Date Printed: May 21, 2018: 06:08 PM

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Original Effective Date: 04/15/01

Reviewed: 02/22/18

Revised: 04/26/18

Subject: Apheresis, Plasmapheresis and Plasma Exchange


Position Statement Billing/Coding Reimbursement Program Exceptions Definitions Related Guidelines
Other References Updates    


Apheresis, Plasmapheresis, and Plasma Exchange

The terms apheresis, plasmapheresis, and plasma exchange (PE) are often used interchangeably. The American Society for Apheresis (ASFA) defines these procedures as follows:

Apheresis: A procedure in which blood of the individual or donor is passed through a medical device which separates out one or more components of blood and returns the remainder with or without extracorporeal treatment or replacement of the separated component.

Plasmapheresis: A procedure in which blood of a individual or the donor is passed through a medical device which separates out plasma from the other components of blood and the plasma is removed (ie, <15% of total plasma volume) without the use of replacement solution.

Plasma exchange (PE): A therapeutic procedure in which blood of the individual is passed through a medical device which separates out plasma from other components of blood; the plasma is removed and replaced with a replacement solution such as colloid solution (eg, albumin and/ or plasma) or a combination of crystalloid/colloid solution.

The rationale for these procedures is based on the fact that circulating substances, such as toxins or autoantibodies, can accumulate in the plasma. Also, it is hypothesized that removal of these factors can be therapeutic in certain situations. PE is essentially a symptomatic therapy, because it does not remove the source of the pathogenic factors. Therefore the success of PE will depend on whether the pathogenic substances are accessible through the circulation and whether their rate of production and transfer to the plasma component can be adequately addressed by PE. For example, PE can rapidly reduce levels of serum autoantibodies; however, through a feedback mechanism, this rapid reduction may lead to a rebound overproduction of the same antibodies. This rebound production of antibodies is thought to render the replicating pathogenic clone of lymphocytes more vulnerable to cytotoxic drugs; therefore, PE is sometimes used in conjunction with cyclophosphamide.

Applications of apheresis, plasmapheresis, and plasma exchange can be broadly subdivided into 2 general categories: (1) acute self-limited diseases, in which PE is used to acutely lower the circulating pathogenic substance; and (2) chronic diseases, in which there is ongoing production of pathogenic autoantibodies. Because PE does not address underlying pathology, and, due to the phenomenon of rebound antibody production, its use in chronic diseases has been more controversial than in acute self-limited diseases. In addition, plasmapheresis has been used in the setting of solid organ transplantation. It has been used as a technique to desensitize high-risk candidates before transplant and also as a treatment of antibody mediated rejection (AMR) reaction occurring after transplant. Before transplant, plasmapheresis has been most commonly used to desensitize candidates receiving an ABO mismatched kidney, often in combination with a splenectomy. As a treatment of AMR, plasmapheresis is often used in combination with intravenous immunoglobulin (IVIg) or anti-CD-20 therapy (ie, Rituxan).

Low-Density Lipid (LDL) Apheresis

Lipid apheresis is used for disorders with marked hyperlipidemia, primarily familial hypercholesterolemia (FH). A dominantly inherited disorder, FH results froms a mutation in the gene that encodes for the specific cell surface receptor responsible for LDL uptake by the cells. The heterozygous form affects about 1 in 500 people. The number of LDL receptors is halved in this condition, resulting in serum low density lipoprotein cholesterol (LDL-C) levels that are approximately 2 to 3 times levels considered acceptable (ie, >300 mg/dL). Affected male patients typically develop coronary heart disease in their thirties and forties, while women develop the disease in their fifties. Depending on the patient, heterozygous FH may or may not respond adequately to lipid-lowering drugs.

The American Heart Association has indicated that adults with heterozygous familial hypercholesterolemia (FH) should be treated with available pharmacotherapy with an initial goal of reducing low-density lipoprotein cholesterol (LDL-C) by at least 50%, usually with a statin. This treatment can be followed by achieving an LDL-C of less than 100 mg/dL (absent coronary artery disease [CAD] or other major risk factors]) or 70 mg/dL (presence of CAD or other major risk factors). The following approach for pharmacotherapy is suggested:

• High-intensity statin therapy to target >50% LDL-C reduction, such as rosuvastatin or atorvastatin

• If the patient is adherent and LDL-C is above the target goal after 3 months, consider adding ezetimibe

• If the patient is adherent and LDL-C is above the target goal after 3 months, consider adding a PCSK9 inhibitor or colesevelam (or other bile acid sequestrant or niacin)

• If the patient is adherent and LDL-C is above the target goal after 3 months, proceed to complex therapy combination such as a 4-drug combination plus LDL apheresis

Low-density lipid (LDL) apheresis is a technique by which cholesterol is removed from the blood by first isolating the plasma, then selectively removing the low density lipoproteins from the plasma by either immunoadsorption, heparin-induced extracorporeal LDL precipitation, or dextran sulfate adsorption. The plasma is then returned to the individual.

LDL apheresis has been developed as a technique to treat those with familial hypercholesterolemia (FH). FH is a dominantly inherited disorder involving a mutation of the gene that encodes for the specific cell surface receptor responsible for LDL uptake by the cells. The heterozygous form affects about 1 in 500 people.The number of LDL receptors is halved in this condition, resulting in serum low-density lipoprotein cholesterol (LDL-C) levels that are approximately 2 to 3 times levels that are considered acceptable (ie, >300 mg/dL). Affected men typically develop coronary heart disease in their thirties and forties, while affected women develop coronary heart disease in their fifties. Depending on the individual, heterozygous FH may or may not respond adequately to lipid-lowering drugs.

Homozygous hypercholesterolemia is rare, only occurring in 1 in 1 million subjects. Serum levels of LDLC may be elevated 6-fold (>500 mg/dL), due to the total lack of functioning LDL receptors. Homozygotes may develop severe aortic stenosis and coronary heart disease by age 20 years. These individuals typically do not adequately respond to drug or diet modification therapy. In the past, those with homozygous FH may have been treated with plasma exchange, but the advent of LDL apheresis provides a more targeted approach by permitting selective removal of LDL from the plasma.

Therapeutic apheresis with selective HDL delipidation and plasma reinfusion is a procedure in which plasma is removed from the body by apheresis, processed through a delipidation device and then returned to the body. The delipidation procedure selectively removes cholesterol from HDL, converting the major alpha HDL to pre-beta-like HDL. The plasma with pre-beta-like HDL is then reinfused to the individual. The pre-beta-like HDL is a form of HDL that enhances cholesterol transport to the liver and is thought to reduce atherosclerosis development and burden.


Apheresis, Plasmapheresis, and Plasma Exchange (36511-36515)

Apheresis, plasmapheresis, and plasma exchange meet the definition of medical necessity for the following conditions:


• Severe multiple manifestations of mixed cryoglobulinemia (MC) such as cryoglobulinemic nephropathy, skin ulcers, sensory motor neuropathy, and widespread vasculitis in combination with immunosuppressive treatment

• Catastrophic antiphospholipid syndrome (CAPS)


• ABO incompatible hematopoietic progenitor cell transplantation

• Hyperviscosity syndromes associated with multiple myeloma or Waldenström macroglobulinemia

• Idiopathic thrombocytopenic purpura in emergency situations

• Thrombotic thrombocytopenic purpura (TTP)

• Atypical hemolytic-uremic syndrome

• Post-transfusion purpura

• HELLP syndrome of pregnancy (a severe form of preeclampsia, characterized by hemolysis [H], elevated liver enzymes [EL], and low platelet [LP] counts)

• Myeloma with acute renal failure

Familial hypercholesterolemia

In conjunction with CAR T-cell therapy


• Acute inflammatory demyelinating polyneuropathy (Guillain-Barré syndrome [GBS]; severity grade 1-2 within 2 weeks of onset severity grade 3-5 within 4 weeks of onset; and children younger than 10 years old with severe GBS)

• Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP)

• Multiple sclerosis (MS), with acute fulminant central nervous system (CNS) demyelination

• Myasthenia gravis in crisis or as part of preoperative preparation

• Paraproteinemia polyneuropathy; IgA, IgG


• Antiglomerular basement membrane disease (Goodpasture syndrome)

• ANCA (antineutrophil cytoplasmic antibody)‒associated vasculitis [eg, Wegener granulomatosis (also known as granulomatosis with polyangitis [GPA]) with associated renal failure

• Dense deposit disease with factor H deficiency and/or elevated C3 Nephritic factor


• ABO incompatible solid organ transplantation:

• Kidney

• Heart (infants)

• Renal transplantation (antibody mediated rejection and HLA [human leukocyte antigen] desensitization)

• Focal segmental glomerulosclerosis after renal transplant

Apheresis, plasmapheresis, and plasma exchange is considered experimental or investigational for all other conditions, including but not limited to the conditions listed below. There is insufficient evidence in the published medical literature to permit conclusions on safety, efficacy and long-term outcomes.

• ABO-incompatible solid organ transplant; liver

• Acute disseminated encephalomyelitis

• Acute inflammatory demyelinating polyneuropathy (Guillain-Barré syndrome) in children younger than 10 years old with mild or moderate forms

• Acute liver failure

• Amyotrophic lateral sclerosis

• ANCA [(antineutrophil cytoplasmic antibody)‒associated rapidly progressive glomerulonephritis (Wegener granulomatosis or GPA without renal failure)

• Aplastic anemia

• Asthma

• Autoimmune hemolytic anemia; warm autoimmune hemolytic anemia; cold agglutinin disease

• Chronic fatigue syndrome

• Coagulation factor inhibitors

• Cryoglobulinemia; except for severe mixed cryoglobulinemia, as noted above

• Dermatomyositis and polymyositis

• Focal segmental glomerulosclerosis (other than after renal transplant)

• Heart transplant rejection treatment

• Hemolytic uremic syndrome (HUS); typical (diarrheal-related)

• Idiopathic thrombocytopenic purpura; refractory or nonrefractory

• Inclusion body myositis

• Lambert-Eaton myasthenic syndrome

• Multiple sclerosis with chronic progressive or relapsing remitting course

• Mushroom poisoning

• Myasthenia gravis with anti-MuSK antibodies

• Overdose and poisoning (other than mushroom poisoning)

• Paraneoplastic syndromes

• Paraproteinemia polyneuropathy; IgM

• Pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS)

• Pemphigus vulgaris

• Phytanic acid storage disease (Refsum disease)

• POEMS (polyneuropathy, organomegaly, endocrinopathy, M protein, skin changes)

• Psoriasis

• Red blood cell alloimmunization in pregnancy

• Rheumatoid arthritis

• Sepsis

• Scleroderma (systemic sclerosis)

• Stiff person syndrome

• Sydenham chorea (SC)

• Systemic lupus erythematosus (including SLE nephritis)

• Thyrotoxicosis

• Hyperviscosity syndromes with renal failure (other than associated with multiple myeloma or Waldenström macroglobulinemia)

Low-density Lipid (LDL) Apheresis (36516, S2120)

Low-density lipid (LDL) apheresis meets the definition of medical necessity for homozygous familial hypercholesterolemia as an alternative to plasmapheresis.

Low-density lipid (LDL) apheresis as an alternative to plasmapheresis meets the definition of medical necessity for heterozygous familial hypercholesterolemia (FH), when ALL of the following are met:

• Failed diet therapy and maximum tolerated combination drug therapy AND meets ONE of the following FDA-approved indications:

• Functional hypercholesterolemic heterozygotes with LDL ≥300 mg/dL, OR

• Functional hypercholesterolemic heterozygotes with LDL ≥200 mg/dL AND documented coronary artery disease*

* Documented coronary artery disease: includes a history of myocardial infarction, coronary artery bypass surgery, percutaneous transluminal coronary angioplasty or alternative revascularization procedure, or progressive angina documented by exercise or non-exercise stress test.

LDL apheresis is considered experimental or investigational for all other conditions, including but not limited to treatment of preeclampsia, nonfamilial hypercholesterolemia, sudden sensorineural hearing loss, severe diabetic foot ulcerations, peripheral artery disease, and non‒arteritic acute anterior ischemic optic neuropathy. There is insufficient to clinical evidence to determine the impact of this procedure on health outcomes.

Therapeutic apheresis with selective high-density lipoprotein (HDL) delipidation and plasma reinfusion (0342T) is considered experimental or investigational. The available clinical evidence does not support clinical value.


CPT Coding:


Therapeutic apheresis; for white blood cells


Therapeutic apheresis; for red blood cells


Therapeutic apheresis; for platelets


Therapeutic apheresis; for plasma pheresis


Therapeutic apheresis; with extracorporeal immunoadsorption, selective adsorption or selective filtration and plasma reinfusion


Therapeutic apheresis with selective HDL delipidation and plasma reinfusion (investigational)

HCPCS Coding:


Low density lipoprotein (LDL) apheresis using heparin-induced extracorporeal LDL precipitation

ICD-10 Diagnosis Codes That Support Medical Necessity for 36511-36515:


Waldenstrom macroglobulinemia


Heavy chain disease


Essential (hemorrhagic) thrombocythemia


Other specified hereditary hemolytic anemias


Hemolytic-uremic syndrome


Other primary thrombocytopenia


Posttransfusion purpura


Other secondary thrombocytopenia


Secondary polycythemia




Multiple sclerosis


Hereditary and idiopathic neuropathy, unspecified


Guillain-Barre syndrome


Chronic inflammatory demyelinating polyneuritis


Myasthenia gravis with (acute) exacerbation


Polyarteritis with lung involvement [Churg-Strauss]


Hypersensitivity angiitis


Thrombotic microangiopathy


Wegener's granulomatosis without renal involvement


Wegener's granulomatosis with renal involvement


Severe pre-eclampsia, unspecified trimester


Severe pre-eclampsia, second trimester


Severe pre-eclampsia, third trimester


HELLP syndrome (HELLP), unspecified trimester


HELLP syndrome (HELLP), second trimester


HELLP syndrome (HELLP), third trimester


Other complications of the puerperium, not elsewhere classified

ICD-10 Diagnosis Codes That Support Medical Necessity for 36516, S2120:


Familial hypercholesterolemia


Refer to section entitled POSITION STATEMENT.


Federal Employee Program (FEP): Follow FEP guidelines.

State Account Organization (SAO): Follow SAO guidelines.

Medicare Advantage products:

The following National Coverage Determination (NCD) was reviewed on the last guideline reviewed date: APHERESIS (Therapeutic Pheresis) (110.14), located at

The following Local Coverage Determinations (LCD) were reviewed on the last guideline reviewed date: Low Density Lipoprotein (LDL) Apheresis (L33381), and Non-Covered Services (L33777), located at


Familial hypercholesterolemia (FH): A recessive genetic disorder caused by a defect on chromosome 19 that makes the liver incapable of metabolizing (or removing) excess LDL. The result is very high LDL levels which can lead to premature cardiovascular disease. There are two forms of FH. If inherited from one parent, the result is heterozygous FH (HeFH). HeFH occurs in 1 in 200 to 500 people worldwide. If inherited from both parents, it is much more severe in its consequences. This form of FH is called homozygous FH (HoFH). It is very rare, occurring in about 1 in 160,000 to one million people worldwide.

Guillain-Barre syndrome: an acute demyelinating neuropathy whose severity is graded on a scale of 1-5.  Plasma exchange is reserved for those with grades 3-5 disease who do not initially respond to prednisone.

HELLP syndrome of pregnancy: a severe form of preeclampsia, characterized by hemolysis [H], elevated liver enzymes [EL], and low platelet [LP] counts).

Myasthenia gravis: an autoimmune disease with autoantibodies directed against the postsynaptic membrane of the muscle end plate.  Clinically, the disease is characterized by fatigable weakness of voluntary muscles.  Initial treatment focuses on the use of cholinesterase inhibitors to overcome the postsynaptic blockade.  Immunosuppressant drugs including corticosteroids and azathioprine are also effective.  Plasma exchange has been used as a short-term therapy in individuals with acute exacerbations associated with severe weakness.

Post-transfusion purpura: a rare disorder characterized by an acute severe thrombocytopenia occurring about 1 week after a blood transfusion in association with a high titer of anti-platelet alloantibodies.

Rapidly progressive glomerulonephritis (RPGN) including Goodpasture’s syndrome: a general term describing the rapid loss of renal function in conjunction with the finding of glomerular crescents on renal biopsy specimens.  There are multiple etiologies of RPGN including vasculitis, the deposition of anti-glomerular basement membrane (GBM) antibodies as seen in Goodpasture’s syndrome, or the deposition of immune complexes as seen in various infectious diseases or connective tissue diseases.  RPGN may also be idiopathic.  Because many cases of RPGN represent an immune-mediated disease of acute onset, RPGN was an early focus of PE research.

Thrombotic thrombocytopenic purpura (TTP)—Hemolytic uremic syndrome (HUS): Once considered distinct syndromes, TTP and HUS are now considered different manifestations of the same disease process, i.e., thrombotic microangiopathy.  The classic signs and symptoms include fever, thrombocytopenia, microangiopathic hemolytic anemia, neurologic abnormalities, and renal involvement. TTP-HUS may be seen in association with other conditions, such as pregnancy or HIV infection. PE has become the primary treatment for TTP-HUS, although a rationale for its effectiveness is unknown. PE is performed daily until a response is noted; the length of treatment averages about once a month, with increasing intervals between PE treatments.


Extracorporeal Photopheresis, 01-90919-02

Tisagenlecleucel (Kymriah) Infusion, 09-J2000-91

Axicabtagene Ciloleucel (Yescarta) Infusion, 09-J2000-95


None applicable


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This Medical Coverage Guideline (MCG) was approved by the BCBSF Medical Policy & Coverage Committee on 02/22/18.



Medical Coverage Guideline developed.


Revised to include coverage information for ECI.


Revised to include ICD-9 diagnosis code for a covered indication for 36521; Add clarification for ICD-9 diagnosis codes that support medical necessity for 36520.


HCPCS coding update.


Reviewed; revised to include additional covered indication.


Medical Coverage Guideline archived.


Medical Coverage Guideline returned to active status. Revised MCG title, description section, position statement, CPT, HCPCS, ICD9, and ICD10 coding; Medicare Advantage program exception, and definitions. Updated references and reformatted guideline.


Revision; updated ICD9 coding section.


Scheduled review. Maintained position statement, revised program exceptions section, and updated references.


ICD-10 coding update: deleted code E78.0; added code E78.01.


Unscheduled revision. Deleted ICD10 code G70.00.


Scheduled review. Maintained position statement. Updated references. Reformatted guideline.


Revision: Revised description section, coverage for low-density lipoprotein (LDL) apheresis, and definitions section. Updated references.


Annual CPT/HCPCS coding update: deleted 36515; revised 36516.


Revision: added CAR T-cell therapy as a covered indication. Updated references.


Revision: updated related guidelines.

Date Printed: May 21, 2018: 06:08 PM