ABSTRACT Introduction: Kidd blood group system has a special importance in transfusion medicine as the antibodies to Kidd antigens tend to go down to undetectable levels but show an anamnestic response on exposure through pregnancy or blood transfusion and cause hemolytic transfusion reaction, most commonly delayed transfusion reaction. Case Report: We report a patient who developed alloantibodies to &apos;Kidd a&apos; antigen leading to delayed hemolytic transfusion reaction. Conclusion: We emphasize the steps for detecting these antibodies and the precautions to be taken once these antibodies are identified

Gagandeep Kaur

Lakhwinder Singh

S S Lehl

Sabita Basu

Sheetal Malhotra

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IJBTI – International Journal of Blood Transfusion and Immunohematology, Vol. 1, 2011. ISSN – [2230 ­ 9020]
Delayed hemolytic reaction due to anti Jkaalloimmunization
Sheetal Malhotra, Gagandeep Kaur, Lakhwinder Singh,Sabita Basu, SS Lehl
ABSTRACT
Introduction: Kidd blood group system has aspecial importance in transfusion medicine asthe antibodies to Kidd antigens tend to go downto undetectable levels but show an anamnesticresponse on exposure through pregnancy orblood transfusion and cause hemolytictransfusion reaction, most commonly delayedtransfusion reaction. Case Report: We report apatient who developed alloantibodies to ‘Kidd a’antigen leading to delayed hemolytictransfusion reaction. Conclusion: We emphasizethe steps for detecting these antibodies and theprecautions to be taken once these antibodiesare identified.
Keywords: Alloimmunization, Kidd blood groupsystem, Delayed hemolytic transfusion reaction,Dosage phenomenon, Anamnestic response
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Malhotra S, Kaur G, Singh L, Basu S, Lehl SS. Delayedhemolytic reaction due to anti Jka alloimmunization.International Journal of Blood Transfusion andImmunohematology 2011;1:16­19.
Article ID: 100004IJBTISM2011
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doi:10.5348/ijbti­2011­4­CR­4
INTRODUCTION
Alloimmunization by Kidd (Jk) blood group systemis uncommon. These antibodies are often immune innature and are produced in response to pregnancy ortransfusion. Owing to their weak serological nature andtheir tendency to show dosage phenomenon, theseantibodies are difficult to detect. Dosage phenomenonrefers to the fact that antibodies of certain blood groupsystems react more strongly with homozygous (doubledose antigen) red cells and may not react when bothantithetical antigens are present on red cells(heterozygous red cells). Moreover these antibodiesoften occur in combination with other antibodies whichfurther complicates the case work up. We report a caseof delayed hemolytic transfusion reaction (HTR) due toalloimmunization by Jka antigens.
CASE REPORT
A 14­years­old female presented with complaints offever with chills, rash all over the body, bleeding frommouth for the past 20 days. There was history oftyphoid three months back. The patient had beentransfused one unit of packed red blood cells (PRBC)from an outside hospital 15 days back. In addition, shehad also received two units of blood components(?platelets ??FFP, definite information could not be
CASE REPORT OPEN ACCESS
Sheetal Malhotra1 , Gagandeep Kaur1 , Lakhwinder Singh1 ,
Sabita Basu2, SS Lehl3
Affi l iations: 1Department of Transfusion Medicine
Government Medical College and Hospital, Chandigarh,
India; 2Professor, Department of Transfusion Medicine,
Government Medical College and Hospital, Chandigarh,
India; 3Professor, Department of General Medicine,
Government Medical College and Hospital, Chandigarh,
India.
Corresponding Author: Dr Sabita Basu, Professor,
Department of Transfusion Medicine, Government
Medical College and Hospital, Chandigarh, India –
1 60032; Postal address - House number 54, Sector 24 A,
Chandigarh - 1 60024; Ph: 91 -1 72-2728945;
Email : drsabitabasu@gmail .com
Received: 05 June 2011
Accepted: 09 August 2011
Published: 31 October 2011
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IJBTI – International Journal of Blood Transfusion and Immunohematology, Vol. 1, 2011. ISSN – [2230 ­ 9020]
obtained) 14 days back. Both these transfusions wereuneventful. Clinically, possibilities of systemic lupuserythematosus (SLE) and thrombotic thrombocytopenicpurpura (TTP) were considered. As such, her samplewas sent to the blood bank for direct Coombs test,indirect Coombs test and a requisition was received forone unit of PRBC and two units of platelet concentrate.Complete blood count of the patient showed anaemia(Hb ­ 4.4 g/dl), leucopenia (Total leukocyte counts ­2400/µl) and thrombocytopenia (Platelet count ­10,000/µl) with increased reticulocyte count (6.8%) andperipheral smear showed marked anisocytosis andpoikilocytosis with microcytes, normocytes, fewmacrocytes, few macro­ovalocytes, fragmented cells,elliptical cells and bite cell, features which wereconsistent with hemolytic anaemia. Liver functionsrevealed hyperbilirubinemia (S. bilirubin ­ 2.3 mg/dl)with mild transaminitis. Renal parameters were withinnormal limits. Her hemoglobin prior to the abovementioned transfusion was 5.2 g/dl.Blood group of the patient was A Rh(D) positive. Thedirect antiglobulin test (DAT) was positive (2+ on geland 1+ on tube) with polyspecific antihuman globulin(anti­IgG and anti­C3d) and with monospecificanti–IgG. With anti­C3d, it was negative on tube andvery weakly positive on gel. The indirect antiglobulintest was negative on immediate spin phase and positiveon AHG phase. Autocontrol was negative on immediatespin phase and showed a mixed field reaction on anti­human globulin (AHG) phase. Antibody screen andidentification panel was put on gel (using commerciallyprepared red cell antigens from Diamed lab) and theresults confirmed the presence of anti Jka antibodies(table 1). It was noted that the strength of the reactionswere stronger in the cells carrying a double dose of Jkaantigens as compared to cells which were heterozygousfor Jka, thereby demonstrating dosage phenomenon. Aneluate was obtained from patient’s red cells (by heatelution method). An antibody screen and identificationpanel of the eluate was put up confirming anti­Jkaantibodies. Alloadsorption with Jka positive cells wasperformed. On elution, Jka antibodies were confirmed.Enzyme treatment with 1% papain was done. Papanizedcells were prepared and reactivities were checked withthe patient’s serum. The strength of the reaction wasincreased as Jk blood group system is known to beenhanced after enzyme treatment. Antibody titres were1:2 on tube. Patient’s phenotype could not be donebecause of recent transfusion 15 days back. AfterDithiothreitol (DTT) treatment, strength of thereactions remained same; confirming IgG nature ofantibodies. So the final inference drawn was IgG typewarm reacting Jka alloantibody, showing dosagephenomenon. As mentioned earlier, autoantibody couldnot be ruled out because of the presence of transfuseddonor cells in circulation. Two random cross matchesdone by the technician before identification of theantibody were found to be compatible on immediatespin phase at 4°C, 22°C and 37°C. These units werechecked for Jka phenotype and compatibility by AHGphase. One unit which was homozygous for Jka, Jk (a+b­)
gave a stronger reaction (1+) than the other unit (weak+) which was heterozygous Jk (a+b+). Thereafter, sixunits of packed red blood cells, blood group A Rh(D)positive were phenotyped for Jka of which one was Jkanegative. It was transfused under close monitoring andthere was a reported rise of Hb by 1g/dl next day. Twounits of platelet concentrate were transfused on thesame day.
DISCUSSION
In 1951, Kidd Blood Group System, ISBT Symbol: JKand ISBT Number: 009, was discovered. It was namedafter Mrs. Kidd in whom an antibody, not previouslyrecognised caused hemolytic disease of newborn andfetus (HDFN) in her sixth child. The antigens in thissystem are well developed at birth with Jka appearing at11 weeks and Jkb at 7 weeks of intrauterine life. Theantigens are also found on neutrophils and in kidneycells. The prevalence of Jk antigens has been variablyestimated in different studies. Thakral found Jk(a+b­) tobe present in nearly 33%, Jk(a­b+) in 17%, Jk(a+b+) in49% and Jk(a­b­) in 0% of the 1420 donors [1]. Inanother study by Nanu et al, the relative frequencies ofthese antigens was estimated as 29%, 22%, 48% and0.5% respectively among more than 6334 donors [2].These antibodies are more commonly implicated inhemolytic transfusion reactions and sometimes inhemolytic disease of fetus and newborn (HDFN). Thereare very few case reports of anti­Jka causing HDFN incontrast to 13 published case reports of HDFN due toanti­Jkb. Franco et al. scrutinized records of allalloimmunized pregnancies at their center from 1959 to2008 and in 20 pregnancies, anti­ Jka was identified. Ofthese, one had severe disease due to anti­ Jka which wasdiagnosed using maternal antibody titer (1:32) andmiddle cerebral artery peak systolic velocity (MCA PSV).This pregnancy required 4 intrauterine transfusions forfetal anaemia [3]. One of the authors have reported acase of HDFN due to anti­Jkb antibody in a woman withhigh risk pregnancy [4].The index case described above elucidates anti­Jkaalloimmunization following a blood transfusion. In thiscase, anti­Jka antibodies could be missed had the AHGcrossmatch and antibody screen not been performed.This highlights the importance of serologicalcompatibility testing at AHG phase and the necessity forperforming the antibody screen using appropriate panelcells. There are a few case reports in literaturedemonstrating anti­ Jka as an allo or auto antibody [5­10]. Sedlmayer et al. reported a case of HTR due to Jkaantibody. In routine cross matching, the antibody wasmissed in both saline and 22% bovine serum albuminafter incubation at 4°C, 20°C and 37°C and was detectedat AHG crossmatch [7]. Sosler reported a case of acutehemolytic anemia associated with a chlorpropamide­induced apparent auto­anti­Jka [8]. Recently Munoz etal. also reported presence of auto Jka antibodies tocomplicate a case of common variableimmunodeficiency and Evan’s syndrome. The patient
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IJBTI – International Journal of Blood Transfusion and Immunohematology, Vol. 1, 2011. ISSN – [2230 ­ 9020]
had a positive DAT with C3d and a serum auto­antibodywith anti­JKa specificity in the eluate prepared from hisred blood cells. Indirect anti­globulin test (IAT) was alsopositive [10].The present case showed a drop in hemoglobin levelsfrom 5.2 g/dl to 4.4 g/dl after her previous transfusionwith peripheral blood picture suggestive of hemolyticanaemia. It can be inferred that she had a delayed HTRdue to the alloimmunization to Jka antigen throughblood transfusion. The nature of antibody was IgG,reacting at body temperature and was clinicallysignificant. Alloimmunization is an immune responsedue to exposure of foreign antigens through pregnancyor blood transfusion in an immunocompetent hostleading to development of corresponding antibodies.had a positive DAT with C3d and a serum auto­antibodywith anti­JKa specificity in the eluate prepared from hisred blood cells. Indirect anti­globulin test (IAT) was alsopositive [10].The present case showed a drop in hemoglobin levelsfrom 5.2 g/dl to 4.4 g/dl after her previous transfusionwith peripheral blood picture suggestive of hemolyticanaemia. It can be inferred that she had a delayed HTRdue to the alloimmunization to Jka antigen throughblood transfusion. The nature of antibody was IgG,reacting at body temperature and was clinicallysignificant. Alloimmunization is an immune responsedue to exposure of foreign antigens through pregnancyor blood transfusion in an immunocompetent hostleading to development of corresponding antibodies.
Since Jka has been identified uncommonly as a cause
of alloimmunization, universal implementation of
antibody screening in all cases may not prove to be cost
effective. However, it cannot be overemphasized that
screening for such uncommon but clinically significant
antibodies including anti­Jka should be carried out at
least in all cases with a prior history of transfusion
and/or pregnancy. The results also emphasize the fact
that whenever anti­Jka antibodies are suspected, use of
red cells homozygous for Jka antigen in antibody screen
and identification panel is essential for their detection
as they may give a weak or a negative reaction with
Jk(a+b+) cells. A special immunohematology card was
issued to our patient stating the presence of Jka
antibodies, as levels of these antibodies are known to go
down to undetectable levels even after a severe HTR and
she was advised to show the card before any subsequent
transfusion. Once anti­Jka antibody is identified, it is of
utmost mportance to review the previous transfusion
records of the patient for all future transfusions. Such
patients should always be transfused Kidd negative
blood units as these antibodies are known to show an
anamnestic response after transfusion of Kidd positive
blood units leading to severe transfusion reaction.
CONCLUSION
It is well established that pre transfusioncompatibility testing by AHG crossmatch technique ismore sensitive compared to immediate spin in detectingclinically significant IgG antibodies. However, in aresource poor setting like ours, primarily because of the
Abbreviations: SC – screening cell; ID –identification; IS – immediate spin; AHG – anti human globulin
Table 1: Results of antibody screen and identification panel on the patient’s serum.
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IJBTI – International Journal of Blood Transfusion and Immunohematology, Vol. 1, 2011. ISSN – [2230 ­ 9020]
financial constraints and also due to lack of awareness,the personnel engaged in transfusion services may omitthis important step of AHG crossmatch and thusincrease the risk of alloimmunization. So werecommended that the indirect Coombs test, which isable to reveal such irregular antibodies, should beroutinely performed as a part of serologicalcompatibility testing.
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Author ContributionsSheetal Malhotra – Substantial contributions toconception and design, Acquisition of data, Analysisand interpretation of data, Drafting the article, Revisingit critically for important intellectual content, Finalapproval of the version to be publishedGagandeep Kaur – Substantial contributions toconception and design, Acquisition of data, Analysisand interpretation of data, Drafting the article, Revisingit critically for important intellectual content, Finalapproval of the version to be publishedLakhwinder Singh – Substantial contributions toconception and design, Acquisition of data, Analysisand interpretation of data, Drafting the article, Revisingit critically for important intellectual content, Finalapproval of the version to be publishedSabita Basu – Substantial contributions to conceptionand design, Acquisition of data, Analysis andinterpretation of data, Drafting the article, Revising itcritically for important intellectual content, Finalapproval of the version to be publishedSS Lehl – Substantial contributions to conception anddesign, Acquisition of data, Analysis and interpretationof data, Drafting the article, Revising it critically forimportant intellectual content, Final approval of theversion to be published
GuarantorThe corresponding author is the guarantor ofsubmission.
Conflict of InterestAuthors declare no conflict of interest.
Copyright© Sheetal Malhotra et al. 2011; This article isdistributed under the terms of Creative Commonsattribution 3.0 License which permits unrestricted use,distribution and reproduction in any means providedthe original authors and original publisher are properlycredited. (Please see www.ijbti.com/copyright­policy.php for more information.)
REFERENCES
1. Thakral B, Saluja K, Sharma RR, Marwaha N.Phenotype frequencies of blood group systems (Rh,Kell, Kidd, Duffy, MNS, P, Lewis, and Lutheran) in
north Indian blood donors. Transfus Apher Sci2010;43:17­22.2. Nanu A, Thapliyal RM. Blood group gene frequencyin a selected north Indian population. Indian J MedRes 1997;106:242­6.3. Franco A, Rossi K, Krugh, O‘Shaughnessy R.Management of anti­Jka alloimmunization. J ReprodMed 2009;54:121­5.4. Thakral B, Malhotra S, Saluja K, Sharma RR,Marwaha N. Hemolytic disease of neworn due toanti­Jkb in a woman with high risk pregnancy.Transfus Apher Sci 2010;43:17­22.5. Guillausseau PJ, Wautier JL, Boizard B, Drouet L,Guillausseau C, Bitoun A et al. Anti­JKa specificity: arare variety of auto­immune hemolytic anemia­report of a case associated with myxoedema. SemHop 1982;58:803­5.6. Preussner S, Roewer J. Hemolytic transfusionaccident due to the blood group antibody anti­Jka.Folia Haematol Int Mag Klin Morphol Blutforsch1975;102:690­6.7. Sedlmayer A. Hemolytic transfusion incident causedby a Kidd­antibody, anti­Jka. Wien Klin Wochenschr1983;95:773­5.8. Sosler SD, Behzad O, Garratty G, Lee CL, PostawayN, Khomo O. Acute hemolytic anemia associatedwith a chlorpropamide­induced apparent auto­anti­Jka. Transfusion 1984;24:206­9.9. Ganly PS, Laffan MA, Owen I, Hows JM. Auto­anti­Jka in Evans' syndrome with negative directantiglobulin test. Br J Haematol 1988;69:537­9.10. Garcia­Munoz R, Anton J, Rodriguez­Otero P,Moreno C, Sanchez­Ibarolla A, Seijo LM et al.Common variable immunodeficiency and Evanssyndrome complicated by autoimmune hemolysisdue to anti­Jka auto­antibodies. Leukemia &Lymphoma 2008;49:1220­22.
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Delayed hemolytic reaction due to anti Jk a alloimmunization

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Delayed hemolytic reaction due to anti Jk a alloimmunization

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