Arno

For acquired maternal IgG antibodies (which may also be transferred postnatally through breast milk), assessing the antibody specificity (AbS) in the newborn, as previously mentioned, appears to be a reasonable approach. In addition, the Direct Antiglobulin Test (DAT) remains key, and performing an elution is important (even if the DAT result is negative). In your case, the negative DAT suggests that either the anti-N antibody did not cross the placenta, possibly due to being a naturally occurring IgM, and/or the baby is N-negative.

For acquired maternal IgG antibodies (which may also be transferred postnatally through breast milk), assessing the antibody specificity (AbS) in the newborn, as previously mentioned, appears to be a reasonable approach. In addition, the Direct Antiglobulin Test (DAT) remains key, and performing an elution is important (even if the DAT result is negative). In your case, the negative DAT suggests that either the anti-N antibody did not cross the placenta, possibly due to being a naturally occurring IgM, and/or the baby is N-negative.

Sorry Neil, but I have to point out that this is not completely accurate.  Any red cell antigens that are adsorbed onto the red cell surface, rather than being an integral part of the red cell membrane remain the type of the patient, rather than the donor.  This is true of the Lewis phenotype (for instance, if the recipient was Le[a+b-], and the donor was Le[a-b+], after the transplant, the red cells will group as Le[a+b-], and not as Le[a-b+]}.  This is also true of antigens within the Chido/Rodgers Blood Group System, and certain others.

If the recipient is a Secretor, they will continue to secrete ABO substance of the original ABO type, which, of course, will also be adsorbed onto the red cell surface (as well as being in the plasma, leading to the phenomenon of "accommodation", and this is why most recipients stay with a reverse group of "AB" after an ABO mis-matched stem cell/bone marrow transplant.

SORRY TO BE A PEDANT, PARTICULARLY AS I AGREE WITH EVERYTHING ELSE YOU HAVE WRITTEN!

Perhaps this is one rare physician who actually reads the medical literature on the subject or has thought things through.
The history of this is very simple.  Based upon the experience of severe or fatal hemolytic transfusion reactions to whole blood, it was discovered that when a patient's ABO type was unknown, and urgent transfusion was life saving, group O was the least likely to result in disaster.  When group O red cells became available during the middle of the last century, with modest amounts of plasma left, it was decided by the then experts that this could be used for non-urgent, routine transfusions of all patients. So-called universal donor O red cells.  The problem, with the 100% accuracy of hindsight, was that we had no evidence this is was good, much less optimal practice. But it was convenient. It meant blood banks didn't have to stock all 8 Rh and ABO types, so it was good for us in the transfusion service. It wasn't good for patients.
Why is that?  Well, there is residual incompatible plasma with anti-A and anti-B in all group O red cells that haven't been washed or thoroughly volume depleted. Well, you might ask, and all of us have assumed for decades, that a few dozen milliliters of incompatible plasma is not a big deal.   The answer, now known to some extent, is that it is a big deal for some patients who are groups A, AB and probably B.  This small residual plasma can on rare occasions cause severe hemolysis.  It's 100% severe if it happens to you as a patient.  This has been known for decades. What is new is the data that recipients of ABO mismatched red cells (Group O in general) have a higher rate of red cell alloimmunization to other red cell antigens, (Transfusion 2012 Mar;52(3):635-40. doi: 10.1111/j.1537-2995.2011.03329.x; 2025 Mar;65(3):588-603. doi: 10.1111/trf.18135. higher rates of febrile and allergic reactions, (Transfusion 2012 Mar;52(3):635-40.doi: 10.1111/j.1537-2995.2011.03329.x.) higher rates of HLA alloimmunization, and perhaps overall higher rates of mortality (Transfusion. 2016 Mar;56(3):550-7.doi: 10.1111/trf.13376).
So, if you are a recipient, you want ABO identical transfusions, or compatible red cells that have had all or almost all of the plasma removed, as by washing, for example.
 
 
 

That was my 1st thought as well!

Neil Blumberg, I'll leave this one to you!

I just answered this question.

My Score PASS  

I wonder if your providers have ever thought of looking at their patients SYMPTOMS, rather than costing a fortune by using a tick box method for ordering tests?????

Of course, I fully realise that this is a suggestion that can only be put forward to your providers by your Pathologist, as doing so yourself would probably get you into deep trouble.

Did you mean that AuntiS.  I fully confess there were times when I did!!!!!!!!!!!!!!!!!!!!!!!!!!!

Agree that in “not recently transfused”patients, eluates are of no clinical use unless you like seeing panagglutinins.😜 Negative eluates occur in some drug dependent examples but the clinical information is paramount in such situations in any case.

Many, many years ago now, when I was working at the old Westminster Hospital in London as a quite junior member of the Blood Transfusion staff, I spent quite a few hours working on a sample from a patient with a positive DAT, trying to determine the specificity, in order to see whether the antibody was an allo- or an auto-antibody.  This included the use of several very rare red cells that I had frozen down and also examining the eluate.  After many happy hours, I had got precisely nowhere, and so sent a sample to my former colleges at the International Blood Group Reference Laboratory.
I received a somewhat "spicy" report from my heroine Joyce Poole, who explained to me, in words of one syllable, that I had rather been wasting my time, rare cell collection and the laboratory's money as, in almost all cases, the specificity would be found to be an auto-anti-Rh17 or auto-anti-Rh18!!!!!
Since then, I have reverted to doing as little as possible on such samples and, when I retired 43 years later, and, as far as I know, none of the patients ever died as a result.  There was a close one once, when I was working on a sample on a Saturday on-call in the Red Cell Reference Laboratory at NHSBT-Tooting Centre.  I was working on a sample that was overtly a case of wAIHA.  After several allo-adsorptions, I was finally able to provide "suitable blood".  It was only at the last minute that the computers came back on after an unplanned downtime, and it appeared that the patient was known, from many years previously as having an allo-anti-Vel!!!!!!!  As you can imagine, I did several more tests before I released the blood (on Pathologist's orders), as there was absolutely no evidence of an anti-Vel (auto- or allo-) in the present sample - but it did give me a bit of a turn!!!!!!!!!!!!
I would recommend a thorough reading of Petz LD, Garratty G.  Immune Hemolytic Anemias.  2nd edition, 2004, Churchill-Livingstone. ISBN  978-0-443-08559-8.
Other than that and, possibly, looking at the patient's sample at a more molecular level (as noelrbrown suggests above), I really wouldn't do much else, except that I would put a little note with the blood to be transfused to remind the doctors and nurses on the ward to be vigilant with their patient observations.
ALL OF THE ABOVE HAVING BEEN SAID, I AM NOT, AND NEVER HAVE BEEN, MEDICALLY QUALIFIED!!!!!!

Hello everyone, 
Here is a new 100% educational opportunity (with PACE credits) for those who are interested in FNAIT. Here is the link to register Webinar | Bio-Rad
 

Hello everyone, 
Here is a new 100% educational opportunity (with PACE credits) for those who are interested in FNAIT. Here is the link to register Webinar | Bio-Rad
 

Hello everyone, 
Here is a new 100% educational opportunity (with PACE credits) for those who are interested in FNAIT. Here is the link to register Webinar | Bio-Rad
 

I thought for the first time I would share one of the educational webinars we have been producing with the ISBT because it is a fascinating topic addressed by a great lecturer (Sue Johnson).
So do miss out on the opportunity to watch the recording of this ISBT educational webinar Could it be drugs? How to differentiate AIHA from DIIHA Start zoom webinar | The International Society of Blood Transfusion (ISBT)
 

My understanding was availability and cost. Probably due to FDA and European drug administrations having very different opinions (that list is long).

The standards probably don't apply to post-mortem transfusions.  I cannot imagine why an organ harvest surgery would require transfusion at all, but I'm not a surgeon.  I've had requests to transfuse platelets and plasma to organ donor patients, which we've uniformly denied.  I'd need some explanation of why transfusion, which is pro-inflammatory, immunomodulatory and pro-thrombotic, would benefit the potential organ recipient.  There is so much misinformation, partially promulgated by the transfusion medicine community, of the "benefits" of transfusion, that it is sometimes difficult to explain to clinicians why transfusion is a bad idea in many situations.
 

I thought for the first time I would share one of the educational webinars we have been producing with the ISBT because it is a fascinating topic addressed by a great lecturer (Sue Johnson).
So do miss out on the opportunity to watch the recording of this ISBT educational webinar Could it be drugs? How to differentiate AIHA from DIIHA Start zoom webinar | The International Society of Blood Transfusion (ISBT)
 

I thought for the first time I would share one of the educational webinars we have been producing with the ISBT because it is a fascinating topic addressed by a great lecturer (Sue Johnson).
So do miss out on the opportunity to watch the recording of this ISBT educational webinar Could it be drugs? How to differentiate AIHA from DIIHA Start zoom webinar | The International Society of Blood Transfusion (ISBT)
 

I thought this would fit quite well with this discussion on new blood group system/antigen discovery
Advancement of new molecular tools for discovery of blood groups - Transfusion Today - October 2024 

Hats off to Nicole and the whole IBGRL team  

I thought this would fit quite well with this discussion on new blood group system/antigen discovery
Advancement of new molecular tools for discovery of blood groups - Transfusion Today - October 2024 

Hats off to Nicole and the whole IBGRL team  

A research team led by NHS Blood and Transplant scientists based in Bristol, at NHSBT’s International Blood Group Reference Laboratory (IBGRL), and supported by colleagues at the University of Bristol, has discovered a new blood group, MAL. 🙌 🩸

They identified the genetic background of the previously known but mysterious AnWj blood group antigen, thus allowing identification and treatment of rare patients lacking this blood group.

Louise Tilley, Senior Research Scientist, IBGRL Red Cell Reference at NHS Blood and Transplant, said: “The genetic background of AnWj has been a mystery for more than 50 years, and one which I personally have been trying to resolve for almost 20 years of my career. It represents a huge achievement, and the culmination of a long team effort, to finally establish this new blood group system and be able to offer the best care to rare, but important, patients."

hashtag#NHSBT hashtag#GiveBlood hashtag#SaveLive hashtag#NHSCareers Activate to view larger image,

I worked in Red Cell Immunohaematology for most of my 43 years before retirement, including two times at the International Blood Group Reference Laboratory (IBGRL), and for over a decade at one of the NHS Blood and Transplant Centres in London.  During that time, I saw some pretty weird Kidd antibodies, but never came across an example of one that reacted with red cells with Jk(a) heterozygous expression, but not with Jk(a) homozygous expression.
One such "weird" type (although I never saw one) was the extremely rare, dominant inhibitor type In(Jk), similar, but, of course, not identical to In(Lu).  These red cells usually type as Jk(a-b-), but their true Kidd type can be ascertained by Adsorption and elution tests..  These red cells are also more resistant to haemolysis by 2M Urea than red cells with "normal" expression of the Kidd antigens, but less resistant to haemolysis by 2M Urea than true "amorphic" Jk(a-b-) red cells.
There are approximately 14, 000 copies of the Kidd carrier molecule per red cell (quite a small number, when compared with some other carrier molecules, such as the D antigen).
The amino acid residue that defines either the Jka or Jkb antigens is very close to the red cell membrane in the 4th extracellular loop but is largely “hidden” by the 3rd extracellular loop (steric hindrance).
 Both facts may contribute to the weak reactions between Kidd antibodies and Kidd antigens.

Schematic of the Kidd carrier molecule (after Wester ES, Storry JR, Olsson ML.  Characterization of Jk(a+weak): a new blood group phenotype associated with an altered JK*01 allele.  Transfusion 2011; 15: 380-392.  DOI: 10.1111/j.1537-2995.2010.02795.x.
In this paper, Wester et al also describe weakened forms of both the Jka and the Jkb antigens, but in each case, the amino acid substitution is remote from position 280 of the mature protein. 
 In addition, an individual with the Trp171Arg mutation with weak Jk(a) expression has produced an anti-Jk3 or anti-Jk3-like antibody, and so they may be “dangerous patients” (Whorley T, Vage S, Kosanka J, Lose SR, Sandquist AR, Copeland TR, Westhoff CM.  JK alleles associated with altered Kidd antigen expression.  Transfusion 2009; 41 (Suppl.): 48A-49A (abstract).
Lastly (for now anyway!), most foetal red cells sensitised by maternal antibodies react only with anti-IgG, but I (and a colleague Grant Webb) have both noticed, but not published, occasions when such red cells also react with anti-C3d and, in one case, only anti-C3d (see genuine photographs below)..