Leaderboard

Not all 'nonspecific reactions' must be antigen typed for Kidd antigens. Evaluate the reactions you see - what do they have in common? Are the reactions occurring where a Kidd antigen is present, especially where it is expressed as a double dose (example: Jka+Jkb-) and not occurring where Kidd antigens are not present. Are the single dose cells (example: Jka+Jkb+) not reacting - which could be the case with an antibody that has a low titer. Keep in mind that some antigen positive cells may not react with an antibody with a low titer, even the double dose cells may not react. If this is what you see, and it looks anti-Jka-ish or anti-Jkb-ish, I would antigen type the patient for the appropriate Kidd antigen. Evaluate your reactions in this way for any antibody that can show dosage, not just potential Jk antibodies, though they are notorious for behaving this way and notorious for causing delayed reactions. You might also see this sort of behavior with newly forming antibodies whose titers are just starting to rise.

I wouldn't suggest that with all non-specific reactions. Just if you get an impression that there might be a kidd, it's better to error on the side of caution. I've certainly called my fair share of unknown/non-specific reactions. I've seen several antibodies who don't react even with all of the homozygous expressions. Honestly, sometimes its not much more than your blood bank "spidey-sense" that leads you to the antibody ID, when you would have been completely correct (per SOPs) to call something unknown.

I agree with the above. Non-specific reactions of any kind cannot be ignored out of hand. You must be careful as with everything in the Lab. Any set of non-specific reactions could indicate an emerging antibody as someone mentioned above. That is why we end up doing an AHG crossmatch when we have such patients, even though there are no other specific allo-antibodies present. Scott

Whatever the reason, do not even think of ever transfusing with group AB blood! anna

I would like to come back to your question about neutral cards not containing AHG. (And apologies for the delay, have been inundated with my day to day work recently). So - IgG antibodies can not usually agglutinate red cells directly. They stick on to the red cells and can cause their destruction, but for us to be able to see that the IgG antibodies are present, we need agglutination. So in order to make IgG antibodies agglutinate, we have to add something that will help them. This 'something else' is either AHG or enzymes. The two react in different ways. The AHG makes a bridge between the IgG molecules attached to the red cells; and the enzymes remove the outer negatively-charged layer of the red cell membrane so that the distance between them is reduced and IgG molecules can agglutinate directly. So, for the AHG test, you need a source of AHG. In the old days (and still in many places today), where the test was done in tubes, this was added to the test after incubation and washing as a liquid. In gel, the AHG is already in the cards. So the 'helper' is present in the gel. For enzymes, the 'helper' is already in the cells, which have been pre-treated with enzymes. Therefore you do not need to have a second helper in the gel. If you put AHG in the gel as well as using enzyme treated cells you are using two different helpers at the same time, when for most cases one is enough. You can choose to use both in an enzyme Coombs technique; it can be helpful for identifying Kidd antibodies; but it is not a good idea to use this as a routine technique unless you want to increase considerably the number of identification panels you have to do, most of which will lead to nothing. Hope that helps anna

Weak ABO: Oh. Then it could be a multitude of other possibilities. So, as routine lab, it might happen that a newborn be "temporarily mis-typed" in cases of weak or subgroups of ABO. As they come of age, they could probably be corrected. Am I getting it right ? Anti-PP1Pk: Interesting as it may seem, the sample had been sent to a reference lab. Confirmed as Anti-PP1Pk. Open and shut case as it may seem. But the curious cat was at it again: 6 year old female DX: Congestive heart disease. Blood group: Indeterminate Solid phase testing: Anti-A : 4+ Anti-B : 0 Anti-D: 4+ Rh Ctrl: 0 A1 Cells: 4+ B Cells : 4+ Ab ID: Confirmed Anti-PP1Pk from reference lab -"Indeterminate" for 6 years. 1st testing 2011 (18 months of age) ^^

I could not agree more. You will see in many text books that there are 14, 000 Kidd antigens per red cell, BUT, if you read around, this is a mean number, with some workers finding as many as 32, 000 antigen sites per red cell, while others as few as 7, 000 antigen sites per red cell. Now, all of these are "estimates" and, of course, it also depends upon the expression of the Kidd antigens (or any other antigens, come to that) of the individual being studied. Let us think for the minute, therefore, about the red cells represented on any antibody identification panel. They will be, to all intents and purposes, representative of the general population (save for the fact that they are often selected because they express homozygosity for many antigens, and because they complement the other red cells represented in the panel, so that the panel is "useful") and so some of the red cells will express the Kidd antigens at the higher end of the scale, and some at the lower end of the scale. Those at the lower end of the scale are those about which AMcCord is talking (I think!).

I would say that the two "enhancement" methods mentioned (enzyme and AHG) above are more complimentary than interchangeable. It also depends on the method. For example, our Papain tube treatment method finishes with an AHG step. Scott

Hi Lingkwyz, Well, in the case of a weak A and a strong B in a newborn, once again, it is impossible to say at the moment. It could be a genuine weak A phenotype, or, it could be, in this case, the B-transferase "winning" against the A-transferase in direct competition. I am VERY jealous of your patient with suspected anti-PP1Pk; I haven't seen one of those for years now! Best wishes, Malcolm

My game plan with the kidds is to honor what antibody I think I see (assuming it agrees with their phenotype). Because titers with kidds are notorious for falling quickly, and their transfusion reactions can be particularly unpleasant, I always think its better to be safe than sorry.

There is a way of confirming it by genoty[ing, but it would cost the Earth for very little return. I would like to know how old is the patient and what is the underlying pathology? You have to remember that the the A, B and H antigens, in common with other carbohydrate-based red cell antigens, are not direct gene products, simply because only proteins can be direct gene products, whilst sugars cannot. In the case of an AB individual, at least two different transferase enzymes are responsible for conferring either the N acetyl-D-galactoseamine residue, in the A antigen, or the D-galactose residue, in the case of the B antigen. These two enzymes are in direct competition with one another as to which one "wins the race" to convert the H backbone to either A or B; sometimes the "A transferase" wins, and sometimes the "B transferase" wins. In this case, it could be that the A-transferase is winning "hands down", and that the B-transferase is "whimping out a bit"! Sorry, that last bit wasn't written exactly scientifically, but I hope you understand what I mean!