Transcript High Resolution Protein Electrophoresis

High Resolution Protein
Electrophoresis
A Clinical
Overview with
Case Studies
By
Lawrence M. Killingsworth, Ph.D.
Human Proteins
Only ~200 of the vast array of human
proteins have been characterized.
Clinical knowledge is limited to 25 – 30
relatively high concentration
components of plasma, CSF, urine and
other fluids.
Of these, 15 or so can be visualized by
high resolution agarose electrophoresis.
Normal Control
Pre-albumin
1-Acid Glycoprotein
-Lipoprotein
1-Antichymotrypsin
Haptoglobin
Albumin
1-Antitrypsin
2-Macroglobulin
Transferrin
-Lipoprotein
C-3
Fibrinogen
IgA
IgG
IgM
Monoclonal Gammopathies
Uncontrolled proliferation of a single
clone of plasma cells at the expense of
other clones.
Protein analysis is valuable in
diagnosing and monitoring
lymphoproliferative diseases.
Evaluation of Monoclonal
Gammopathies
1. Serum and Urine High Resolution
Protein Electrophoresis
(24-hour urine preferred)
2. Quantitative Serum Immunoglobulins
3. Serum and Urine IFE
SPIFE ImmunoFix
IFE is the method
of choice to identify
suspicious serum
or urine electrophoretic bands.
Periodic evaluation
by serum and urine
electrophoresis
and by quantitative
Ig assay can help
monitor therapy.
Monoclonal Gammopathies
Variable mobility and band appearance.
Case 1: IgG Kappa Monoclonal
Patient: 78 year-old male
History & Physical: Severe pain right leg
and right lumbar region.
SPE: Monoclonal band in gamma region.
IFE: IgG Kappa.
Control
Hospital Course: Bulging disk surgically
decompressed; referred to hematologist/
oncologist for follow-up & treatment.
Patient
Case 2: IgG Kappa
Monoclonal
Patient: 78 year-old male
History & Physical: Recent
chemotherapy for lymphadenopathy.
SPE: Hypoalbuminemia and
monoclonal band in 2 region.
IEP: IgG Kappa.
Control
Patient
Hospital Course: Treated with
transfusions and plasmapheresis.
Symptomatic improvement.
Discharged for outpatient
re-evaluation.
Case 3: IgA Lambda
Monoclonal
Patient: 74 year-old female
History & Physical: Myeloma. Pain in
lower thoracic and upper lumbar spine,
right shoulder and left anterior ribs.
SPE: Large monoclonal band in 2 region.
IEP: IgA Lambda.
Control
Patient
Hospital Course: Radiation therapy.
Transferred to hospital closer to home
for continued radiation and
chemotherapy.
Case 4: IgM Kappa
Monoclonal
Patient: 68 year-old male
History & Physical: Anemia, elevated
IgM, edema in ankles, petechiae.
SPE: Marked M-component in 2
region; also in urine.
IEP: IgM Kappa in serum; free Kappa
light chains in urine.
Control
Patient
Hospital Course: Bone marrow biopsy
non-diagnostic. Discharged for outpatient treatment and followup for
possible macroglobulinemia, chronic
lymphatic leukemia or lymphoma.
Case 5: Lambda Light Chain
Patient: 78 year-old male
History & Physical: Anemia, azotemia;
admitted for dialysis.
SPE:  1AT and Hp,  pre-albumin,
albumin & transferrin (consistent with
acute inflammation); 2 small M-proteins
in  region. Urine:  albumin,1AT,
transferrin; large M-protein in  region
and smaller cathodal band.
IEP: Monoclonal lambda light chain in
urine and serum. No heavy chain.
Control
Patient
Hospital Course: Bone marrow biopsy
confirmed multiple myeloma.
Hemodialysis, plasmapheresis and
chemotherapy improved symptoms.
Case 6: Lambda Light Chain
Patient: 82 year-old male
History & Physical: Fractured left hip,
suspected frontal lobe infarction.
SPE:  albumin, acute inflammation,
 Hp (consistent with in-vivo hemolysis
or  RBC turnover), mild hypogammaglobulinemia. Urine: Several small
monoclonal bands in  region.
IEP: Monoclonal free lambda light chain
in urine; no monoclonal proteins in
serum.
Serum
Control
Urine
Patient
Hospital Course: Acute left cerebral
infarction confirmed. B12 anemia
treated. Died due to post-operative
pneumonia following hip surgery.
Multiple Myeloma
Clinical Presentation
Bone pain, especially in spine, pelvis or
ribs
Renal failure of unknown etiology
Recurrent bacterial infections
Physical exam usually unremarkable – no
lymphadenopathy or hepatosplenomegaly
Macroglobulinemia
Clinical Presentation
Fatigue
Generalized weakness
Skin and mucosal bleeding
Visual disturbances
Headache
Other neurological signs and symptoms
Cardiopulmonary abnormalities due to
increased plasma volume and viscosity
Recurrent bacterial infections
Physical exam may reveal purpura,
lymphadenopathy and hepatosplenomegaly
Genetic Deficiencies
1-Antitrypsin Deficiency
Linked to hepatitis and cirrhosis in
neonates; chronic obstructive pulmonary
disease and hepatic cirrhosis in adults
Electrophoresis useful in initial
evaluation
Quantitative immunochemical assays
and phenotyping required
Genetic Deficiencies
Immunoglobulin Deficiencies
Isolated IgA deficiency
Isolated IgM deficiency
X-linked immunodeficiency with  IgM
Wiskott-Aldrich Syndrome
Transient hypogammaglobulinemia of infancy
Ataxia Telangiectasia
Severe combined immunodeficiency (SKID)
Common variable immunodeficiency
–Pan hypogammaglobulinemia
–IgG and IgA deficiency
–Isolated IgG deficiency
Inflammatory Response
ACUTE
SUBACUTE
CHRONIC
Pre-albumin




Albumin







ALPHA-1 -lipoprotein
1-acid
glycoprotein



1-antitrypsin




ALPHA-2 Cerulopasmin
Haptoglobin
BETA-1 Transferrin








 or N
BETA-2 C-3

Fibrinogen
 or N


IgA

GAMMA IgM

IgG

CRP




Liver Diseases
Chronic Hepatocellular Disease & Cirrhosis
Most common pattern includes diffuse
increase in IgG with proportionally greater
increases in IgA and sometimes IgM
1-antitrypsin is the most sensitive indicator
for hepatocellular disease
Pre-albumin is the most sensitive monitor in
cirrhosis; 2-macroglobulin and ceruloplasmin
also very elevated
All other proteins usually normal or decreased
Case 7: Chronic
Hepatocellular Disease
Patient: 39 year-old male
Pre-albumin
Albumin
-Lipoprotein
1-Antitrypsin
2-Macroglobulin
Haptoglobin
Transferrin
C-3
Immunoglobulins
Normal Patient
History & Physical: Long-term
alcohol abuse; ascites, leg swelling,
shortness of breath, right side pain,
enlarged liver and spleen.
SPE: Hypoalbuminemia with normal
migration.  pre-albumin,
-lipoprotein and transferrin,
consistent with chronic disease.
Diffuse IgA, IgG .
Hospital Course: Ascites , right
lung abcess treated. Liver tests
normal at 4 weeks. Discharged in
good condition.
Liver Diseases
Hepatitis
Often associated with acute phase
inflammatory response in the early stages
Diffuse elevations in one or more of the
immunoglobulins with chronic disease
Case 8: Cirrhosis
Pre-albumin
Albumin
Patient: 54 year-old female
-Lipoprotein
History & Physical: Chronic
alcoholism; deeply jaundiced, rapid
pulse, hepatomegaly, splenomegaly.
1-Antitrypsin
2-Macroglobulin
Haptoglobin
Transferrin
-Lipoprotein
C-3
Immunoglobulins
Normal
Patient
SPE: Hypoalbuminemia ( anodic
mobility due to bilirubin binding).
 pre-albumin,  -lipoprotein and
 transferrin, consistent with
chronic disease. Diffuse IgA, IgG .
Hospital Course: Rehydrated and
stabilized. Discharged in good
condition.
Protein Losing Disorders
Selective Protein Loss
Nephrosis can result in elevations in serum
concentrations of large proteins with decreases
in smaller components.
Serum pattern shows:
– Increased 2-macroglobulin, -lipoprotein
and polymeric forms of haptoglobin.
– Decreased pre-albumin, albumin, 1-acid
glycoprotein, 1-antitrypsin, transferrin.
– IgM usually elevated, IgG usually decreased.
Case 9: Acute Renal Failure
Patient: 57 year-old male
Albumin
-Lipoprotein
1-Antitrypsin
2-Macroglobulin
Haptoglobin
Transferrin
-Lipoprotein
C-3
Immunoglobulins
Normal
Patient
History & Physical: Rapid onset
abdominal pain and enlargement,
edema, decreased urine output.
SPE:  albumin,  2-macroglobulin
and  -lipoprotein, consistent with
selective protein loss due to
glomerular-type proteinuria.
Hospital Course: Received albumin
and hemodialysis. Discharged in
improved condition with limited
outpatient dialysis. Final diagnosis:
Acute renal failure due to tubular
necrosis, possibly of a toxic nature.
Protein Losing Disorders
Nonselective Protein Loss
Whole blood loss
Congestive heart failure
Liver failure
Hemodilution
Malnutrition
Protein-losing enteropathies – greater
decrease in immunoglobulins than other
plasma proteins
Pregnancy &
Hyperestrogenism*
Moderate decreases in prealbumin, albumin,
1-acid glycoprotein and IgG
Large relative increases in 1-antitrypsin,
ceruloplasmin, transferrin and fibrinogen
Moderate increase in -lipoprotein
Slight increase in 2-macroglobulin and
hemopexin
Haptoglobin and C-3 essentially normal
*Hyperestrogenism
(i.e. contraceptive pills, estrogen medications)
can mask pathological changes
Case 10: Infant w/ Hepatic
Involvement
Patient: 5 month-old female
Pre-albumin
Albumin
-Lipoprotein
1-Antitrypsin
2-Macroglobulin
Haptoglobin
Transferrin
C-3
Immunoglobulins
Normal Patient
History & Physical: Previously
healthy; 104º fever/24 hrs,
jaundice, hepatomegaly.
SPE: Hypoalbuminemia ( anodic
mobility due to bilirubin binding),
 1-AT,  Hp,  -lipoprotein,
 transferrin; consistent with acute
inflammation. Age-appropriate
hypogammaglobulinemia.
Hospital Course: Blood culture
positive for gram negative rods.
Treated with antibiotics and
discharged.
Case 11: Acute Renal Failure
Pre-albumin
Albumin
-Lipoprotein
1-Antitrypsin
2-Macroglobulin
Haptoglobin
Transferrin
C-3
Immunoglobulins
C-reactive protein
Normal
Patient
Patient: 52 year-old male
History & Physical: Weakness,
progressive shortness of breath,
tachycardia, anemia, azotemia, mild
hepatomegaly, edema.
SPE: Hypoalbuminemia,  1-AT,
 Hp,  -lipoprotein,  transferrin;
consistent with acute inflammation.
Low normal gammaglobulins. CRP?
Hospital Course: Blood culture
positive for Staph aureus. Vigorous
antibiotic therapy. Died 5 days postadmission.
Case 12: Chronic Renal Failure
Patient: 68 year-old male
Pre-albumin
Albumin
-Lipoprotein
1Antitrypsin
2-Macroglobulin
Haptoglobin
Transferrin
-Lipoprotein
C-3
Immunoglobulins
Normal
Patient
History & Physical: Chronic
bladder outlet obstruction;
abdominal pain, hematuria,
urinary or bladder infection.
SPE: Hypoalbuminemia with
 anodal mobility;  1-AT,  Hp,
 transferrin; consistent with acute
inflammation. Random urine
pattern consistent with mixed
glomerular-tubular proteinuria.
Hospital Course: Continued
antibiotics, hemodialysis.
Case 13: Acute & Subacute
Inflammation
Pre-albumin
Albumin
-Lipoprotein
1-Antitrypsin
2-Macroglobulin
Haptoglobin
Transferrin
-Lipoprotein
C-3
Immunoglobulins
Normal Patient
Patient: 74 year-old male
History & Physical: Pneumonia,
2 weeks duration.
SPE: Hypoalbuminemia with
 anodal mobility;  1-AT,  Hp,
 transferrin,  a-lipoprotein,
and  C-3; consistent with acute
and subacute inflammation.
Hospital Course: Antibiotics,
discharged in good condition.
Case 14: Diffuse Hypergammaglobulinemia with Lymphoma
Pre-albumin
Albumin
-Lipoprotein
1-Antitrypsin
2-Macroglobulin
Haptoglobin
Transferrin
-Lipoprotein
C-3
Immunoglobulins
Normal
Patient
Patient: 63 year-old female
History & Physical: Pruritis,
sweats and fatigue, multiple
dermal nodules.
SPE: Non-specific findings –
diffuse increase in immunoglobulins, suggesting chronic
inflammation.
Hospital Course: Biopsy reports
consistent with lymphoma;
patient discharged for outpatient
treatment and followup.
Urinary Proteins of
Plasma Origin
Normal Urinary Protein
< 150 mg/day
Albumin
Primarily Filtered Plasma
Proteins – albumin, low MW
species, immunoglobulin
components
Sometimes
Transferrin
Remainder – derived from
urinary tract
Urine
Serum
Electrophoretic pattern of
normal urine – trace albumin,
sometimes transferrin
Urinary Proteins of
Plasma Origin
Proteinuria
Glomerular – results from increased passage of
proteins through the glomerulus; characterized
by loss of plasma proteins the size of albumin or
larger
Tubular – results from decreased capacity of
tubules to reabsorb proteins; characterized by
inceased excretion of very small proteins such
as 2-microglobulin
Systemic – exercise, postural, pregnancy,
overflow
Urinary Proteins of
Plasma Origin
High Resolution protein electrophoresis
developed with a sensitive protein stain
Excellent analytical technique
Easily distinguishes & characterizes the various
types of proteinuria
Provides useful insight on specific functions
within the nephron
“Biochemical biopsy”
Differential diagnosis & monitoring of patients
with renal dysfunction
Urinary Proteins of
Plasma Origin
Glomerular Proteinuria
Renal glomeruli are ultrafilters for macromolecules
Damage to renal glomeruli leads to increased
urinary excretion of proteins (30,000 to 100,000
daltons) which are normally retained
Some selectivity remains – very large proteins
(>500,000 daltons) still retained by glomerulus
In early disease, very LMW proteins (<15,000
daltons) are still reabsorbed by tubules and absent
from urine
Urinary Proteins of
Plasma Origin
Glomerular Proteinuria
Urine Protein Pattern
- strong band of albumin
- strong, broad 1 zone due to 1-acid glycoprotein
and 1-antitrypsin
- strong band of transferrin (1)
Serum Protein Pattern
- marked decrease in albumin
- marked decrease in 1-acid glycoprotein and
1-antitrypsin
- increases in large proteins: 2-macroglobulin,
-lipoprotein
Urinary Proteins of
Plasma Origin
Severe Proteinuria / Nephrotic Syndrome
Total Protein > 3.5 g/day
Hypoalbuminemia and hyperlipidemia
Massive edema
Urinary Proteins of
Plasma Origin
Disorders Associated
with Nephrotic Syndrome
Glomerular diseases
Proliferative glomerulonephritis
Other diseases
- Infections
- Neoplasia
- Miscellaneous
- Drugs
- Multisystem diseases
- Hereditary disorders
Case 1: Nephrotic Syndrome
with Glomerular Proteinuria
Patient: 45 year-old white male
Albumin
Albumin
1 acid
glycoprotein
1AT
2-Macro
1 AT
HP
Transferrin
Transferrin
-Lippo
C-3
IgA
IgM
IgG
Normal
Serum
Urine
History & Physical: Diabetes
mellitus / nephrotic syndrome.
SPE:  pre-albumin, albumin
and transferrin with  2-macroglobulin and -lipoprotein;
consistent with selective renal
protein loss.
Urine Elp:  albumin,
1-antitripsin and transferrin
with trace pre-albumin and
2-components; consistent with
sieving glomerular-type protein
loss.
Urinary Proteins of
Plasma Origin
Tubular Proteinuria
Normal tubules reabsorb and catabolize 95 to 99%
of proteins from glomerular filtrate
Tubular disease reduces capacity to reabsorb and
catabolize, resulting in increased urinary excretion
Causes of tubular proteinemia:
- Chronic metal exposure (cadmium, gold, lead, mercury)
- Acute and chronic pyelonephritis
- Renal transplant rejection
- Toxicity due to aminoglycoside therapy
- Balkan nephropathy
- Uremic medullary cystic disease
Urinary Proteins of
Plasma Origin
Tubular Proteinuria
Serum Protein Pattern
- little or no change since LMW proteins are
present in very low levels
Urine Protein Pattern
- faint albumin band
- double band in 2 area due to 2-microglobulin
- strong band in mid- region due to
2-microglobulin
- diffuse background in  region due to
free light chains
Urinary Proteins of
Plasma Origin
Mixed Glomerular/Tubular Proteinuria
Chronic renal disease or renal failure
Combined pattern with both “glomerular-type”
and “tubular-type” proteins in the urine
Case 2: Heavy Metal Toxicity
with Tubular Proteinuria
Albumin
Albumin
1-AT
2-Macro
2Microglobulin
HP
 2Microglobulin
Transferrin
-Lipo
Patient: 52 year-old black
male
History & Physical: Metal
worker.
SPE: Essentially normal.
Urine Elp: Trace albumin,
 2-microglobulin and
2-microglobulin; consistent
with tubular-type proteinuria.
C-3
IgA
IgM
IgG
Normal
Serum
Urine
Urinary Proteins of
Plasma Origin
Other Conditions with Increased
Urinary Protein Excretion
Exercise Proteinuria – strenuous muscular exercise
increases excretion of HMW and LMW proteins
Postural or Orthostatic Proteinuria – present/upright,
absent/recumbent – benign or underlying cause?
Pregnancy – usually transitory, may be associated
with toxemia, delivery, UTI, or asymptomatic
Overflow Proteinuria – increased plasma concentration of LMW proteins, e.g. BJP, myoglobin,
hemoglobin, acute phase reactants
Case 3: Septicemia
with Overflow Proteinuria
Patient: 65 year-old white female
Albumin
Albumin
1-acid
glycoprotein
1AT
1-AT
2-Macro
Acute phase
reactants
HP
Transferrin
-Lipo
C-3
IgA
IgM
IgG
Normal
Serum
Urine
History & Physical: High fever,
chills, sweats, joint and muscle
aches.
SPE:  pre-albumin, albumin,
-lipoprotein and transferrin,
 1-antitrypsin, haptoglobin, C3
& C-reactive protein; consistent
with acute inflammation.
Urine Elp: Trace albumin and
transferrin,  1-acid
glycoprotein, faint acute phase
reactants; consistent with
overflow proteinuria
Cerebrospinal
Fluid Proteins
CSF Proteins versus Plasma Proteins
CSF Total Protein:
Much less than in plasma
150 – 450 mg/L, ages 10 – 40 years, lumbar
Slightly higher, ages 40+
Slightly higher for verticular & cisternal specimens
CSF Production:
Primarily ultrafiltration and active transport of
proteins, ions, water and other components
through the choroid plexus.
Small amount produced within CNS
Cerebrospinal
Fluid Proteins
CSF Protein Composition
Pre-albumin
Albumin – major protein
present, 55 – 75% of the total
Albumin
1-Antitrypsin
1 – primarily 1-antitrypsin,
-lipoprotein absent
Haptoglobin
Transferrin
CSF
2 – essentially absent
TF
1 – transferrin detectable
2 – carbohydrate-deficient
“CSF-specific” transferrin
Oligoclonal Bands
Normal CSF
Abnormal
Patient CSF
 – almost exclusively IgG,
faint “-trace”
Cerebrospinal
Fluid Proteins
Permeability of Blood-CSF Barrier
Increased permeability caused by
- bacterial or viral menigitis
- neoplastic infiltration of meninges
- polyneuropathies
- disk herniations
- cerebral infarctions
Integrity of blood-CSF barrier
- Total CSF protein
- 2-macroglobulin
- Protein ratios
Cerebrospinal
Fluid Proteins
Abnormal CNS Protein Production
Demyelinating Diseases
Increased IgG synthesis in Multiple Sclerosis and
Subacute Sclerosing Panencephalitis
IgG as Percentage of Total Protein
Considers increased permeability vs. synthesis.
IgG >10% suspicious; >13% abnormal production likely.
CSF/Serum Ratios
Considers increased plasma concentration.
86% of MS patients show values above reference range.
Oligoclonal Banding
Indicative of MS; new more sensitive procedure is IEF.
Cerebrospinal
Fluid Proteins
Oligoclonal Banding
Multiple, restricted bands
in the gamma fraction
Detectable by high
resolution electrophoresis
and IEF methods
90% of MS patients exhibit
oligoclonal banding
New CSF IEF methods have become the gold
standard for diagnosing MS in Europe.
Cerebrospinal
Fluid Proteins
Isoelectric Focusing
IEF followed by
immunoblotting
Oligoclonal banding
in unconcentrated
CSF but not serum
is diagnostic of MS
Gold Standard in
Europe
S = Serum
C = CSF
Cerebrospinal
Fluid Proteins
Laboratory Protocol to Rule Out MS
1. Draw both CSF and serum samples.
2. Note CSF color and appearance. Determine
total protein, glucose, white cell count,
differential, red cell count.
3. Perform high resolution protein electrophoresis
on concentrated CSF.
4. Perform high resolution protein electrophoresis
on serum for presence or absence of banding.
5. In borderline cases, determine CSF and serum
albumin and IgG ratios.
Cerebrospinal
Fluid Proteins
Laboratory Findings in Multiple Sclerosis
CSF Appearance: Clear
NSC
Patient Serum
Leukocytes: Usually normal
Total Protein: Usually normal
Glucose: Normal
Patient CSF
Electrophoresis: Oligoclonal
banding in 90% of cases
Normal CSF
IgG Ratio: Elevated in 90% of
cases
Cerebrospinal
Fluid Proteins
Clinical
Manifestations of MS
40% of patients
present with optic
neuritis
60 to 70% present
with evidence of
spinal cord or
brainstem lesion
Case 1: Multiple Sclerosis
Patient: 33 year-old female
Normal CSF
Patient CSF
Patient Serum
NSC
History & Physical: left-side
numbness - 9 months; fuzzy
vision - 2 weeks.
SPE: Normal.
CSF: Clear, colorless. Cell
count, differential, glucose
and total protein all normal.
CSF Elp: Increased gamma
globulins, strong oligoclonal
banding. Consistent with
demyelinating disease.
Case 2: Multiple Sclerosis
Patient: 31 year-old male
Normal CSF
Patient CSF
History & Physical: Unsteady
walk, leg numbness, inability to
concentrate, irritability, slurred
speech, disturbed vision,
urinary urgency.
SPE: Normal.
Patient Serum
NSC
CSF: Clear, colorless. Normal
glucose. 29 WBC/mm3 (9%
lymphocytes, 1% moncytes).
Total Protein 55 mg/dL.
CSF Elp: Gamma globulin
increase, strong oligoclonal
banding; consistent with MS.
Case 3: Multiple Sclerosis
Patient: 36 year-old female
Normal CSF
Patient CSF
History & Physical: numbness in
legs – 1 month; urinary urgency
and blurred vision – 4 months;
tires easily.
SPE: Normal.
Patient Serum
NSC
CSF: Clear, colorless. Normal total
protein, WBC count, and glucose.
CSF Elp: Profound gamma globulin
increase, very strong oligoclonal
banding. (IgG & ratios markedly
elevated.) Consistent with MS.
Case 4: Suspected
Viral Meningitis
Patient: 25 year-old white female
Normal CSF
Patient CSF
Patient Serum
NSC
History & Physical: Progressive
headache, lethargy, altered mental
status; “flu” – 4 weeks prior.
SPE: Borderline hypoalbuminemia.
CSF: Clear, colorless. Normal
glucose. 158 WBC/mm3 (1oo%
moncytes). Total Protein 83 mg/dL.
CSF Elp: Increased gamma globulins,
prominent oligoclonal banding.
Considering  total protein;
consistent with viral encephalitis.
Discharged for outpatient followup.
Case 4: Suspected Viral
Meningitis (cont’d)
Patient: Readmitted 8 days later with redeveloped headache.
Normal CSF
Patient CSF
Patient Serum
NSC
Normal CSF
Patient CSF
CSF: Clear, colorless. Normal glucose
and protein. 103 WBC/mm3 (90%
lymphocytes, 10% neutrophils).
CSF Elp: Gamma globulins and
oligoclonal banding decreased from
previously. Transient increase
consistent with CNS infection /
inflammation.
SPIFE 3000 Analyzer
Automated sample
application, separation
and staining of visible
analytes
Automated reagent
application for enzymatic
assays
On-board cooling for
excellent separation and
resolution
On-board availability of
two stains
SPIFE Assays
Cholesterol Profile
Serum Proteins
Split-Beta SPE
Urine Proteins
Immunofixation
Urine Immunofixation
Hi Resolution Proteins
Alkaline Hemoglobins
Acid Hemoglobins
CK* & LD Isoenzymes
Alk Phos Isoenzymes*
CSF IgG IEF*
Lipoproteins
*Pre-market approval pending 4/02
SPIFE Hi Res Proteins
Excellent separation
Active cooling
preserves pattern
integrity
Acid violet stain for
added sensitivity
Urine
SPIFE IFE 15, 9, 6 & 3
Up to 210 profiles in
8 hours
Highest sensitivity
antisera
Acid violet
for best
sensitivity
Built in QC
wells
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