Malcolm Needs

No problem Mabel, BUT, what I don't understand is why your Pathologist didn't tell the OB doctors "to get knotted" when they asked for the antibody to be titrated.  As far as I am aware, there has only ever been one peer-reviewed paper suggesting that a maternal anti-Le(a) has caused "clinically significant" HDFN (Carreras Vescio LA, Torres OW, Virgilio OS, Pizzolato M.  Mild hemolytic disease of the newborn due to anti-Lewisa.  Vox Sang 1993; 64: 194-195.  DOI: 10.1111/j.1423-0410.1993.tb05387.x.) and, from memory, I believe that this was not, how should I put it, universally accepted!
More to the point though, given that there a[[ears to be no detectable anti-Le(a) in the plasma at the moment, have you checked the lady's present Lewis phenotype?  It could be that she is now Le(a+b-), or even Le(a-b+).  Excuse me asking, as I am sure you probably know this, but there may be others reading this who do not, it has been known for many years that pregnant women may become transiently Le(a-b-) and may even produce Lewis antibodies.  It was originally thought that pregnant women produced less Lewis glycolipid, but it is now thought that this is not so.  It has been theorised that the increased incidence of the Le(a-b-) phenotype during pregnancy may be a result of increased concentration of plasma lipoproteins during pregnancy (Hammar L, Mansson S, Rohr T, Chester MA, Ginsburg V, Lundblad A, Zopf D.  Lewis phenotype of erythrocytes and Leb-active glycolipid in serum of pregnant women.  Vox Sang 1981; 40: 27-33.  DOI: 10.1111/j.1423-0410.1981.tb00665.x.).  In pregnant women, the ratio of lipoprotein to red blood cell mass increases more than fourfold, so that much more Lewis glycolipid is attached to plasma lipoprotein than is available for the red blood cell surface.
I shall now shut up and let others comment!!!!!!!!!!!!!!!!!!!!!!

No problem Mabel, BUT, what I don't understand is why your Pathologist didn't tell the OB doctors "to get knotted" when they asked for the antibody to be titrated.  As far as I am aware, there has only ever been one peer-reviewed paper suggesting that a maternal anti-Le(a) has caused "clinically significant" HDFN (Carreras Vescio LA, Torres OW, Virgilio OS, Pizzolato M.  Mild hemolytic disease of the newborn due to anti-Lewisa.  Vox Sang 1993; 64: 194-195.  DOI: 10.1111/j.1423-0410.1993.tb05387.x.) and, from memory, I believe that this was not, how should I put it, universally accepted!
More to the point though, given that there a[[ears to be no detectable anti-Le(a) in the plasma at the moment, have you checked the lady's present Lewis phenotype?  It could be that she is now Le(a+b-), or even Le(a-b+).  Excuse me asking, as I am sure you probably know this, but there may be others reading this who do not, it has been known for many years that pregnant women may become transiently Le(a-b-) and may even produce Lewis antibodies.  It was originally thought that pregnant women produced less Lewis glycolipid, but it is now thought that this is not so.  It has been theorised that the increased incidence of the Le(a-b-) phenotype during pregnancy may be a result of increased concentration of plasma lipoproteins during pregnancy (Hammar L, Mansson S, Rohr T, Chester MA, Ginsburg V, Lundblad A, Zopf D.  Lewis phenotype of erythrocytes and Leb-active glycolipid in serum of pregnant women.  Vox Sang 1981; 40: 27-33.  DOI: 10.1111/j.1423-0410.1981.tb00665.x.).  In pregnant women, the ratio of lipoprotein to red blood cell mass increases more than fourfold, so that much more Lewis glycolipid is attached to plasma lipoprotein than is available for the red blood cell surface.
I shall now shut up and let others comment!!!!!!!!!!!!!!!!!!!!!!

It is true that anti-Lea is quoted in the literature as having caused haemolytic transfusion reactions, but only if the anti-Lea is IgG and lytic. Even then, the reactions are self-limiting.
If a patient has a reaction to the first part of the unit, very often you can leave it for a bit and then resume the transfusion, and the patient has no further reaction whatsoever (although I wouldn't advocate you trying this as an experiment!!!!!!!!!!).
This is because the Le(a) substance in the plasma that is transfused inhibits the anti-Lea.
In addition, because the Lewis immuno-dominant sugar residues (both L-Fucose) are on a Type 1 backbone, they are not truely blood group antigens per se (they are adsorbed onto the surface of the red cell, rather than being an integral part of the red cell membrane) and, as such, can be eluted naturally from the surface of the red cell. By this, I mean that, if you put, for example, Le(a+) red cells in the plasma of an Le(a-b-) individual, the red cells will become Le(a-b-).
This also happens in vivo, so that, if you transfuse an Le(a+) or Le(b+) patient with Le(a-b-) blood, the transfused red cells will become Le(a+) or Le(b+) respectively. In other words, they take on the Lewis type of the recipient.
This is also true of a stem cell or bone marrow transplant. When the graft takes, the blood groups of the red cells will be, as you would expect, those of the donor, BUT the red cells will be the Lewis type of the recipient, and will remain so, as these red cells will adsorb the recipient's Lewis substance from the recipient's plasma.
We would NOT our hospitals with Lewis typed blood (in fact, for a number of years now, we have not even typed out units for Lewis).
:blahblah::blahblah:

Lewis antibodies do not cause HDFN and do not need titration.  We do not Lewis phenotype transfusions to patients with anti-Lewis antibodies, but do a manual antiglobulin crossmatch to find units that do not react. I'm sure there are rare patients whose antibodies can cause removal of Lewis positive red cells at an accelerated rate, but this is not something that needs to be considered unless the patient shows signs of hemolysis or rapid red cell removal.  Never come across this in 50 years of practice :).  But never say never in medicine.

Sorry Yanxia, but are you absolutely certain that the bloody urine wasn't a result of the burns, rather than the anti-Lea?

It is true that anti-Lea is quoted in the literature as having caused haemolytic transfusion reactions, but only if the anti-Lea is IgG and lytic. Even then, the reactions are self-limiting.
If a patient has a reaction to the first part of the unit, very often you can leave it for a bit and then resume the transfusion, and the patient has no further reaction whatsoever (although I wouldn't advocate you trying this as an experiment!!!!!!!!!!).
This is because the Le(a) substance in the plasma that is transfused inhibits the anti-Lea.
In addition, because the Lewis immuno-dominant sugar residues (both L-Fucose) are on a Type 1 backbone, they are not truely blood group antigens per se (they are adsorbed onto the surface of the red cell, rather than being an integral part of the red cell membrane) and, as such, can be eluted naturally from the surface of the red cell. By this, I mean that, if you put, for example, Le(a+) red cells in the plasma of an Le(a-b-) individual, the red cells will become Le(a-b-).
This also happens in vivo, so that, if you transfuse an Le(a+) or Le(b+) patient with Le(a-b-) blood, the transfused red cells will become Le(a+) or Le(b+) respectively. In other words, they take on the Lewis type of the recipient.
This is also true of a stem cell or bone marrow transplant. When the graft takes, the blood groups of the red cells will be, as you would expect, those of the donor, BUT the red cells will be the Lewis type of the recipient, and will remain so, as these red cells will adsorb the recipient's Lewis substance from the recipient's plasma.
We would NOT our hospitals with Lewis typed blood (in fact, for a number of years now, we have not even typed out units for Lewis).
:blahblah::blahblah:

I think it very much depends upon one's definition of the wording used as to what causes a problem.  It could be clinical or serological or both.

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)..

Auto-anti-M is VERY rare, but is negative with papain/ficin treated red cells.

Auto-anti-M is VERY rare, but is negative with papain/ficin treated red cells.

Lol, I somehow knew Malcolm would know one (or many) more this is true for :-D 
 

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)..

I should have also said that there is an excellent Blood Group Review available, viz Hamilton JR.  An update to Kidd blood group system.  Immunohematology 2024; 40: 28-33.  DOI:  10.2478/immunohematology-2024-005.

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)..

You are quite right Jason.  I also remember a similar paper, written by Jill Storry, entitled "Long term preservation of red cell antibody identification panels in low ionic strength solution."  This was published in Medical Laboratory Sciences 1987; 44 (4): 350-355, but was based on the winning Margaret Kenwright award presentation at the Annual Scientific Meeting of the British Blood Transfusion Society, London, UK on 4th September 1986.  This was when Jill was a Senior Medical Laboratory Scientific Officer at the South Western Regional Transfusion Centre of the National Blood Transfusion Service in Southmead Road, Bristol.  She has done rather well for herself since then, now being a Professor at Lund University.  Unfortunately, I don't have a DOI for this paper.
 
At the time, I was working at Mayday Hospital in Croydon, London, and wrote to her to clear up a couple of queries I had.  In early January 1988 she wrote back to me and, in this reply, she stated,

"Can I also draw your attention to the fact that the original trial (her original trial) was done using frozen re-constituted red cells.  It has subsequently been pointed out to me that when using fresh cells for screening purposes there is significant loss of Fy(a) and Fy(b) antigens over a two week period.  This phenomenon has been well documented (see below) and is due to the release of proteases upon leucocyte aminoglycoside interaction.  Gentamicin is of course, an aminoglycoside antibiotic.  We have overcome this problem completely by leucocyte depletion using a Sepacell 500 filter,  and I hope to submit a short communication to the IMLS journal describing the results of this modification."  I haven't got a reference for this.
The paper to which Jill was referring to in her letter was:
Malyska H, Kleeman JE, Masouredis SP, Victoria EJ.  Effects on Blood Group Antigens from Storage at Low Ionic Strength in the Presence of Neomycin.  Vox Sanguinis 1983; 44 (6): 375-384.  DOI: 10.1111/j.1423-0410.1983.tb03660.x
All that having been said, I would be surprised if all screening cells and antibody identification cells were not now leukodepleted.  In addition, of course, apart from certain areas of Asia, neither the Fy(a), nor the Fy(b) antigens can be regarded as high prevalence antigens, and those antigens within the Duffy Blood Group System that can be regarded as high prevalence (Fy3, Fy5 and Fy6) are vey different to both Fy(a) and Fy(b), and so it is doubtful that these would weaken substantially upon storage.

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)..

I should have also said that there is an excellent Blood Group Review available, viz Hamilton JR.  An update to Kidd blood group system.  Immunohematology 2024; 40: 28-33.  DOI:  10.2478/immunohematology-2024-005.

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)..

I should have also said that there is an excellent Blood Group Review available, viz Hamilton JR.  An update to Kidd blood group system.  Immunohematology 2024; 40: 28-33.  DOI:  10.2478/immunohematology-2024-005.

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)..

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)..

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)..

You are quite right Jason.  I also remember a similar paper, written by Jill Storry, entitled "Long term preservation of red cell antibody identification panels in low ionic strength solution."  This was published in Medical Laboratory Sciences 1987; 44 (4): 350-355, but was based on the winning Margaret Kenwright award presentation at the Annual Scientific Meeting of the British Blood Transfusion Society, London, UK on 4th September 1986.  This was when Jill was a Senior Medical Laboratory Scientific Officer at the South Western Regional Transfusion Centre of the National Blood Transfusion Service in Southmead Road, Bristol.  She has done rather well for herself since then, now being a Professor at Lund University.  Unfortunately, I don't have a DOI for this paper.
 
At the time, I was working at Mayday Hospital in Croydon, London, and wrote to her to clear up a couple of queries I had.  In early January 1988 she wrote back to me and, in this reply, she stated,

"Can I also draw your attention to the fact that the original trial (her original trial) was done using frozen re-constituted red cells.  It has subsequently been pointed out to me that when using fresh cells for screening purposes there is significant loss of Fy(a) and Fy(b) antigens over a two week period.  This phenomenon has been well documented (see below) and is due to the release of proteases upon leucocyte aminoglycoside interaction.  Gentamicin is of course, an aminoglycoside antibiotic.  We have overcome this problem completely by leucocyte depletion using a Sepacell 500 filter,  and I hope to submit a short communication to the IMLS journal describing the results of this modification."  I haven't got a reference for this.
The paper to which Jill was referring to in her letter was:
Malyska H, Kleeman JE, Masouredis SP, Victoria EJ.  Effects on Blood Group Antigens from Storage at Low Ionic Strength in the Presence of Neomycin.  Vox Sanguinis 1983; 44 (6): 375-384.  DOI: 10.1111/j.1423-0410.1983.tb03660.x
All that having been said, I would be surprised if all screening cells and antibody identification cells were not now leukodepleted.  In addition, of course, apart from certain areas of Asia, neither the Fy(a), nor the Fy(b) antigens can be regarded as high prevalence antigens, and those antigens within the Duffy Blood Group System that can be regarded as high prevalence (Fy3, Fy5 and Fy6) are vey different to both Fy(a) and Fy(b), and so it is doubtful that these would weaken substantially upon storage.

I haven't seen a rebuttal but the FY system is reported to be a problem with storage. It was reported by :
Williams D, Johnson CL, Marsh WL. Duffy antigen changes on red blood cells stored at low temperature. Transfusion. 1981 May-Jun;21(3):357-9. doi: 10.1046/j.1537-2995.1981.21381201813.x. PMID: 7233520.

Could be an antigen within the Knops Blood Group System.  They are notorious for "going off" on older red cells, but the antibodies are not renowned for being clinically significant.