongation of the QRS interval ("sine wave" pattern). Conduction delay can

manifest as bundle branch or AV nodal block, and ventricular fibrillation or asystole can result. (See "Clinical manifestations and treatment of hyperkalemia").

If more advanced electrocardiographic features of hyperkalemia are present, medical management should be initiated immediately with continuous ECG monitoring. Medical therapy is administered while emergency hemodialysis is being arranged, (See "Clinical

manifestations and treatment of hyperkalemia", section on Treatment).

Although there is no general consensus concerning the optimal strategy, the following is our general approach to the dialysate potassium concentration [2] : Predialysis potassium <4.0

meq/L — If the predialysis serum potassium level is less than 4.0 meq/L, we recommend that the dialysate potassium bath should be adjusted to 4.0 meq/L [2] . This is done to prevent the development of hypokalemia and its complications. Predialysis potassium

between 4.0 and 5.5 meq/L — If the predialysis serum potassium level is between 4.0 and 5.5 mEq/L, the typical potassium concentration in the dialysate for acute hemodialysis

usually ranges from 2.0 to 4.0 mEq/L. We suggest using a dialysate potassium of 3.5 meq/L if the predialysis serum potassium is between 4.0 to 4.5 mEq/L, and 3.0 meq/L if the

predialysis serum potassium is between 4.5 to 5.5 meq/L. However, if a rapid increase in extracellular potassium is anticipated prior to the next hemodialysis session (eg, due to

marked rhabdomyolysis), then a dialysate potassium of 2.0 meq/L should be used to ensure normokalemia in the lower range of normal. Predialysis potassium >5.5 meq/L and <8.0

meq/L — If patients have a predialysis serum potassium level greater than 5.5 meq/L and less than 8.0 meq/L, then a 2.0 meq/L dialysate potassium bath should be used. However, the dialysate concentration should be increased to 2.5 or 3.0 meq/L in patients at risk for

cardiac arrhythmia or those receiving digitalis [2] . (See "Complications with potassium removal" below). Severe hyperkalemia, potassium >8.0 meq/L — In cases of severe

hyperkalemia (eg, >8.0 meq/L), a dialysate potassium concentration of 1.0 mEq/L can be used to rapidly decrease the serum potassium to a more tolerable level. However, this

should be done with a high degree of caution to avoid hypokalemia .

Although rarely recommended, a zero potassium bath has also been used to rapidly decrease the serum potassium in a short period of time [3,4] . After four hours of

hemodialysis in one study, for example, a dialysate free of potassium was more effective

than a 1.0 or 2.0 mEq/L potassium dialysate bath in removing serum potassium, removing 85 percent more potassium than a 2.0 meq/L bath and 46 percent more than a 1.0 meq/L bath

[3].

However, to minimize the risk of hypokalemia and dialysis-induced arrhythmias, we do NOT recommend use of a zero potassium dialysate bath for the treatment of severe

hyperkalemia. If a rapid fall in serum potassium is desired because of severe hyperkalemia, we suggest using a 1.0 meq/L potassium bath and checking a serum potassium every 30 to 60 minutes. Once the serum potassium is between 6 and 7 meq/L, the dialysate potassium concentration can be changed to 2.0 meq/L for the remainder of the hemodialysis session,

depending upon many other prescriptive components discussed below.

In patients with underlying cardiac disorders or those taking digoxin, the dialysate concentration can be changed to 3.0 meq/L once the serum potassium is approximately 5.5

meq/L to avoid possibly life-threatening arrhythmias, with the postdialysis serum potassium goal of 4.0 meq/L. Although not studied in the acute setting, this overall approach decreases

the risk of hypokalemia and dialysis-induced arrhythmias, particularly in patients with predisposing risk factors delineated below. (See "Complications with potassium removal"

below).

The amount of potassium removal is proportional to the gradient between the serum and dialysate concentrations. The administration of insulin, intravenous glucose, beta-agonists,

or bicarbonate either concurrently or prior to hemodialysis results in intracellular translocation of potassium, lower serum levels, and therefore lower rates of potassium

removal during dialysis.

Dialysate glucose concentration — The dialysate glucose concentration is another factor that can modulate potassium removal, since the glucose load enhances insulin secretion which drives potassium into the cells. Thus, in the presence of endogenous insulin, the standard

dialysate glucose concentration (200 mg/dL [11.1 mmol/L]) results in significantly decreased potassium removal relative to glucose-free dialysate solution [5].

Thus, in cases of severe hyperkalemia where potassium removal is critical, a lower dialysate glucose concentration may be used. We suggest a dialysate glucose concentration of 100

mg/dL (5.6 mmol/L) if severe hyperkalemia (eg, >8.0 meq/L) is present. We do NOT use glucose-free dialysate because of the risk of hypoglycemia. Standard dialysate glucose concentration (200 mg/dL [11.1 mmol/L]) should be used in cases of mild to moderate

hyperkalemia.

Complications with potassium removal — The hemodialysis treatment can provoke ventricular arrhythmias, which are related to dialysis-induced reductions in the serum

potassium. Multiple studies have demonstrated that potentially life-threatening dialysis-induced arrhythmias with potassium removal are independently associated with risk factors

such as coronary artery disease, left ventricular hypertrophy (LVH), digoxin use, hypertension, and advanced age [6,7].

In one study in chronic dialysis, for example, 23 stable ESRD patients were evaluated using a Holter monitor [7] . Nine (39 percent) had ventricular tachycardia (VT) during and after

hemodialysis performed with a dialysate potassium concentration of 2.0 meq/L. Episodes of frequent or complex ventricular arrhythmias were more likely in patients on digoxin (8/9

versus 1/14 without arrhythmias) and those with LVH (9/9 versus 7/14 without arrhythmias). It was concluded that a low dialysate potassium concentration can induce ventricular arrhythmias in hemodialysis patients on digoxin and with LVH. It is unknown if, in the

absence of underlying risk factors (cardiac arrhythmias, digoxin, or heart disease), a dialysate potassium concentration of 2.0 meq/L causes serious ventricular arrhythmias [4].

To lower the risk of potentially life-threatening dialysis-induced arrhythmias among patients with underlying risk factors, the goal is to obtain a postdialysis serum potassium

concentration of approximately 4.0 meq/L by using a dialysate potassium concentration no lower than 3.0 meq/L.

Periodic measurements of postdialysis potassium may be helpful. The immediate postdialysis value is generally the lowest and potassium rebound, while rapid, depends upon

the factors previously discussed. However, the degree of potassium rebound is highly variable. Poor perfusion states and underlying illnesses all affect potassium rebound.

Poor systemic perfusion may have a potentially large impact in two ways. First, potassium removal during hemodialysis is associated with a larger reduction in serum potassium due to less potassium efflux from cells. Second, after dialysis, potassium rebound will be less by the

same mechanism. Such patients warrant closer monitoring of the serum potassium, with a postdialysis measurement at two to four hours.

In addition, we recommend that patients with underlying cardiac disorders who undergo acute hemodialysis should be placed on a cardiac rhythm monitor during the dialysis

session.

Sodium modeling and hemodialysis hypotension — The choice of the dialysate sodium concentration can have a significant impact on the patient's volume and hemodynamic

status. During the early days of hemodialysis, low dialysate sodium concentrations were routinely used to help decrease volume overload and hypertension. However, a low

dialysate sodium during a 3 to 4 hour hemodialysis session acutely decreases the intravascular volume over a short period of time as the result of the net negative sodium

balance that is produced by diffusion. This approach can cause significant hypotension and discomfort in the form of nausea, vomiting, muscle cramping, fatigue, and dizziness.

Since the early 1980s, high-sodium bicarbonate-based dialysate has mostly eliminated hypotension and discomfort during hemodialysis. However, the widespread use of these

high-sodium solutions has caused dialysis salt loading with resultant postdialysis thirst, interdialytic weight gain, and hypertension [8] . The problem of postdialytic weight gain and

hypertension is mostly seen in the chronic hemodialysis population, but can also have bearing in the acute setting, particularly in patients with an intact thirst mechanism and the

ability to drink fluid based on their thirst.

During acute intermittent hemodialysis, particularly in the ICU setting, hypotension is common since patients usually have compromised hemodynamic factors due to cardiac, hepatic, infectious, or bleeding complications. The hypotension that can develop during maximal rates of solute removal often compromises clearance and ultrafiltration targets.

To avoid hemodynamic instability during acute intermittent hemodialysis, sodium modeling can be administered by utilizing a higher dialysate sodium concentration at the beginning of

hemodialysis and progressively decreasing it throughout the session to avoid lowering the plasma osmolarity abruptly.

A concise mechanism describing sodium profiling is best described by the following quotation [9]:

"A high dialysate sodium concentration is used initially with a progressive reduction toward isotonic or hypotonic levels by the end of the procedure. This method allows for a diffusive

sodium influx early in the session to prevent the rapid decline in plasma osmolality resulting from the efflux of urea and other small molecular weight solutes. During the remainder of

the procedure, when the reduction in osmolality accompanying urea removal is less abrupt, the lower dialysate sodium level minimizes the development of hypertonicity and any

resultant excessive thirst, fluid gain, and hypertension in the interdialytic period".

Although sodium modeling has been studied mostly in the chronic hemodialysis population, a randomized, cross-over study of 10 patients evaluated sodium modeling in acute renal

failure patients in the ICU [10] . The study used either a fixed dialysate sodium regimen (140 mEq/L) with a fixed ultrafiltration (UF) rate spread over the entire dialysis time, or a variable

dialysate sodium profile which varied dialysate sodium (160 mEq/L to 140 mEq/L) in a stepwise fashion. The group's UF profile was varied in a similar fashion to the sodium

profiling prescription (half of the fluid being removed during the first third of the treatment, and the remaining half over the last two thirds).

The following results were observed: Sodium modeling with variable UF rate was associated with greater hemodynamic stability compared to the fixed regimen. Significantly less

frequent interventions involving nursing and volume replacement was noted in the sodium modeling and variable UF rate arm. Relative blood volume changes were less during sodium

modeling .

The group concluded that sodium and ultrafiltration profiling may be the preferred dialysis prescription for ARF patients in the ICU at risk for hemodynamic instability while undergoing

intermittent hemodialysis [10].

Several sodium modeling prescriptions exist. Multiple sodium modeling prescriptions are programmed in most hemodialysis machines. Patients may respond to only one or all

available prescriptions. Thus, trials are required to find the best sodium modeling prescription in ARF patients on hemodialysis.

The same sodium modeling principles used for intradialytic hypotension in the chronic hemodialysis population can also be used in ARF patients. We recommend using combined

sodium and UF profiling if hypotension occurs while on intermittent hemodialysis (IHD) in the acute setting.

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 ultrafiltration rate is minimized or stopped. Ultrafiltration only

occurs during the high sodium period to draw out intracellular water due to the extracellular hypernatremia. Another sodium modeling prescription is to set the initial dialysate sodium

at a high level (eg, 150 to 160 meq/L). Subsequently, 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 pre-dialysis serum sodium

concentration (approximately within 1.0 to 2.0 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 [11] .

Other methods to treat hypotension are reviewed below. Since lower blood flows through the dialyzer may result in less hemodynamic instability, sustained low efficiency

hemodialysis (SLED) over 6 to 12 hours or continuous renal replacement therapy (CRRT) can be used if sodium modeling on IHD does not improve the blood pressure. (See "Sustained

low efficiency or extended daily dialysis").

Dialysate sodium composition — The choice of dialysate sodium concentration depends upon the predialysis serum sodium concentration, hemodynamic status, the diffusion

gradient for sodium, method of serum sodium measurement, and Gibbs-Donnan effect. Issues surrounding dialysate sodium concentration in patients with dysnatremias or

hemodynamic instability are discussed in the next and previous sections, respectively. (See "Dysnatremias" below and see "Sodium modeling and hemodialysis hypotension" above).

With respect to the additional factors that affect the choice of the dialysate sodium concentration: The diffusion gradient for sodium lies between its ionic activity in dialysate

and blood water [8,12] . Since laboratories use a variety of methods to measure serum sodium concentration (flame photometry, indirect ionometry and direct ionometry), there is

a subtly different relationship between the gradient and sodium ionic activity for each method used. The Gibbs-Donnan effect denotes the reduced sieving coefficient of the

dialysis membrane for sodium that arises as a result of negatively charged plasma proteins [13] .

As a result of all of these factors, a high sodium dialysate for the majority of patients would be characterised by a sodium concentration of approximately 141 mEq/L, and a low sodium

dialysate by a sodium concentration of approximately 137 mEq/L. For individual patients, the dialysate sodium concentration that results in no net transfer of sodium has been

estimated in various studies to be between 0.1 to 3.0 mEq/L below that of the pre-dialysis serum sodium concentration [11,14-16] . For most patients with normal or near-normal

serum sodium levels, we use a sodium dialysate concentration of approximately 137 mEq/L.

Dysnatremias — Rapid correction of an abnormal serum sodium concentration should be avoided during dialysis to avoid neurologic complications [17] . Failure to adjust the dialysis prescription may lead to cerebral edema in the patient with severe chronic hypernatremia

and osmotic demyelination (pontine and extrapontine myelinolysis) in the patient with severe chronic hyponatremia. Although uremia may provide some protection against

osmotic demyelination, case reports of this complication following dialysis of severely hyponatremic patients lead us to recommend a cautious approach in most patients.

The overall dialysis strategy for the management of dysnatremias is the same as that in the non-dialysis general population. Large, rapid changes in the serum sodium concentration are

very rarely indicated.

Only patients with hyperacute salt poisoning (eg, due to the suicidal ingestion of sodium chloride or the inadvertent intravenous 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 ever be allowed to undergo aggressive initial correction of their serum sodium concentration. In such patients with hyponatremia, for example,

aggressive initial correction at a rate of 1.5 to 2 meq/L per hour, may be indicated for the first three to four hours or until the symptoms resolve. However, the plasma sodium

concentration should probably be raised by less than 10 meq/L in the first 24 hours and less than 18 meq/L in the first 48 hours. (See "Treatment of hyponatremia").

In the vast majority of patients with more chronic dysnatremias, the treatment during a single dialysis session should be adjusted to provide a rate of correction that does not

exceed the generally recommended rate. If the serum sodium concentration is very high or very low, it may be impractical to avoid a rapid change solely by adjusting the dialysate

sodium concentration. In many such patients, it may be necessary to either cut the dialysis session short or to offset the effect of dialysis by concurrent infusions of hypertonic saline or D5W. Hourly measurements of the serum sodium concentration during the course of dialysis

are mandatory. (See "Treatment of hyponatremia", section on rate of correction).

Another possibility is to use continuous renal replacement therapy. This modality is far less efficient at changing serum sodium concentrations, which may therefore change more

slowly than with the use of intermittent hemodialysis.

Some authorities also favor the following approach [18] : Among patients with severe chronic hyponatremia (predialysis serum sodium level less than 130 meq/L), a cautious

strategy is to set the dialysate sodium concentration at a level that is no higher than 15 to 20

meq/L above the plasma level of the patient [18] . The goal would be correction of the hyponatremia only after multiple hemodialysis sessions that are performed over a period of several days. In those with hypernatremia, 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. Thus, a reasonable and safe

approach would be to use a dialysate sodium concentration within 2 meq/L of the plasma sodium concentration in the first dialysis session. Subsequently, correction of the

hypernatremia could be performed with the administration of hypotonic solutions. (See "Treatment of hypernatremia") .

Buffer solutions — Acetate was the predominant buffer used during the early days of hemodialysis. However, acetate is presently not routinely used because of associated cardiac

and hemodynamic instability.

The main dialysate buffer currently used in IHD is bicarbonate. This buffer is inexpensive and generally well tolerated without the hemodynamic problems seen with acetate.

The main disadvantage of bicarbonate is that it precipitates as an insoluble salt when stored together with divalent cations calcium and magnesium, thereby requiring the buffer and electrolytes to be stored separately prior to hemodialysis [19] . In addition, possible side

effects with bicarbonate include hypoxemia due to decrease respiratory drive with higher pH, and altered mental status, weakness, cramping, and lethargy due to acute metabolic

alkalosis [20].

The dialysate bicarbonate concentration should vary based upon the acid-base status of the patient. The usual dialysate bicarbonate concentration in chronic hemodialysis is

approximately 33 to 35 mEq/L. We suggest that this high concentration bicarbonate solution be used in cases of moderate metabolic acidosis in ARF. In severe metabolic acidosis, the

concentration of the bicarbonate solution may be maximized (eg, 40 mEq/L) and extended duration of hemodialysis may be necessary. In addition, in patients being mechanically

ventilated using low-tidal volume ventilation, an increased dialysate bicarbonate concentration may be required to compensate for the respiratory acidosis resulting from "permissive hypercapnea." 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.

Acute hemodialysis patients can also be alkalemic. The severity of the alkalemia and the process generating the alkalosis are the main issues to help determine the optimal dialysate bicarbonate concentration. In particular, the clinician must investigate whether there is on-

going generation versus a one-time insult causing the alkalosis. A one-time insult can be resolved with a single hemodialysis treatment, whereas on-going generation of alkalosis may

require frequent and/or long hemodialysis sessions with a lower bicarbonate dialysate.

If the predialysis serum bicarbonate level is above 28 mEq/L or respiratory alkalosis is present, the usual dialysate bicarbonate concentration should not be used [21] . In this

setting, a lower bicarbonate dialysis concentration would be appropriate.

Modern machines can adjust dialysate bicarbonate in 1 mEq/L increments (from 40 to 20 mEq/L). In addition, the frequency and duration of the dialysis treatment(s) as well as the

volume of ultrafiltrate must all be considered when determining the specific concentration of bicarbonate in the dialysate.

Calcium — In chronic hemodialysis patients, the standard dialysate calcium concentration is 2.5 meq/L. In addition to helping manage secondary hyperparathyroidism, this level is used to avoid the development of hypercalcemia and elevated calcium-phosphorus product that can occur with higher dialysate calcium concentrations. (See "Active vitamin D analogs and

calcimimetics to control hyperparathyroidism in chronic kidney disease").

In the acute hemodialysis setting, the dialysate calcium concentration may be chosen to treat the presence of either hypo- or hypercalcemia. According to some authorities, the

dialysate calcium concentration for acute hemodialysis should be 3.0 to 3.5 meq/L, and the routine use of the standard concentration for chronic hemodialysis is inappropriate

considering the risk of developing hypocalcemia in the acute setting [21] . In addition, a higher dialysate calcium concentration used in the setting of predialysis hypocalcemia may

prevent further worsening of hypocalcemia with the correction of acidosis [21].

A higher dialysate calcium concentration can also improve intradialytic hypotension by improving cardiac performance. As an example, one prospective crossover study compared

the effect of high dialysate calcium concentration (3.5 meq/L) with low dialysate calcium concentration (2.5 meq/L) on hemodynamic stability in patients on IHD [22] . The study

patients had a history of intradialytic hypotension and were also administered therapy with either midodrine, cool dialysate, or a combination of these two therapies.

Compared with low-dialysate calcium, the following results were reported: High-dialysate calcium significantly increased posthemodialysis mean arterial pressure (MAP). High-

dialysate calcium improved the lowest intradialytic MAP, but was not statistically significant. The improvements in blood pressure with high-dialysate calcium were not associated with

similar reductions in symptoms or interventions for intradialytic hypotension .

Hypocalcemia is fairly common in ICU patients, particularly those with sepsis [23] . This combination is reportedly associated with increased mortality [24].

This observation has led some to postulate that treatment of hypocalcemia in those with sepsis may improve outcomes. However, calcium administration to rodents with sepsis

appears to be harmful [25,26] . Its administration may therefore be associated with higher mortality in critically ill patients with sepsis. Thus, administering calcium to treat

hemodynamic instability during acute intermittent hemodialysis may be harmful to septic patients and should be considered carefully. (See "Management of severe sepsis and septic

shock in adults")

Since total plasma calcium levels are poorly predictive of the ionized

level, the ionized plasma calcium level should be measured prior to

hemodialysis in acutely ill patients with significant hypocalcemia or

hypercalcemia. This is particularly important since acute phase

responses (eg, sepsis) and changes in pH during dialysis and mechanical

ventilation can affect ionized calcium levels independent of the total

plasma calcium concentration. (See "Relation between total and ionized plasma calcium concentration")

We suggest the following concerning the dialysate calcium concentration: We favor adjusting the dialysate calcium concentration to avoid hypercalcemia or clinical

hypocalcemia. If the measured total plasma calcium level is used in this setting (although ionized plasma calcium is preferred), it is important that this level is corrected based upon

the serum albumin level and other factors given that the total plasma calcium concentration will change in parallel to the albumin concentration. (See "Relation between total and

ionized plasma calcium concentration", for details concerning this issue and the correction formula). We use a dialysate calcium concentration of 3.0 to 3.5 mEq/L in the patient with

significant hypocalcemia (total plasma calcium level <8.0 mg/dL [<2.0 mmol/L]), particularly if the patient is symptomatic. If the patient has severe hypercalcemia (total plasma calcium

level >12.0 mg/dL [>3.0 mmol/L]), we use a dialysate calcium concentration of 2.0 to 2.5 mEq/L. For patients with mild hypocalcemia, normocalcemia, or mild hypercalcemia (total

plasma calcium level between 8.0 to 12.0 mg/dL [2.0 to 3.0 mmol/L]), we use a dialysate calcium concentration of 2.5 mEq/L. To treat intradialytic hypotension, increasing the

dialysate calcium may be used in combination with sodium profiling and a lower dialysate temperature. We do not use a dialysate calcium concentration above 3.5 mEq/L for this

purpose. The development of hypercalcemia must be avoided with this strategy. However, the ideal level of ionized calcium in critically ill patients is not known, and may not be the

same as in normal subjects. (See "Ultrafiltration and blood pressure control" below and see "Dialysate sodium composition" above) .

BLOOD FLOW RATE — Deciding upon the optimal blood flow rate through the dialyzer is determined by various factors. For patients with chronic kidney disease who are initiated on

hemodialysis, the blood flow rate is increased incrementally over several sessions to avoid the rapid removal of accumulated blood solutes that can lead to the development of the

dialysis disequilibrium syndrome and to evaluate the angioaccess. (See "Dialysis Disequilibrium Syndrome").

With ARF, blood solutes have usually not had time to accumulate to the degree observed in the ESRD population. However, if the BUN has been >100 mg/dL for at least three days in

the patient with ARF, there may be enough osmole accumulation in the CNS to justify a slow removal for the first and second dialysis sessions. Thus, lower blood flow rates should be

prescribed at the initiation of therapy in such patients.When this is not necessary, high blood flow rates can be initiated at the onset of acute IHD without fear of precipitating the

disequilibrium syndrome. (See "Dialysis Disequilibrium Syndrome").

Blood flow rate in acute hemodialysis is dependent upon temporary dialysis catheter performance, length, and location. Dialysis catheters must be long enough to reach either the superior vena cava (SVC) or inferior vena cava, where the venous blood flows are the

highest. Left-sided internal jugular (IJ) and subclavian catheters tend to provide unreliable blood flow, at a rate that is typically up to 100 mL/min lower than elsewhere because their

tips abut the walls of either the SVC or innominate vein [27] . The best blood flows are attained with femoral vein and right-sided IJ catheters. (See "Acute hemodialysis vascular

access", for a detailed discussion of these issues).

Higher blood flows are necessary during IHD to provide sufficient overall solute clearance because of the relatively shorter duration of the session, whereas lower blood flows are

sufficient to achieve adequate clearance by CRRT due to its continuous nature [27] . However, the use of higher blood flows with IHD may result in rapid reduction in serum

osmolality promoting water movement into cells, thus reducing effective circulating volume.

This may exacerbate intradialytic hypotension despite measures to treat intradialytic hypotension, particularly in critically ill patients suffering from septic shock, cardiac

decompensation, bleeding, or hepatic insufficiency. Non-compliant dialyzers, smaller surface area dialyzers, and ultrafiltration control minimize the need to decrease blood flow rate.

We use a dialysis blood flow rate of 400 mL per minute. If a lower blood flow (or lower ultrafiltration rate) is required because of hemodynamic instability, the best dialysis

modality is unclear. Until further data are available, we suggest slower solute removal over six to 12 hours by sustained low-efficiency dialysis (SLED) or by continuous renal

replacement therapy (CCRT). (See "Continuous renal replacement therapy in acute kidney injury (acute renal failure)" and see "Renal replacement therapy (dialysis) in acute kidney injury (acute renal failure): Indications, timing, and dialysis dose", section on CRRT versus

intermittent hemodialysis).

DIALYSATE TEMPERATURE — Vasoconstriction due to lower body temperatures has been used to increase vascular resistance and improve hemodynamic stability during IHD in ESRD. Cool temperature dialysate typically uses a temperature of 35.0 degrees Celsius, which may

be associated with symptoms. (See "Cool temperature hemodialysis: Hemodynamic effects", for a discussion of this issue).

Hypothermia, however, may be undesirable in critically ill patients due to adverse effects upon myocardial function, end-organ perfusion, blood clotting, and possibly renal recovery

[28] . With blood temperature monitoring, the patients' blood temperature is maintained precisely at target value by a series of feedback loops controlling thermal transfer to and

from the dialysate [29] . It is effective in ameliorating hemodynamic instability for ESRD patients [30].

Blood temperature monitoring might conceivably allow for controlled cooling in critically ill ARF patients without the risk of hypothermic damage. However, it has not been evaluated in this setting. Our recommendations concerning the use of cold temperature hemodialysis are

presented in the next section.

ULTRAFILTRATION AND BLOOD PRESSURE CONTROL — Determining optimal ultrafiltration (UF) requirements in critically ill ARF patients is challenging. This is determined in part by

physical examination, laboratory values, and hemodynamic indices. In general, no one specific test or parameter is sufficient in isolation.

The following two over-riding principles should be recognized: The target weight in ESRD patients undergoing chronic maintenance dialysis 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, extracellular volume status in critically ill ARF patients is not necessarily an end-point itself. The volume expansion that is frequently observed in such patients is often necessary to maintain optimal circulatory and

oxygen transport status. The clinician should appreciate that the relationship between blood volume and hypotension is different in patients with ESRD and critically ill individuals with

ARF. Autonomic function and circulating humoral agents all mediate and mitigate this relationship, and these factors are not comparable between the two groups. This can be illustrated by considering blood volume monitoring, which is a biofeedback system that

automatically adjusts ultrafiltration rate and dialysate sodium content in response to a fall in circulating intravascular volume. Although these systems can convincingly reduce the occurrence of intradialytic hypotension in ESRD patients [31] , they are ineffective for

ameliorating hypotension in critically ill ARF patients [32] . 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 ESRD patients. However, in hemodynamically unstable

patients, target intravascular volume should be titrated to invasive or non-invasive (bio-impedance analysis, pulse contour analysis [PiCCO], or echocardiography) monitoring, which

should guide the UF goals for a given IHD session.

Ultrafiltration during IHD can result in significant intradialytic hypotension, which can be treated by reducing or discontinuing ultrafiltration, and/or a reducing the blood flow rate. In

addition to these maneuvers, modifying other dialysis-dependent factors of intradialytic hypotension (eg, cooling dialysate temperature and improving autonomic reflexes) can help

deliver effective hemodialysis while optimizing ultrafiltration and hemodynamic tolerance.

In order of efficacy, the following measures help prevent intradialytic hypotension during IHD in ARF: Minimize UF rate requirements by increasing frequency of treatments and/or

increased duration of treatments Sodium/ultrafiltration profiling Cool temperature dialysate Higher dialysate calcium concentration Midodrine (alpha-1 adrenergic agonist used in autonomic dysfunction), which may be administered in the absence of more powerful

pharmacologic forms of pressor support .

(See "Hemodynamic instability during hemodialysis: Overview" for further discussion concerning intradialytic hypotension in patients undergoing chronic intermittent

hemodialysis.)

We recommend initially treating intradialytic hypotension with the first three measures listed above. In addition to these interventions, normal saline intravenous boluses given

during hemodialysis can transiently increase blood pressure.

Despite the above-mentioned measures, 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 IHD sessions are not successful, switching to SLED or CRRT

usually improves hemodynamics while maintaining an acceptable rate of ultrafiltration and solute clearance.

ANTI-COAGULATION — Issues surrounding anti-coagulation in patients undergoing acute hemodialysis are presented separately. (See "Hemodialysis Anticoagulation")

PRE- AND POSTHEMODIALYSIS LABORATORY VALUE MONITORING — Specific laboratory values are usually required either before or after an acute hemodialysis session. A predialysis

basic metabolic profile should be reviewed prior to some acute hemodialysis sessions since electrolyte and acid/base status can profoundly change between treatments and require

alterations to the dialysate bath.

Drug monitoring — Therapeutic drug monitoring levels can be measured posthemodialysis to help guide supplemental dosing. The following equation can be used to calculate the

supplemental dose that takes the patient from the measured level to the desired peak level of drug [33]:

   Supplemental Dosage = Vd * IBW * (Desired Peak Level – Measured Level)

where Vd is the volume of distribution of the drug and IBW is the ideal body weight.

As an example, a patient with an ideal body weight of 70 kg is receiving Vancomycin, with the Vancomycin Vd 0.75, and the measured Vancomycin level of 12 mg/L. The desired

Vancomycin peak level in this case is 30 mg/L. The calculated supplemental dose of Vancomycin would be 945 mg after hemodialysis to achieve a peak level of 30 mg/L.

DIALYSIS DOSE — Dialysis dose in acute renal failure is increasingly recognized as an important issue. This is briefly reviewed in this section, and in detail separately. (See "Renal

replacement therapy (dialysis) in acute kidney injury (acute renal failure): Indications, timing, and dialysis dose").

The delivered IHD dose tends to be low in critically ill ARF patients, and lower than that prescribed [34,35,35] . Two studies support a relationship between acute IHD dose and

mortality: A retrospective observational study showed that a delivered single pool Kt/V >1.0 per treatment was associated with significantly improved outcome in patients with

intermediate illness severity [36] . This study did not attempt to relate outcomes to the frequency of IHD. A prospective controlled trial demonstrated substantially improved

outcomes with a cumulative single pool Kt/V of 6.0 per week versus 3.0 per week (by simple addition), and daily versus alternate day treatments [37] . Despite initial concerns about the

study conduct and methods, there is now general acceptance of this result. However, the time averaged BUN in the lower dose group (approximately 100 mg/dL) indicates under-

dialysis by modern standards, probably exaggerating the benefit in the higher dose group .

As described elsewhere in UpToDate, the VA/NIH Acute Renal Failure Trial Network (ATN) study did not find a difference in mortality associated with a more intensive dosing strategy for renal replacement therapy. Based on the results of the ATN study, we recommend that

intermittent hemodialysis be provided three times per week with monitoring of the delivered dose of therapy to ensure a minimum delivered Kt/V of 1.2 per treatment. There is

no evidence that more frequent hemodialysis is associated with improved outcomes unless necessitated for specific indications (eg, hyperkalemia, volume excess, hypotension, etc).

(See "Renal replacement therapy (dialysis) in acute kidney injury (acute renal failure): Indications, timing, and dialysis dose").

SUMMARY AND RECOMMENDATIONS Indications for renal replacement therapy (RRT) in patients with acute renal failure (ARF) generally include volume overload refractory to

diuretics, hyperkalemia, metabolic acidosis, uremia, and toxic overdose of a dialyzable drug. (See "Indications" above and see "Renal replacement therapy (dialysis) in acute kidney injury (acute renal failure): Indications, timing, and dialysis dose"). Once the decision to initiate RRT

has been made, the specific modality of dialytic support must be chosen. This includes peritoneal dialysis or hemodialysis and its variations (eg, hemofiltration), and the acute

dialysis prescription determined. (See "Modality" above and see "Continuous renal

replacement therapy in acute kidney injury (acute renal failure)"). When acute hemodialysis is chosen as the dialytic support modality, vascular access must be established prior to

initiating treatment. Placement of the venous dialysis catheter must be considered carefully. (See "Vascular access" above and see "Acute hemodialysis vascular access"). In the setting of

ARF, the optimal choice of artificial dialysis membrane is unclear. We suggest that biocompatible dialysis membranes be used in this setting. If the water system is of high

quality, high flux biocompatible dialysis membranes should be used. By comparison, low flux biocompatible dialysis membranes or a prefilter added to the dialysis machine should be

used if the water system is not of high quality. (See "Hemodialyzer membranes" above). The dialysate solution composition consists of potassium, sodium, bicarbonate buffer, calcium,

magnesium, chloride, and glucose. The dialysate composition in acute hemodialysis is routinely altered each treatment to correct the metabolic abnormalities that can rapidly

develop during ARF. (See "Dialysate composition" above). There is not a standard or fixed dialysate potassium concentration in the acute hemodialysis prescription because of wide

variability in the serum potassium level prior to initiating the hemodialysis session. The typical potassium concentration in the dialysate for acute hemodialysis ranges from 2.0 to

4.0 mEq per L. The dialysate bath potassium is determined by both the absolute predialysis serum potassium and the rate of rise in the inter-dialytic period. A rapid rate of rise of the

serum potassium may best be treated by daily hemodialysis rather than lowering the dialysate potassium bath concentration. (See "Potassium dialysate composition" above). The

hemodialysis treatment can provoke ventricular arrhythmias, which are related to dialysis-induced reductions in the serum potassium. They are independently associated with

numerous risk factors such as coronary artery disease, left ventricular hypertrophy (LVH), digoxin use, systolic blood pressure, and advanced age. We therefore recommend that patients with underlying cardiac disorders who undergo acute hemodialysis should be

placed on a cardiac rhythm monitor during the dialysis session. (See "Complications with potassium removal" above). The choice of the dialysate sodium concentration can have a

significant impact on the patient's volume and hemodynamic status. (See "Sodium modeling and hemodialysis hypotension" above). The dialysate bicarbonate concentration should vary

based upon the acid-base status of the patient. The usual dialysate bicarbonate concentration in chronic hemodialysis is approximately 33 to 35 mEq/L. We recommend that

this high concentration bicarbonate solution be used in cases of moderate metabolic acidosis in ARF. In severe metabolic acidosis, the concentration may be maximized (eg, 40

mEq/L) and extended duration of hemodialysis may be necessary. Acute hemodialysis patients can also be alkalotic. The severity of the alkalosis and the process generating the

alkalosis are the main issues to help determine the optimal dialysate bicarbonate concentration. (See "Buffer solutions" above). We recommend adjusting the dialysate

calcium concentration to avoid hypercalcemia or clinical hypocalcemia. (See "Calcium" above). We use a dialysis blood flow rate of 400 mL per minute. If a lower blood flow rate is

required because of hemodynamic instability, the best dialysis modality is unclear and the subject of ongoing study. Until further data are available, we suggest slower solute removal

over six to 12 hours by sustained low-efficiency dialysis (SLED) or by continuous renal replacement therapy (CCRT). (See "Blood flow rate" above). Determining the ultrafiltration goals in ARF patients can be challenging. The estimation of target intravascular volume will

guide the ultrafiltration goals for a given intermittent hemodialysis session. Ultrafiltration

during IHD can result in significant intradialytic hypotension. This can be treated by minimizing UF rate requirements by increasing frequency of treatments and/or increased

duration of treatments, as well as sodium/ultrafiltration profiling, and using cool temperature dialysate. (See "Ultrafiltration and blood pressure control" above). We

recommend that intermittent hemodialysis be provided at least three-times per week (alternate days) with monitoring of the delivered dose of dialysis to ensure delivery of a Kt/V

of at least 1.2 per treatment (Grade 1B). (See "Dialysis dose" above). However, more frequent dialysis may be necessary for specific clinical scenarios, such as intractable

hyperkalemia, volume overload, or severe hypotension .

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