Facts about Jka and Jkb antigens and antibodies:
- Part of the Kidd blood group system.
- Jka is one of the most immunogenic red cell antigens, surpassed only by ABO, RhD, and K antigens. Jkb is not very immunogenic.
- Antibodies rarely cause HDFN.
- Antibodies are not very stable in storage and can disappear from patients' circulation quickly making them difficult to detect pre-transfusion. They typically become undetectable by serology after approximately 14 days.
- Capable of causing acute hemolytic transfusion reactions but more commonly associated with delayed hemolytic transfusion reactions.
- Can cause acute transplant rejection, specifically acute renal transplant rejection. Due to the frequency of this, they are thought to behave as histocompatibility antigens.
- Jk(a-b-) phenotype is very rare but found more commonly in Polynesians. These RBCs will also lack urea transporter. The phenotype is detected using 2M Urea treatment. Normal RBCs will swell and burst in 2M Urea. Jk(a-b-) cells resist 2M Urea treatment and will shrink but not lyse. There are 2 possible pathways to this phenotype:
- Jknull Amorphic lacks Jka, Jkb, and Jk3. When exposed to the antigens, patients easily form anti-Jk3. Jk3 is an inseparable anti-JkaJkb and will react with all cells except those negative for both antigens. Anti-Jk3 is seen in severe hemolytic transfusion reactions but not HDFN.
- The other pathway to this phenotype is a Jknull In(Jk) suppressor in which the cells type negative for the antigens but can be found in trace amounts. In(Jk) suppressor has one dominant inhibitor gene which expresses as Jk(a-b-) serologically but there are trace amounts of the antigen present, thus it is not truly a Jknull phenotype. Since there are Jk antigens present, they will lyse in 2M Urea. As a result, 2M Urea can differentiate between these two phenotypes. These patients do not make anti-Jk3. No diseases are associated with this phenotype.
- Anti-Jka and Anti-Jkb can bind complement about 50% of the time. Because of this, sometimes using a polyspecific AHG reagent can enhance detection. Enzyme treatment of RBCs can also enhance reactivity if an Anti-Jka or Anti-Jkb is suspected.
Table 8. Kidd Blood Group System Facts.| Ag/Ab | Ag Frequency (White) | Ag Frequency (Black) | Dosage | Enzyme Interaction | Antibody Class | Complement Binding | Clinically Significant |
| Jka | 77% | 92% | Yes | Enhanced by | IgG | Yes | Yes |
| Jkb | 74% | 49% | Yes | Enhanced by | IgG | Yes | Yes |
