10/12/23, 7:22 PM Therapeutic apheresis (plasma exchange or cytapheresis): Indications and technology - UpToDate

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Therapeutic apheresis (plasma exchange or

cytapheresis): Indications and technology
AUTHORS: Joy L Fridey, MD, Andre A Kaplan, MD
SECTION EDITOR: Lynne Uhl, MD
DEPUTY EDITOR: Jennifer S Tirnauer, MD

All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: Sep 2023.

This topic last updated: Sep 29, 2023.

INTRODUCTION

Therapeutic apheresis (TA) is an extracorporeal treatment that selectively removes abnormal

cells or substances in the blood that are associated with or cause certain disease states. It
can also be used to administer cells or plasma constituents that are present in
subtherapeutic concentrations.

An overview of indications for which TA is used and practical information for performing
apheresis are presented here. Many indications for TA are presented in separate reviews
about specific clinical conditions treated with TA.

Complications of TA are discussed separately. (See "Therapeutic apheresis (plasma exchange

or cytapheresis): Complications".)

TERMINOLOGY

The following terminology is used to describe procedures related to apheresis and TA:

● Apheresis – A general term for "taking away" a targeted cell type or substance from
blood. Apheresis includes plasmapheresis (plasma) and cytapheresis (blood cells).

● Plasmapheresis – A general term to denote selective removal of plasma. Plasma can

be separated from blood with centrifugation or filtration. Plasmapheresis is mostly
used to collect plasma from a healthy blood donor for transfusion (ie, plasma
donation). (See "Clinical use of plasma components", section on 'Plasma products'.)
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● Therapeutic apheresis (TA) – A general phrase that denotes replacement of plasma

with another fluid such as colloid, crystalloid, or allogeneic plasma; or removal or
replacement of abnormal or excessive cells for the purpose of achieving a clinical
benefit.

● Therapeutic plasma exchange (TPE) – This phrase was historically used synonymously
with "therapeutic apheresis" because generally only plasma was used as replacement
fluid. However, TPE is now applied specifically to procedures that involve replacement
solely with plasma. TPE is also referred to as plasma exchange or therapeutic
plasmapheresis and involves removal of patient plasma and replacement with
allogeneic or autologous plasma. Plasma removed during plasma exchange must not
be used for transfusion to another individual, according to regulations from the US
Food and Drug Administration (FDA).

● Therapeutic cytapheresis (hemapheresis) – A term used to denote selective removal

of abnormal blood cells (eg, sickled cells [erythrocytapheresis, red blood cell exchange])
or excessive numbers of cells (eg, platelets [thrombocytapheresis], white blood cells
[leukocytapheresis]).

● Dialysis – A diffusion-based treatment best suited for the removal of fluid or small
molecules (eg, uremic toxins, some drugs) from the blood using a filter. Fluid is
removed by filtration (convection); solutes are removed by diffusion.

● Plasma filtration – A technique that separates plasma from cellular components with a
highly permeable filter (plasma filter) using a dialysis or hemofiltration machine. (See
"Therapeutic plasma exchange (plasmapheresis) with hemodialysis equipment".)

OVERVIEW OF INDICATIONS

Rationale and benefits of therapeutic apheresis — The basic premise of TA is that by

removing or decreasing levels of certain pathologic substances from the plasma, prevention
of further damage or reversal of a pathologic process can occur ( table 1). The pathologic
substance may be an autoantibody, immune complex, cryoglobulin, myeloma light chains,
endotoxin, cholesterol-containing lipoprotein, or other substances.

TA involves the passing of venous blood through an extracorporeal device that separates
blood into its components, cells and plasma, shunts much of the targeted pathologic cells or
plasma into a discard container and returns most of the remaining blood to the patient
along with replacement fluid and normal cells and a short-acting anticoagulant, usually
citrate.

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Potential replacement fluids include the patient's own plasma from which an unwanted
substance has been removed, or allogeneic (donor) plasma, colloid, or crystalloid. In some
cases, use of allogeneic plasma is preferred because it provides needed proteins,
immunoglobulins, clotting factors, or other substances. However, allogeneic plasma should
only be used as replacement fluid for specific indications such as thrombotic
thrombocytopenic purpura (TTP) that is associated with ADAMTS13 deficiency. In other
clinical situations, use of appropriate non-plasma replacement fluid eliminates unnecessary
exposure to allogeneic plasma.

At least one of the following conditions must be present for therapeutic plasma exchange
(TPE) to be considered as a rational therapeutic choice:

● The substance targeted for removal must have a sufficiently long half-life so that
extracorporeal removal is more rapid than endogenous clearance pathways.

● The substance to be removed must be acutely toxic and/or resistant to conventional

therapy so that rapid elimination from the extracellular fluid by TA is indicated.

● The substance to be removed should be large, with a molecular weight >15,000

daltons, so that it cannot be easily removed by less expensive purification techniques
such as hemofiltration or high-flux hemodialysis.

TA is highly effective for the removal of pathologic autoantibodies. Immunoglobulin G (IgG)

has an average molecular weight >150,000 daltons and a half-life of approximately 21 days
[1]. Thus, even if immunosuppressive therapy could immediately inhibit new antibody
production, the plasma concentration would decrease by only approximately 50 percent
within 21 days. Such a delay may not be acceptable with an aggressive autoantibody such as
that seen in anti-glomerular basement membrane (anti-GBM) antibody disease. (See "Anti-
GBM (Goodpasture) disease: Treatment and prognosis".)

TA has other potential benefits, including unloading of the reticuloendothelial system, which
can enhance endogenous removal of circulating toxins; stimulation of lymphocyte clones to
enhance cytotoxic therapy; and the possibility of reinfusing plasma volumes in such a way
that the risk of intravascular volume overload can be decreased [2,3].

The infusion of allogeneic plasma is particularly important in immune or congenital TTP. For
immune TTP, TPE using plasma as replacement fluid may be lifesaving. TPE works in TTP
both by removing very high molecular weight von Willebrand factor (VWF) multimers and
autoantibodies against ADAMTS13 (the VWF multimer-cleaving protease), as well as by
providing ADAMTS13. (See "Immune TTP: Initial treatment".)

For some indications, TA is considered first-line therapy (eg, TTP, acute Guillain-Barré
syndrome), whereas for others such as light chain cast nephropathy in multiple myeloma,

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apheresis may need to be used in combination with other established treatments such as
chemotherapy to inhibit antibody production. (See "Kidney disease in multiple myeloma and
other monoclonal gammopathies: Treatment and prognosis", section on 'Extracorporeal
methods for light chain removal'.)

Common uses of therapeutic apheresis — In the United States, most TA procedures are
performed for neurologic, immunologic, or hematologic diseases ( table 2). A collaborative
survey by the Association for the Advancement of Blood & Biotherapies (AABB) and the
American Society for Apheresis (ASFA) showed that more than one-half of all procedures
were performed for neurologic conditions such as Guillain-Barré syndrome or myasthenia
gravis [4,5].

The Canadian Apheresis Group has reported a growing use of TA for hematologic disorders,
which constituted 55 percent of all TA procedures in 2003; use of TA for neurologic
conditions had decreased from 50 percent in 1988 to 40 percent in 2003 [6,7]. This change
reflects the growing use of evidence-based practice and advances in pharmacologic
treatments that in some instances replace apheresis as standard treatment for some
conditions.

The more common indications for TA are discussed in separate topic reviews. Examples
include the following:

● Immune thrombotic thrombocytopenic purpura (TTP) – (See "Immune TTP: Initial

treatment" and "Thrombotic microangiopathy after kidney transplantation".)

● Renal diseases – (See "Granulomatosis with polyangiitis and microscopic polyangiitis:

Induction and maintenance therapy" and "Anti-GBM (Goodpasture) disease: Treatment
and prognosis".)

● Hyperviscosity – (See "Treatment and prognosis of Waldenström macroglobulinemia"

and "Kidney disease in multiple myeloma and other monoclonal gammopathies:
Treatment and prognosis".)

● Neurologic syndromes – (See "Guillain-Barré syndrome in adults: Treatment and

prognosis" and "Overview of the treatment of myasthenia gravis" and "Chronic
inflammatory demyelinating polyneuropathy: Treatment and prognosis".)

Previously, multiple sclerosis, systemic lupus erythematosus, and rheumatoid arthritis were
treated with TA, but this practice often was not based on data from controlled studies. Use of
this complex and expensive treatment in the absence of supporting data prompted the
development of evidence-based guidelines rather than reliance on anecdotal reports or data
from small series or uncontrolled trials ( table 2). (See 'ASFA therapeutic categories' below.)

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Common uses of therapeutic cytapheresis — In contrast to routine TA, therapeutic

cytapheresis is used to lower abnormally high cell counts and to remove abnormal cells such
as in sickle cell disease, in which sickle hemoglobin (Hb S)-containing cells can be removed
and simultaneously replaced with blood cells (RBC) from blood donors who lack the Hb S
variant.

In most conditions, a complete blood count (CBC) will demonstrate whether cell counts have
been lowered.

● For hyperleukocytosis, the post-procedure target white blood cell count (WBC) is
<100,000/microL.
● For thrombocytosis, the target platelet count is <1,000,000/microL [8].

For RBC exchange in sickle cell disease, the total Hb and percent of Hb S are measured to
determine the efficacy of apheresis. (See "Red blood cell transfusion in sickle cell disease:
Indications and transfusion techniques", section on 'Simple versus exchange transfusion'.)

ASFA therapeutic categories — A comprehensive review of indications for TA based on

literature reviews is published approximately every two to three years by the American
Society for Apheresis (ASFA) [9-13]. Conditions are assigned to one of four categories based
on evidence of clinical efficacy as determined by evaluation of peer-reviewed literature.
These guidelines are not intended to mandate TA for conditions in which it is clearly not
effective, nor are they intended to deny or exclude patients from receiving TA when a benefit
may be potentially achievable. Given the complexity and expense of the procedure, however,
the guidelines provide a framework for clinical decision-making.

ASFA categorizations are summarized in the 2023 guidelines (9th edition) ( table 2) [13].

The categories are defined as follows:

● Category I – Disorders for which apheresis is accepted "as first-line therapy, either as
primary stand-alone treatment or in conjunction with other modes of treatment."
Examples include TA in Guillain-Barré syndrome or immune TTP, and
erythrocytapheresis in sickle cell disease with certain complications such as stroke. (See
"Red blood cell transfusion in sickle cell disease: Indications and transfusion
techniques", section on 'Exchange blood transfusion'.)

● Category II – Disorders for which apheresis is accepted "as second-line therapy,"

either as a stand-alone treatment or in conjunction with other treatments. Examples
include TA for life-threatening hemolytic anemia for cold agglutinin disease or Lambert-
Eaton myasthenic syndrome. (See "Lambert-Eaton myasthenic syndrome: Treatment
and prognosis", section on 'Plasma exchange'.)

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● Category III – Disorders for which the "optimum role of apheresis therapy is not
established." Decision-making should be individualized. Examples include TPE for
hypertriglyceridemic pancreatitis or extracorporeal photopheresis for nephrogenic
systemic fibrosis. (See "Hypertriglyceridemia-induced acute pancreatitis", section on
'Plasmapheresis' and "Nephrogenic systemic fibrosis/nephrogenic fibrosing
dermopathy in advanced kidney disease", section on 'Treatment'.)

● Category IV – Disorders for which "published evidence demonstrates or suggests

apheresis may be ineffective or harmful." Examples include TPE for active rheumatoid
arthritis.

The efficacy of TPE in some conditions and intoxications that are not addressed in the ASFA
guidelines are available in a separate publication [14].

Opinions and small studies regarding TA for treating coronavirus disease 2019 (COVID-19) or
COVID-19 syndromes such as cytokine release syndrome (CRS) or hyperviscosity have been
published, but standards-of-practice guidelines have not been determined. A 2021
International Society of Blood Transfusion (ISBT) Working Group preliminarily suggested a
role for TA in treating COVID-19-associated syndromes, particularly CRS, applying ASFA
guidelines for multiple organ dysfunction to assign a category III, 2B classification to COVID-
19-associated CRS; however, the authors cited lack of high-quality evidence for TA [15].

The value of the ASFA guidelines lies not only on the comprehensive nature of the literature
reviews but also the concise format for each listed disease state or condition. Categories and
recommendation ratings are provided for each condition, as well as a succinct literature
synopsis, evidence grading, and recommendations for the treatment schedule, replacement
fluids, exchange volumes, and procedure frequency.

TECHNOLOGY

Therapeutic plasma exchange (TPE) is most commonly performed with centrifugation

devices referred to as apheresis instruments, also used for blood component collection in
healthy donors. These instruments offer the additional advantage of allowing selective cell
removal (cytapheresis).

The use of a highly permeable filter with standard hemodialysis equipment is discussed
separately. (See "Therapeutic plasma exchange (plasmapheresis) with hemodialysis
equipment".)

Venous access — Successful TA requires reliable vascular access, which may consist of two
large, durable peripheral veins or a central dual-lumen catheter that is adequately rigid to
withstand significant flow pressures; appropriate lines are apheresis/dialysis catheters.
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Radiographic confirmation of catheter placement is critical to prevent perforation of adjacent

tissues or organs and also because cardiac arrhythmias may result if citrate anticoagulant,
which binds ionized calcium, is infused in close proximity to the sinoatrial node.

Use of peripheral veins may avoid complications associated with central venous catheters
but is associated with slower blood flow and longer procedures that may eventually render
peripheral veins ineffective or create patient discomfort. It may be more practical to insert a
central catheter to manage conditions that warrant several procedures over a longer period
of time.

Exchange volumes — For most conditions, it has become standard practice to perform 1 to
1.5 plasma volume exchanges per procedure. Exchange of the first 1 to 1.5 plasma volumes
removes the greatest concentration of the targeted substance, with diminishing amounts
removed in each subsequent exchange procedure. A single plasma volume exchange in an
average-sized adult uses approximately 3 liters of replacement fluid.

In general, large molecular weight compounds equilibrate slowly between the vascular
space and the interstitium. Thus, calculations of the rate of removal by TA can be simplified
to first-order kinetics. A single plasma volume exchange will lower plasma macromolecule
levels by 60 percent, and an exchange equal to 1.4 times the plasma volume will lower
plasma levels by 75 percent [16,17].

The following formula can be used to estimate the plasma volume in most adults [18]:

Estimated plasma volume (in liters) = 0.07 x weight (kg) x (1 - hematocrit)

The app of the American Red Cross Compendium of Transfusion Practice Guidelines, 4th
edition, offers a function for calculating total blood, red cell, and plasma volumes [19].

Exchanging more than 1 to 1.5 plasma volumes in a single treatment increases procedure
time, challenges patient tolerance, and increases cost. As an example, cell separators can
perform one complete volume exchange in 1.5 to 2 hours; two to three plasma exchanges
will double or triple the time required to perform the procedure.

Replacement fluids — The patient's fluid volume removed by apheresis must be replaced to
prevent marked volume depletion. Albumin (5 percent), normal saline, or a combination of
albumin and normal saline are the replacement fluids of choice for most conditions.

The optimal choice often varies with the clinical setting. Albumin is used for most conditions;
normal saline for hyperviscosity; and some combination of albumin and normal saline if cost
is a consideration.

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We prefer 5 percent albumin or a crystalloid-colloid (albumin-normal saline) combination as

the replacement fluid, rather than normal saline alone. It is generally recommended that
plasma only be used as the replacement fluid for conditions in which constituents of plasma
are necessary, such as in thrombotic thrombocytopenic purpura (TTP). Albumin 25 percent
should not be used unless it is diluted to 5 percent concentration by the hospital pharmacy.

● Five percent albumin – The advantages of 5 percent albumin are the markedly
lowered risks of pathogen transmission and anaphylactic reactions [20]. However, a
post-apheresis dilutional coagulopathy due to coagulation factor depletion and a net
loss of immunoglobulins can occur.

● Albumin-saline combination – When colloid and crystalloid solutions are used in

combination, the amount of colloid should not be less than 50 percent of the total
infused. An appropriate replacement solution would consist of 1:1 ratio of 5 percent
albumin to whole blood and a 2:1 ratio of saline to whole blood for the remainder. For
example, if a 3000 mL exchange is performed and 1500 mL of 5 percent albumin is
used, 3000 mL of saline solution should be used to replace the other 1500 mL of
patient fluid [8,21].

● Saline – Normal saline alone provides insufficient oncotic pressure and tends to lead to
significant edema and/or hypotension. Thus, we prefer 5 percent albumin or an
albumin-normal saline combination. However, there may be medically compelling
reasons for the use of normal saline in some cases, for example, if albumin is not
available or for complications such as allergies occurring with albumin or plasma.

● Plasma – Plasma can be provided in the form of Fresh Frozen Plasma (FFP), Plasma
Frozen Within 24 hours After Phlebotomy (PF24), Thawed Plasma, or other products.
(See "Clinical use of plasma components", section on 'Plasma products'.)

Plasma replaces proteins removed by apheresis so that significant depletion of

coagulation factors or immunoglobulins does not occur with multiple or consecutive
daily procedures. However, other complications are more common with plasma than
with albumin. (See "Therapeutic apheresis (plasma exchange or cytapheresis):
Complications", section on 'Donor plasma or red blood cell exposure'.)

Additional information about replacement fluids, apheresis schedules, and other technical
information have also been published for each listed condition by the American Society for
Apheresis (ASFA) [13].

Apheresis schedule — The TA schedule should be based on the nature of the targeted
pathologic substance and by the desired endpoint, (eg, clinical improvement or reduction in
the level of the pathologic entity). In immunologically mediated, paraproteinemic, or

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hyperviscosity conditions, immunoglobulin compartmental shifts, especially of IgG and IgM,

must be considered [8]. In many of these cases, TA only serves an adjunct role, as the
patients are receiving concomitant chemotherapy or immunosuppressive therapy.

● IgM – Approximately 75 percent of IgM is intravascular. As a result, only one or two

procedures are usually required to rapidly reduce IgM levels.

● IgG – Only 45 percent of IgG is intravascular, and within 48 hours, plasma IgG returns
to approximately 60 percent of the pre-apheresis level [14,17]. IgG production is also
characterized by a "rebound" phenomenon, especially if the patient is not on
immunosuppressive therapy. Consequently, a more rigorous regimen involving several
TA procedures and the institution of immunosuppressive therapy are important to
significantly reduce IgG levels [22].

If, as a result of concurrent immunosuppressive therapy, one assumes a negligible

production rate of immunoglobulin, and the rate of extravascular to intravascular
equilibration to be approximately 1 to 2 percent per hour, then five separate procedures over
7 to 10 days are required to remove 90 percent of the total initial body immunoglobulin
burden [23]. Additional treatments may be required if new antibody production occurs.

The AABB general recommendation for conditions requiring TA is that one exchange be
performed every second or third day, each exchange consisting of 1 to 1.5 plasma volumes
for, in most cases, a total of three to five procedures. Exceptions include the following:

● In immune TTP, TPE is usually performed daily. (See "Immune TTP: Initial treatment".)

● Treatment for Goodpasture's syndrome (anti-GBM mediated disease) is generally also

performed on a daily or every-other-day basis. (See "Anti-GBM (Goodpasture) disease:
Treatment and prognosis".)

Laboratory evaluation — Laboratory assessment is based on the desired endpoint of

therapy, the number of planned procedures, and the type of replacement fluid.

For TA performed without plasma, a baseline complete blood count (CBC), immunoglobulin
levels, and coagulation and electrolyte studies should be obtained. If serial or several closely
spaced procedures are planned, more frequent subsequent laboratory evaluation may be
warranted.

For therapeutic cytapheresis, the appropriate cell count determines adequacy of response.
(See 'Common uses of therapeutic cytapheresis' above.)

SUMMARY AND RECOMMENDATIONS

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● Definitions – Therapeutic apheresis (TA; plasma exchange or cytapheresis) is an

extracorporeal technique for the removal of large molecular weight substances or cells
from the blood or plasma, respectively. (See 'Terminology' above.)

● Indications (general principles) – For apheresis to be an appropriate therapeutic

choice, the substance to be removed should be sufficiently large so that it cannot be
easily removed by hemofiltration or high-flux hemodialysis, must have a sufficiently
long half-life, or must be acutely toxic and/or resistant to conventional therapy.
Examples include pathogenic autoantibodies, immune complexes, cryoglobulins,
myeloma light chains, endotoxin, cholesterol-containing lipoproteins. (See 'Rationale
and benefits of therapeutic apheresis' above.)

● Indications (cytapheresis) – Therapeutic cytapheresis (ie, removal of white blood cells,

platelets, or red blood cells) can be performed to reduce excessive numbers of cells or
pathologically abnormal cells; this may be used for hyperleukocytosis, marked
thrombocytosis, or red blood cell exchange transfusion. (See 'Common uses of
therapeutic cytapheresis' above.)

● ASFA categories – The American Society for Apheresis (ASFA) guidelines for TA are
based on literature reviews of multiple disease states. Conditions are assigned to one
of four categories based on evidence of clinical efficacy ( table 2). (See 'ASFA
therapeutic categories' above.)

● Venous access – Successful TA requires reliable vascular access with either two large,
durable peripheral veins or a central dual lumen catheter that is rigid enough to
withstand significant flow pressures. (See 'Venous access' above.)

● Choice of replacement fluid – The intravascular volume removed by TA must be

replaced to prevent marked volume depletion. Albumin, normal saline, or a
combination of albumin and normal saline are the replacement fluids of choice for
most conditions. Plasma is appropriate in some conditions that require replacement of
a plasma protein or substance with low or absent levels (eg, ADAMTS13 in immune
thrombotic thrombocytopenic purpura [TTP]). For most conditions, it should be
adequate to perform 1 to 1.5 plasma volume exchanges per procedure. A single plasma
volume exchange in an average-sized adult uses approximately 3 liters of replacement
fluid. (See 'Replacement fluids' above.)

● Frequency – The apheresis schedule should be determined by the patient's condition,

the pathologic substance targeted for removal, and the desired clinical and/or
laboratory endpoint. Only one or two procedures may be required to rapidly reduce
IgM levels; a more rigorous regimen involving several apheresis procedures may be
warranted to significantly reduce IgG levels. Adjunctive use of immunosuppressive

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therapy may be required, depending on the patient's diagnosis. (See 'Apheresis

schedule' above.)

● Complications – Complications of TA are discussed separately, including hypocalcemia;

depletion of coagulation factors, immunoglobulins, or medications; angiotensin-
converting enzyme (ACE) inhibitor-related symptoms; and adverse reactions to donor
plasma such as anaphylaxis, transfusion-related acute lung injury (TRALI), and exposure
to infectious pathogens. (See "Therapeutic apheresis (plasma exchange or
cytapheresis): Complications" and "Approach to the patient with a suspected acute
transfusion reaction".)

ACKNOWLEDGMENT

The UpToDate editorial staff acknowledges extensive contributions of Arthur J Silvergleid,

MD to earlier versions of this and many other topic reviews.

Use of UpToDate is subject to the Terms of Use.

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ican Red Cross, 2021.
20. Tabor E. The epidemiology of virus transmission by plasma derivatives: clinical studies
verifying the lack of transmission of hepatitis B and C viruses and HIV type 1.
Transfusion 1999; 39:1160.
21. Technical Manual, 11th ed, Walker RH (Ed), American Association of Blood Banks, Bethes
da 1993. p.37.

22. Therapeutic Apheresis, Kolins J, Jones JM (Eds), American Association of Blood Banks, Arli
ngton 1983. p.2.
23. Keller AJ, Urbaniak SJ. Intensive plasma exchange on the cell separator: effects on serum
immunoglobulins and complement components. Br J Haematol 1978; 38:531.

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Topic 7941 Version 32.0

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GRAPHICS

Pathologic substances removed by therapeutic apheresis

Pathologic substance Diseases

Immunoglobulins Hyperviscosity syndrome

Waldenström macroglobulinemia

Multiple myeloma

Autoantibodies Myasthenia gravis

Anti-GBM antibody disease

Systemic lupus erythematosus

Systemic vasculitis

Factor VIII inhibitors

Thrombotic thrombocytopenic purpura

Lipoproteins Hypercholesterolemia

Leukocytes Hyperleukemic leukostasis

Platelets Severe thrombocytosis

Abnormal red cells Sickle cell disease (pain crisis, acute chest syndrome,
stroke)

Circulating immune complexes Immune complex glomerulonephritis

Systemic lupus erythematosus

Systemic vasculitis

Protein-bound substances and Thyroid storm

toxins
Amanita phalloides toxins

Hyperparasitemia Malaria, babesiosis

Graphic 60280 Version 4.0

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American Society for Apheresis 2023 indications for therapeutic apheresis

and cytapheresis procedures

Indication Modality Category Evidence

Acute disseminated encephalomyelitis TPE II 2C

(ADEM): Steroid refractory

Acute fatty liver of pregnancy TPE III 2B

Acute inflammatory demyelinating TPE I 1A

polyradiculoneuropathy (Guillain-Barré
syndrome): Primary treatment IA I 1B

Acute liver failure TPE III 2B

TPE-HV I 1A

Age-related macular degeneration, dry, DFPP III 2B

high-risk

Alzheimer disease, mild or moderate TPE III 2A

Amyloidosis, systemic, dialysis-related Beta2 microglobulin II 2B

adsorption

Anti-glomerular basement membrane disease (Goodpasture syndrome)

Diffuse alveolar hemorrhage (DAH) TPE I 1C

Dialysis-independence TPE I 1B

Dialysis-dependence, no DAH TPE III 2B

Atopic dermatitis (atopic eczema), ECP/IA/TPE/DFPP III 2B

recalcitrant

Autoimmune dysautonomia TPE III 2C

Autoimmune hemolytic anemia (AIHA), severe

Severe cold agglutinin disease TPE II 2C

Severe warm AIHA TPE III 2C

Babesiosis, severe RBC exchange III 2C

Burn shock resuscitation TPE III 2B

Cardiac neonatal lupus TPE III 2C

Catastrophic antiphospholipid syndrome TPE I 2C

(CAPS)

Chronic acquired demyelinating polyneuropathies

IgG/IgA/IgM related TPE I 1B

Anti-myelin-associated glycoprotein TPE III 1C

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Chronic ataxic neuropathy, TPE III 2C

ophthalmoplegia, IgM paraprotein,
cold agglutinins, and disialosyl
antibodies (CANOMAD)/Chronic
ataxic neuropathy with disialosyl
antibodies syndrome (CANDA)

Chronic focal encephalitis (Rasmussen TPE/IA III 2C

encephalitis)

Chronic inflammatory demyelinating TPE/IA I 1B

polyradiculoneuropathy (CIDP)

Coagulation factor deficiency and inhibitors IA III 2B

TPE III 2C

Complex regional pain syndrome, chronic TPE III 2C

Cryoglobulinemia, severe/symptomatic TPE/DFPP II 2A

IA II 2B

Cutaneous T cell lymphoma (CTCL)

Erythrodermic mycosis ECP I 1B

fungoides/Sézary syndrome

Non-erythrodermic mycoses ECP III 2B

fungoides

Dilated cardiomyopathy, idiopathic, NYHA IA II 1B

II-IV
TPE III 2C

Erythrocytosis

Polycythemia vera Erythrocytapheresis I 1B

Secondary erythrocytosis Erythrocytapheresis III 1C

Erythropoietic protoporphyria, liver disease TPE/RBC exchange II 2C

Familial hypercholesterolemia

Homozygous individuals LA I 1A

Heterozygous individuals LA II 1A

All patients TPE II 1B

Focal segmental glomerulosclerosis (FSGS)

Recurrent in kidney transplant TPE/IA I 1B

All types LA II 2C

Steroid resistant in native kidney TPE III 2C

Graft-versus-host disease (GVHD)

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Acute ECP II 1B

Chronic ECP II 1B

Hemophagocytic lymphocytosis (HLH) TPE III 2C

Heparin-induced thrombocytopenia and thrombosis

Pre-procedure TPE/IA III 2C

Refractory or with thrombosis TPE III 2C

Hereditary hemochromatosis Erythrocytapheresis I 1B

Hyperleukocytosis Leukocytapheresis III 2B

Hypertriglyceridemic pancreatitis

Severe TPE/LA III 1C

Prevention of relapse TPE/LA III 2C

Hyperviscosity in hypergammaglobulinemia

Symptomatic TPE I 1B

Prophylaxis for rituximab TPE I 1C

Idiopathic inflammatory myopathies

Anti-synthetase-syndrome TPE III 2B

Clinically amyopathic TPE III 2B

dermatomyositis

Immune-mediated necrotizing TPE III 2B

myopathies

IgA nephropathy (Berger's disease)

Chronic progressive TPE III 2C

Crescentic TPE III 2B

Immune checkpoint inhibitors, immune- TPE III 2C

related adverse events

Immune thrombocytopenia (ITP), refractory TPE/IA III 2C

Inflammatory bowel disease

Ulcerative colitis Adsorptive II 1B

cytapheresis

Crohn disease Adsorptive III 1B/2C

cytapheresis/ECP

Lambert-Eaton myasthenic syndrome TPE II 2C

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Lipoprotein(a) hyperlipoproteinemia, LA II 1B
progressive atherosclerotic cardiovascular
disease

Malaria, severe* RBC exchange III 2B

Multiple sclerosis

Acute attack/relapse TPE/IA II 1A/1B

Chronic TPE/IA III 2B

Myasthenia gravis

Acute, short-term treatment TPE/DFPP/IA I 1B

Long-term treatment TPE/DFPP/IA II 2B

Myeloma cast nephropathy TPE II 2B

Nephrogenic systemic fibrosis ECP/TPE III 2C

Neuromyelitis optical spectrum disorders (NMOSD)

Acute attack/relapse TPE/IA II 1B/1C

Maintenance TPE III 2C

N-methyl-D-aspartate receptor antibody TPE/IA I 1C

encephalitis

Overdose, envenomation, and/or poisoning

Mushroom poisoning TPE II 2C

Envenomation TPE III 2C

Other TPE/RBC exchange III 2C

Paraneoplastic autoimmune retinopathies TPE III 2C

Paraneoplastic neurologic syndromes TPE/IA III 2C

Pediatric autoimmune neuropsychiatric disorders

Pediatric autoimmune TPE II 1B

neuropsychiatric disorder associated
with group A streptococci
(PANDAS)/Pediatric acute-onset
neuropsychiatric syndrome (PANS),
exacerbation

Sydenham chorea, severe TPE III 2B

Pemphigus vulgaris, severe TPE III 2B

IA/ECP/DFPP III 2C

Peripheral vascular diseases LA II 1B

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Phytanic acid storage disease (Refsum TPE/LA II 2C

disease)

Post-transfusion purpura (PTP) TPE III 2C

Progressive multifocal TPE III 1C

leukoencephalopathy (PML) associated
with natalizumab

Pruritus due to hepatobiliary disease, TPE III 1C

treatment resistant

Psoriasis, disseminated pustular ECP III 2B

Adsorptive III 2C
cytapheresis

TPE IV 2C

Red blood cell alloimmunization, pregnancy complications

Hemolytic disease of the fetus and TPE III 2C

newborn

RhD alloimmunization prophylaxis RBC exchange IV 2C

after transfusion

Sepsis with multiorgan failure TPE III 2A

Sickle cell disease

Acute stroke RBC exchange I 1C

Acute chest syndrome, severe RBC exchange II 1C

Other acute complications RBC exchange/TPE III 2C

Stroke prophylaxis RBC exchange I 1A

Pregnancy RBC exchange II 2B

Recurrent vaso-occlusive pain RBC exchange II 2B

Preoperative management RBC exchange III 2A

Steroid-responsive encephalopathy TPE II 2C

associated with autoimmune thyroiditis
(Hashimoto encephalopathy)

Stiff-person syndrome TPE III 2C

Sudden sensorineural hearing loss LA/DFPP/TPE III 2A

Systemic lupus erythematosus (SLE): Severe TPE II 2C

complications

Systemic sclerosis ECP III 2A

TPE III 2C

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Thrombocytosis

Symptomatic Thrombocytapheresis II 2C

Prophylactic or secondary Thrombocytapheresis III 2C

Thrombotic microangiopathy

Coagulation-mediated, due to TPE III 2C

pathogenic variants in THBD, DGKE,
or PLG

Complement-mediated, due to factor TPE I 2C

H autoantibodies

Complement-mediated, due to TPE III 2C

pathogenic variants in complement
regulatory genes

Drug-associated: Ticlopidine ¶ TPE I 2B

Drug-associated: Clopidogrel TPE III 2B

Drug-associated: Gemcitabine TPE IV 2C

Drug-associated: Quinine TPE IV 2C

Infection-associated, from Shiga TPE/IA III 2C

toxin-producing Escherichia coli
(STEC-HUS), severe

Infection-associated, from TPE III 2C

Streptococcus pneumoniae (pHUS)

Pregnancy associated, severe TPE III 2C

Pregnancy associated, extremely TPE/LA III 2C

preterm preeclampsia, severe

Thrombotic thrombocytopenic TPE I 1A

purpura (TTP; immune, with
ADAMTS13 deficiency)

Transplantation-associated TPE III 2C

Thyroid storm TPE II 2C

Toxic epidermal necrolysis (TEN), refractory TPE III 2B

Transplantation, heart

Cellular/recurrent rejection ECP II 1B

Rejection prophylaxis ECP/TPE II 2A/IC

Desensitization TPE II 1C

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Antibody-mediated rejection TPE III 2C

Transplantation, hematopoietic stem cell, ABO incompatible

Major ABO incompatible, TPE II 1B

hematopoietic cells obtained from
bone marrow

Major ABO incompatible, TPE II 2B

hematopoietic cells obtained by
apheresis

Minor ABO incompatible, RBC exchange III 2C

hematopoietic cells obtained by
apheresis

Pure RBC aplasia TPE III 2C

Transplantation, hematopoietic stem cell, TPE III 2C

HLA desensitization

Transplantation, intestine

Antibody mediated rejection TPE III 2C

Desensitization TPE III 2C

Transplantation, kidney, ABO compatible

Antibody mediated rejection TPE/IA I 1B

Desensitization/prophylaxis, living TPE/IA I 1B

donor

Transplantation, kidney, ABO incompatible

Desensitization, living donor TPE/IA I 1B

Antibody-mediated rejection TPE/IA II 1B

Transplantation, liver

Desensitization, ABO incompatible, TPE I 1C

living donor

Desensitization, ABO incompatible, TPE III 2C

deceased donor

Antibody-mediated rejection ECP/TPE III 2B/2C

Immune suppression withdrawal ECP III 2B

Desensitization, ABO incompatible ECP III 2C

Transplantation, lung

Chronic allograft dysfunction ECP II 1C

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Bronchiolitis obliterans syndrome ECP II 1C

Antibody-mediated TPE III 2C

rejection/desensitization

Desensitization TPE III 2C

Vaccine-induced thrombotic TPE III 2C

thrombocytopenia, refractory

Vasculitis, ANCA-associated

Microscopic polyangiitis TPE III 1B

Granulomatosis with polyangiitis TPE III 1B

Eosinophilic granulomatosis with TPE III 2C

polyangiitis (EGPA; Churg-Strauss)

Vasculitis, IgA (Henoch-Schönlein purpura)

Crescentic rapidly progressive TPE III 2C

glomerulonephritis (RPGN)

Severe extrarenal manifestations TPE III 2C

Vasculitis, other

Hepatitis B polyarteritis nodosa TPE II 2C

Kawasaki disease TPE III 2C

Multisystem inflammatory syndrome TPE III 2C

in children (MIS-C)

Voltage-gated potassium channel (VGKC) TPE/IA II 1B

antibody-related disease

Wilson disease, fulminant TPE I 1C

Refer to UpToDate topics on individual conditions for specific treatment recommendations. Due
to UpToDate styling and alphabetization, the order of diseases in this table may differ slightly
from the original source publication.

Category
Category I: Disorders for which apheresis is accepted as first-line therapy, either as a
standalone treatment or in conjunction with other therapies.
Category II: Disorders for which apheresis is accepted as second-line therapy, either as a
standalone treatment or in conjunction with other therapies.
Category III: Disorders for which the optimal role of apheresis therapy is not established.
Category IV: Disorders for which published evidence demonstrates or suggests apheresis to
be ineffective or harmful.

Evidence
Evidence grade 1: Strong recommendation.
Evidence grade 2: Weak recommendation.

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Evidence quality A: High-quality evidence.

Evidence quality B: Moderate-quality evidence.
Evidence quality C: Low-quality or very low-quality evidence.

TPE: therapeutic plasma exchange; IA: immunoadsorption; TPE-HV: high-volume therapeutic

plasma exchange; ECP: extracorporeal photopheresis; DFPP: double filtration plasmapheresis;
NYHA: New York Heart Association; RBC: red blood cell; LA: lipoprotein apheresis; Ig:
immunoglobulin; HLA: human leukocyte antigen.

* UpToDate authors do not use RBC exchange for severe malaria.

¶ UpToDate authors consider this entity (thrombotic microangiopathy [TMA] in the setting of
ticlopidine) to be immune thrombotic thrombocytopenic purpura (iTTP) rather than drug-induced
TMA because the patients had severe ADAMTS13 deficiency.

From: Connelly-Smith L, Alquist CR, Aqui NA, et al. Guidelines on the use of therapeutic apheresis in clinical practice -
Evidence-based approach from the Writing Committee of the American Society for Apheresis: The Ninth Special Issue. J
Clin Apher 2023; 38:77. https://onlinelibrary.wiley.com/doi/10.1002/jca.22043. Copyright © 2023 Wiley Periodicals LLC.
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Contributor Disclosures
Joy L Fridey, MD No relevant financial relationship(s) with ineligible companies to disclose. Andre A
Kaplan, MD No relevant financial relationship(s) with ineligible companies to disclose. Lynne Uhl,
MD Grant/Research/Clinical Trial Support: NHLBI [Myocardial infarction and transfusion].
Consultant/Advisory Boards: Abbott [Transfusion Medicine educational services]. All of the relevant
financial relationships listed have been mitigated. Jennifer S Tirnauer, MD No relevant financial
relationship(s) with ineligible companies to disclose.

Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these
are addressed by vetting through a multi-level review process, and through requirements for
references to be provided to support the content. Appropriately referenced content is required of all
authors and must conform to UpToDate standards of evidence.

Conflict of interest policy

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