The Osler Institute

Blood Bank I
D. Joe Chaffin, MD
Summit Pathology, Greeley, CO
Bonfils Blood Center, Denver, CO

I. Get Ready, Get Set…

A. Blood Bank I
• Blood Groups
B. Blood Bank II
• Blood Donation
• Pretransfusion Testing
C. Blood Bank III
• Component Therapy
D. Blood Bank IV
• Transfusion Complications
* Noninfectious (Transfusion Reactions)
* Infectious (Transfusion-transmitted Diseases)
E. Blood Bank Practical
• Management of specific clinical situations
• Calculations, Antibody ID, and no-pressure sample
questions

Blood Bank I
Blood Groups
I. Basic Antigen-Antibody Testing
A. Basic Red Cell-Antibody Interactions
1. Agglutination
a. Clumping of red cells due to antibody coating
b. Main reaction we look for in Blood Banking
c. Two stages:
1) Coating of cells (“sensitization”)
a) Affected by specificity of antibody,
electrostatic charge of RBCs, temperature,
relative amounts of antigen and antibody
b) Substances like Low Ionic Strength Saline
(LISS) and Polyethylene glycol (PEG) aid in
sensitization by helping to overcome physical
barriers to let antigens and antibodies get
closer to each other
2) Formation of bridges
a) Lattice-like structures formed by antibodies
and red cells
b) IgG isn’t good at this; it is usually too small
to bridge the gap between red cells by itself
c) IgM is much better at forming bridges

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2. Hemolysis
a. Direct lysis of a red cell as a result of antibody
coating is uncommon, but is just as much a
“positive” as agglutination
1) Requires complement fixation
2) IgM antibodies do this more than IgG
B. Tube Testing
1. Immediate spin “phase”
a. Serum and 2-5% RBC solution together in tube,
centrifuge for 15-30 sec, and examine.
1) Most common: 2 drops serum, 1-2 drops RBCs.
2. 37 C “phase”
a. Take above mixture and incubate at 37 C for
specified time, centrifuge, and examine.
1) 10-15 minutes if LISS used to potentiate
2) 15-30 minutes if albumin or PEG used
3) 30-60 minutes if no potentiation used
3. Indirect antiglobulin (a.k.a., “antihuman globulin”)
“phase”
1) Wash above mixture to remove unbound
globulins.
2) Add antihuman globulin, centrifuge, and
examine.
C. Alternatives to tube testing
1. Column agglutination technology
a. Gel testing (Ortho)
1) Multiple microtubes filled with gel particles and
anti-IgG reagent
a) Gel particles separate red cell clusters by size
(i.e., larger clumps of cells are stopped from
migrating through gel while individual cells
cruise right on through to the bottom)
b) Anti-IgG grabs onto red cells coated by IgG
2) Add red cells and plasma to top of tube,
incubate, then centrifuge
3) More coating of red cells by antibody = larger
agglutinates and more attraction to antiglobulin
in gel = less transport through gel
a) Negative gel tests show cells in a button at
the bottom of the microtube
b) Positive tests have cells spread in varying
degrees through the microtube
4) Can be automated (ProVue machine)
b. Affinity column testing (REACT; not currently
available)
1) Similar appearance, but no antiglobulin
2) IgG-binding proteins in column

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2. Solid-phase Red Cell Adherence Testing (Immucor
Gamma)
1) Uses binding of antibody to RBCs that are
themselves bound to the sides of microwells
2) Manufacturer binds RBCs carrying antigens we
are interested in to small wells.
3) Lab adds patient serum, incubates, washes
a) Antibody binds to test RBCs
4) Indicator RBCs (coated with monoclonal anti-
IgG) attach to test RBCs via bound antibody
5) Centrifuge and interpret
a) Negative solid phase tests have cells in a
button at the bottom of the microplate,
because the indicator cells don’t bind to the
test RBCs on the microplate wall
b) Positive solid phase tests have cells spread in
a “carpet” all along the microplate wall,
because the indicator cells have bound to test
RBCs all along the wall
6) Can be automated (Galileo and Galileo Echo
machines)
D. The Antiglobulin Test (“Coomb’s Test”)
1. Indirect: described above; checks for in-vitro coating
of RBCs with antibody or complement.
2. Direct: Red cells taken directly from patient, washed,
then mixed with anti-human globulin; checks for in-
vivo coating of RBCs with antibody and/or
complement.

3. IAT Variations
a. Can be used to check for an unknown antibody by
using red cells with a known antigen profile, as in
an antibody screen
b. Can be used to check for an unknown red cell
antigen by using serum with known antibody
specificity, as in RBC antigen testing
c. Can be used to check for a reacting unknown
antigen and unknown antibody, as in the
crossmatch procedure
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4. Specificities of the antiglobulin
a. Anti-IgG, -C3d (“polyspecific”)
1) Will detect red cells coated with either of the
above, and may also detect other
immunoglobulins (because the anti-IgG is not
specific)
b. Anti-IgG and anti-IgG (heavy chains)
1) Both detect IgG-coated red cells; anti-IgG may
also detect light chains associated with other
antibody classes (IgA, IgM)
c. Anti-C3b, -C3d
1) Detects either of the above complement
components
2) Useful in evaluating IgM-related hemolysis, cold
agglutinin disease, and certain warm
autoimmune hemolysis without IgG
5. IgG-coated red cells (“Coomb’s control”)
a. Used after negative DAT or IAT to ensure proper
functioning of antiglobulin reagent
b. IgG-coated RBCs added to AHG-cell mixture
c. Negative = bad AHG or no AHG added
d. Other errors in the process (leaving out the test
serum, bad processing technique, etc) would not be
detected by Coomb’s Control test

E. Dosage
1. Certain antibodies do not react as strongly with RBCs
that have antigens coded for by a single gene.
2. For example, imagine a hypothetical anti-Z
a) Patient 1 genotype: ZZ (Homozygous for Z)
b) Patient 2 genotype: ZY (Heterozygous for Z)
c) If anti-Z shows dosage, it will react stronger with
patient 1’s RBCs (see below)
RBC Genotype Reaction with anti-Z
ZZ 3+
ZY 1+

3. Most common in Kidd, Duffy, Rh, and MNSs blood

groups

F. Neutralization
1. A particular substance, when mixed with an antibody,
eliminates the activity of that antibody against test red
cells
2. Some of these are pretty weird! (See table on next
page)

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Neutralization of Antibodies

ABO Saliva (secretor)

Lewis Saliva (secretor for Leb)

Hydatid cyst fluid,
P1
Pigeon egg fluid
Sda Urine
Chido,
Serum
Rodgers

II. Blood Groups

A. General Characteristics
1. Guidelines
a. “Clinically significant” = Blood group antibody
which causes HTRs or HDN
b. Most significant antibodies are “warm reactive”;
meaning they react best at 37 C or IAT.
c. Most insignificant antibodies are “cold reactive”;
meaning they react best below 37 C.
d. Warm antibodies are most often IgG, while colds
are usually IgM.
e. IgM antibodies are usually “naturally occurring”,
meaning no transfusion or pregnancy is required for
their formation.

“WARM-REACTIVE” “COLD-REACTIVE”
ANTIBODIES ANTIBODIES
IgG IgM
Require exposure Naturally occurring
Cause HDN No HDN*
Cause HTRs No HTRs*
“Significant” “Insignificant”*
f. *Note that the ABO blood group is the exception in
the table above.
2. The “Enzyme Classification”

Enzyme-enhanced Enzyme-decreased Enzyme unaffected

ABO Family MNSs Blood Group Kell Blood Group
ABO Blood Group Duffy Blood Group
Lewis Blood Group
I/i Blood Group
P Blood Group
Rh Blood Group
Kidd Blood Group

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B. ABO Blood Group
1. Basic biochemistry (see figure below)
a. Type I and II chains
1) Type I: Think of them as primarily glycoproteins
in secretions and plasma.
2) Type II: Think of them as primarily
glycosphingolipids on RBCs.
b. Se gene
1) “Secretor” gene on chromosome 19
a) A secretor is a person able to make A or B
antigens in their secretions (saliva, etc)
2) Codes for an enzyme that adds fucose to type I
chains at terminal galactose; product is H
antigen (sometimes called “type I H”)
3) 80% gene frequency
c. H gene
1) Closely linked to Se on chromosome 19
2) Enzyme product adds fucose to terminal
galactose of type II chains; product is H
antigen (“type II H”)
2) Virtually 100% gene frequency (lack of H =
“Bombay phenotype” (more later).
d. H antigen (type II) is required before A and/or B
antigens can be made on red cells; type I H is
required before A and/or B are made in secretions
1) A single sugar is added to an H antigen chain to
make A or B antigens; when this happens, the
chain no longer has H activity.
a) Group A sugar: N-acetylgalactosamine
b) Group B sugar: Galactose

2) Relationship is reciprocal; the more A or B is

made, the less H remains.
a) Relative amounts of H by blood group
• O > A2 > B > A2B > A1 > A1B
2. ABO antigens and antibodies
a. Antigens based on combinations of three genes on
chromosome 9: A, B, and O.

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b. Antibodies are clinically significant and “naturally
occurring”
c. Group O
1) Generally the most common blood group
2) Genotype: OO
3) Antigen: H
a) Lectin of Ulex europaeus agglutinates cells
with abundant H antigen.
b) Note lectin chart for various specificities

Lectin Specificity
Dolichos biflorus A1, Sda
Ulex europaeus H
Vicea graminea N

4) Antibodies: anti-A, anti-B, and anti-A,B

a) Antibodies characteristically very strong
b) Antibodies in group O people are mostly
IgG, so they may cross the placenta to cause
mild HDFN (most common HDFN)
d. Group A
1) Genotypes: AA, AO
2) Antigens: A, H
3) Antibodies: anti-B (primarily IgM).
4) A subgroups
a) A1 (80%) and A2 (~20%) most important.
b) A1 red cells have about 4 times more A
antigen on RBC surfaces than A2 cells.
c) Despite this quantitative difference,
qualitative differences also exist in the
interactions and shapes of the antigens
d) Small % of A2’s (1-2% of A2 and 25% of
A2B) form anti-A1.
• Anti-A1 is usually clinically insignificant
but it can cause discrepancies in ABO
testing
e) Lectin of Dolichos biflorus agglutinates A1
RBCs, to differentiate A1 from A2
e. Group B
1) Genotypes: BB, BO
2) Antigens: B, H
3) Antibodies: Anti-A (primarily IgM).
4) B Subgroups: Unimportant and less frequent
f. Group AB
1) Least frequent ABO blood type (about 4%)
2) Antigens: A and B (very little H)
a) Can be further subdivided into A1B or A2B
depending on the status of the A antigen

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3) Antibodies: none
3. ABO Testing
a. Cell Typing (“forward grouping”)
1) Patient red cells agglutinated by known sera
(anti-A, anti-B).
b. Serum Typing (“reverse grouping”, “back typing”)
1) Patient serum (or plasma) against A1 and B
RBCs.

Forward Reverse
ABO
Anti- Anti- A1 B Group
A B cells cells
4+ 0 0 4+ A
0 4+ 4+ 0 B
4+ 4+ 0 0 AB
0 0 4+ 4+ O

c. Note the opposite reactions!

1) If forward reactions are not opposite of reverse,
an ABO discrepancy is present.
d. Both serum and cell typing are required unless
testing babies < 4 months of age or reconfirming
testing done elsewhere (cell typing only)
4. ABO discrepancies
a. Disagreement between the interpretations of
forward and reverse grouping (e.g., forward
grouping looks like group A, reverse like group O);
generally caused by either antigen or antibody
problems
b. Antigen problems
1) Lack of expected antigens
a) A or B subgroups
b) Transfusion or transplantation
2) Unexpected antigens
a) Acquired B phenotype (more below)
b) Recent marrow/stem cell transplant,
c) Polyagglutinable RBCs, nonspecific
agglutination
c. Antibody problems
1) Lack of expected antibodies
a) Immunodeficiency
b) Abnormally HIGH concentrations of Ab
(prozone phenomenon)
c) Neonates, elderly, or immunocompromised
d) Transplantation or transfusion
2) Unexpected antibodies
a) Cold auto- or alloantibodies

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b) Anti-A1
c) Rouleaux (false positive)
d) Transfusion or transplantation
5. Weird stuff about ABO
a. Acquired B Phenotype
1) Seen in colon cancer, intestinal obstruction,
gram-negative sepsis
2) AB forward (with weak reactions with reagent
anti-B), A reverse
Forward Grouping Reverse Grouping
Anti- Anti- A1 B
Interp Interp
A B cells cells
4+ 1-2+ AB 0 4+ A

3) Bacteria deacetylate group A sugar (GalNAc);

remaining galactosamine cross-reacts with
reagent anti-B.
4) Acidify serum (no reaction with anti-B), acetic
anhydride (re-acetylates), autoincubation (no
reaction), BS-1 lectin (no reaction).
b. B(A) Phenotype
1) Similar to acquired B, but with group B (i.e.,
they are really group B but forward test like an
AB, with a weak reaction with anti-A)
2) Problem is a cross-reaction with a particular
form of anti-A; testing using a different anti-A is
shows the patient truly to be group B
c. Bombay (Oh) Phenotype
1) Total lack of H, A, and B antigens due to lack of
H and Se genes.
2) Develop strong anti-H, anti-A, and anti-B.
3) Testing: O forward, O reverse, but antibody
screen wildly positive and all units incompatible.
4) Require other Bombay donors
5) Para-Bombay phenotype
a) Similar, but these patients have Se to partially
compensate for their lack of H.
b) Phenotypes: Ah, Bh, ABh
c) Red cells may type like Bombays, but serum
testing shows H and A or B antigen (unless
group O)
d) These patients have anti-H in serum
6. Consequences of ABO incompatibility
a. Severe acute hemolytic transfusion reactions
1) Most frequent blood bank fatalities
2) Clerical errors
b. Most frequent HDFN; usually mild, however.
C. Lewis Blood Group
1. Biochemistry (see figure below)
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a. Type I chains only
b. One gene: Le
c. Gene product adds fucose to subterminal GlcNAc
1) This makes Lea (Lewis A) antigen
2) In a non-secretor, Lea is the only Lewis antigen
possible
d. In secretors, Se product adds fucose, then Le
product adds fucose; this makes Leb (Lewis B)
1) So, the majority of secretor’s chains are Leb

e. Unlike ABO, antigens are not tightly bound

(remember, they are made from Type I chains);
rather, they adsorb onto the surface of RBCs
1) Leb does this better than Lea, so this is another
reason that most adults with both Le and Se will
be Le(a-b+).
2) Le(a-b+) people still have Lea (since not all
chains have been converted), it just may not be
detectable on RBCs.
f. Same chain can carry Le antigen and ABO antigen.
2. Lewis antigens and antibodies
a. Lea, Leb
b. Leb is seen more frequently
c. 22% of blacks are Le(a-b-), vs. only 6% of
whites
d. Antibodies are naturally occurring
1) Primarily in Le(a-b-)
2) Cold reacting IgM
3) Neutralize with saliva
3. Consequences of incompatibility
a. Rare HTRs (more commonly anti-Lea)
b. No HDFN (antibody doesn’t cross placenta and
antigen isn’t present on fetal RBCs).
4. Weird stuff about Lewis
a. Lewis antigens decrease during pregnancy
1) Pregnant patients may have transient,
insignificant Lewis antibodies
b. Le(a-b+) people don’t make anti-Lea.

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a
1) As above, these people still have Le , just not on
their red cells.
c. Children’s Lewis type may vary, as antigen chains
are converted (they may have more Lea than Leb)

D. I/i Blood Group

1. Antigens built on chains related to ABO.
2. Expression is age-dependent
a. Simple chains found on neonates make i antigen.
b. More branched chains in adults make I antigen.
c. “Big I in big people, little i in little people”
3. Antibodies
a. Cold reacting IgM
b. Naturally occurring
c. Autoantibodies very common
4. Classic associations
a. Auto-anti-I
1) Cold agglutinin disease
2) Mycoplasma pneumoniae infection
b. Auto-anti-i
1) Associated with Infectious mononucleosis
2) Less often a problem than auto-anti-I

E. P Blood Group (the cool one)

1. Also built on ABO-related chains.
2. P1 most frequent antigen
a. P, Pk are others
1) Combination of these three antigens makes the P
phenotype
2) Most common P phenotype is P1 (positive for P1
and P, and negative for Pk)
b. Very rare people lack all three and make anti-
PP1Pk.
1) Associated with acute HTRs, HDFN, and early
abortions
c. P antigen is Parvovirus B19 receptor.
3. Antibodies (anti-P1)
a. Cold reacting, naturally occurring, insignificant
IgM
b. Neutralized by hydatid (Echinococcus) cyst fluid
and pigeon egg fluid (Really! I’m not kidding!)
4. Association with Paroxysmal Cold Hemoglobinuria
a. Biphasic IgG with anti-P specificity
1) Binds in cold temps, hemolyzes when warmed
2) “Donath-Landsteiner biphasic hemolysin”
b. Classically associated with syphilis, now with viral
infections in children

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F. Rh Blood Group
1. Second most important blood group (after ABO)
2. Terminology systems
a. Fisher-Race (DCE or CDE)
1) Five major antigens: D, C, E, c, e
a) “Rh positive” really means “D positive”.
b) Absence of D designated “d” (later found not
to be a real antigen)
2) Eight potential combinations (“haplotypes”)
named based on presence of genes for above
antigens (i.e., “DCe”, “dce”, etc.)
b. Wiener (Rh-Hr)
1) Different names for the five main antigens; these
are not used very often by non-geeky people
2) Believed that main Rh genes (for presence or
absence of D, for C or c, and for E of e) were
inherited as one genetically linked group, or
“haplotype”.
3) Gave shorthand names to the eight potential
combinations alluded to above; this
nomenclature is still in use and is essential to
know (even though his theory of how these are
inherited has been disproved).

Wiener’s “Haplotypes”
(with DCE Equivalents)
R1: DCe r’: dCe
R2: DcE r”: dcE
R0: Dce r: dce
Rz: DCE ry: dCE

a) Rules for converting Wiener’s shorthand into

Fisher-Race terminology:
• “R” = D, “r” = d
• “1” or “prime” = C
• “2” or “double prime” = E
• “0” or “blank” = ce
• Any superscript letter = CE
c. “The Big Four”
1) Fortunately, only four of the above combinations
occur frequently enough to memorize their
relative order: R1, R2, R0, and r. (~97% of
blacks and whites use only these four)
a) How to remember?
• R0 is most common in blacks, least
common in whites.
• r is always second in frequency.
• R1 always comes before R2.

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“The Big Four”
Whites: R1 > r > R2 > R0
Blacks: R0 > r > R1 > R2

2) FYI, Asians have much less r; the order in that

group is R1 > R2 > r and R0
3. Rh antibodies
a. Exposure required
b. Warm-reacting IgG
4. Consequences of Rh incompatibility
a. Unexposed: 80% (reported as wide range of 30-
85%) of D-negative patients make anti-D with a
one unit D-pos RBC transfusion.
b. Exposed: HTRs with extravascular hemolysis
c. Most severe and prototypical HDN
5. Weird stuff about Rh
a. Weak D phenotype (Formerly known as Du)
1) Some D+ individuals require an Indirect
Antiglobulin Test (IAT) to detect D antigen.

2) Possible reasons for weak D

a) C on opposite chromosome to D (“C in
trans”)
b) Weak form of R0 gene
c) Mosaic forms of D antigen (“partial D”, “D
mosaic”) lack portions of D antigen
• Probably better considered separately from
first two.
• Patients with partial D may develop
antibodies against portions of the antigen
they lack; this may lead to what looks like
an anti-D in a D-positive person.
3) Requirements
a) Weak D test for all D negative blood donors
b) Not required for D negative blood recipients
(though often done; especially for pregnant
women)
b. Rhnull phenotype
1) No Rh antigens whatsoever
2) Hemolytic anemia with stomatocytes

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3) Also associated with altered activity of S, s, and

U antigens (See MNSs system later)
4) Rhmod is a similar, though less severe form, also
associated with hemolysis
c. Warm autoimmune hemolytic anemia
1) Antibody seems to have relative specificity to
basic Rh structural antigens
d. Compound Rh antigens
1) G = antigen present when either C or D are
present
2) f = antigen present when c and e are on the same
chromosome (as in r and R0)
G. Kidd Blood Group
1. Kidd antigens
a. Jka, Jkb
b. Jka slightly more common
2. Kidd antibodies
a. Exposure required
b. Warm reacting IgG
1) Unusually good at fixing complement, in
contrast to most IgG antibodies
c. Marked dosage effect
1) A Kidd antibody may not react at all against
cells with heterozygous expression of Kidd
antigens, but may react very strongly against a
homozygous cell
d. Variable antibody expression
1) Antibody often disappears with time/storage
3. Weird stuff about Kidd
a. Delayed HTRs
1) Kidd’s most famous association
2) Anamnestic response
3) Intravascular and often severe
b. Mild HDFN at worst
1) Child can only be one antigen different from
mom; remember dosage discussion above.
H. MNSs Blood Group
1. Basic biochemistry
a. Glycophorin A carries M and N antigens.
b. Glycophorin B carries S, s, and U antigens.
2. MNSs antigens
a. M frequency roughly equals N
b. s>S
c. If S-s-, may also be U negative if black (see earlier
discussion of racial differences).
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3. MNSs antibodies
a. M and N antibodies are mostly opposite of S, s, and
U antibodies (see below)
b. Enzymes destroy M, N, and S antigens, but do not
greatly affect s antigens.
Anti-M & anti-N Anti-S, -s, and –U
Naturally occurring Require exposure

Cold IgM Warm IgG

Dosage Minimal dosage

Insignificant Significant

c. Anti-M is generally insignificant, but has been

associated uncommonly with HDFN
4. Weird stuff about MNSs
a. N-like antigen (‘N’)
1) Glycophorin B has a terminal 5 AA sequence
that matches glycophorin A’s last 5 when coding
for actual N antigen; this is known as ‘N’
a) This is not really true N antigen, but it is
close enough that it prevents most M+N-
people from making anti-N
2) Everyone except those who lack glycophorin B
(S-s-U-) have ‘N’.
a) For this reason, the majority of people who
make clinically significant anti-N are
African-Americans (<1% lack S, s, and U)
b. Anti-N induced by hemodialysis
1) Formaldehyde sterilization of machine
2) Modification of N antigen
c. Another lectin!
1) Vicea graminea lectin used commonly as an N-
typing reagent
I. Duffy Blood Group
1. Duffy antigens
a. Fyb > Fya
b. Fy(a-b-) is the most common Duffy phenotype in
blacks (68%)
c. Fya is much more common in Asians than in
Caucasians.
2. Duffy antibodies
a. Anti-Fya much more common and significant than
anti-Fyb
b. Require exposure
c. Warm-reacting IgG
d. Marked dosage
e. May have variable expression like Kidd antibodies.

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3. Consequences of incompatibility
a. Severe HTRs, usually delayed and extravascular
b. Generally mild HDFN (for same reason as Kidd
above)
4. Weird stuff about Duffy
a. Fy(a-b-) and malarial resistance
1) Fy(a-b-) humans are resistant to Plasmodium
vivax and P. knowlesi infection
J. Kell Blood Group
1. Extremely important group clinically and serologically
2. Kell antigens
a. Low frequency: K, also known as “K1” (9%
whites, 2% blacks), Jsa, Kpa
b. High frequency: k, also known as “K2” (99.8%),
Jsb, Kpb
c. Kx: important antigen that may help stabilize RBC
membrane (more later); is closely associated with
K antigens on the red cell membrane
1) Kx has a strange relationship to Kell antigens
2) When Kell antigens decrease in number, Kx
increases (as in “Kell null” phenotype, aka K0);
thought to be due to decrease in masking Kell
antigens
a) This led to Kx originally postulated as a
precursor; not true
3) When Kx decreases (as in “McLeod phenotype”,
see later), Kell antigens decrease, too
a) Kx may be required for proper Kell antigen
expression
d. Kell system antigens destroyed by thiol reagents (2-
ME, DTT, ZZAP) but not by enzymes alone.
3. Kell antibodies
a. Anti-K
1) Very common (most common non-ABO
antibody after anti-D)
2) Warm reacting IgG
b. Anti-k
1) Very uncommon due to high antigen frequency
2) Analogous to anti-K
4. Consequences of incompatibility
a. Severe HTRs
1) May be acute or delayed; usually extravascular.
b. Severe HDN
5. Weird stuff about Kell
a. Kell null phenotype (“K0”)
1) Absence of all Kell antigens
2) Kx increased
3) Significant anti-Ku (“universal”) with exposure
b. McLeod phenotype
1) Absence of Kx

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2) Markedly decreased (not absent) Kell system
Ags
3) No anti-Ku!
4) Hemolytic anemia with acanthocytes

5) Occasional association with X-linked Chronic

Granulomatous Disease.
a) NADPH oxidase deficit
b) Organisms phagocytized but not killed
c) Catalase-positive organisms (Staph)
6) Also associated with cardiac and nervous system
abnormalities
K. A Few Other Antigens (in brief)
1. Lutheran
a. Lua and Lub antigens
b. Linked to Se on chromosome 19
c. Antibodies uncommon and not usually significant
d. Enzymes decrease Lu antigen activity
2. Xg
a. Gene carried on X chromosome (“X-linked”)
1) Seen in approximately 2/3 of males and 90% of
females
b. Antibody insignificant
3. Diego System
a. Two pairs of antigens, Dia/Dib, Wra/Wrb (“Wright
A” and “Wright B”)
b. Anti-Dia may be significant, but is uncommon
c. Anti-Wra is common but is not usually significant
4. Sda (“Sid”)
a. High frequency
b. Refractile immune complexes
c. Lectin of Dolichos biflorus agglutinates Sid
positive RBCs (like A1).
d. Neutralize with urine of the guinea pig!
5. HTLA (“High titer, low avidity”)
a. High frequency
b. Chido, Rodgers most frequent
1) Complement components (C4)
c. Clinically insignificant (no HTRs or HDN)
d. Neutralize with serum.

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