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In a delayed haemolytic transfusion reaction due to an apparently typical complement-binding IgG anti-Jka, it was possible to show that transfused Jk (a+b+) cells were destroyed progressively over a period of about 3 weeks. The slow destruction may have been due partly to the fact that the patient had been splenectomised.
Data on centromeric linkage for trisomies 13 and 18 are presented. There is no substantial evidence that any of these loci studied are on either chromosome. There is weak evidence relating the locus defining the Kidd groups to chromosome 18.
Water homeostasis is regulated in large part by the proper operation of the urinary concentrating mechanism. In the renal inner medulla, urea recycling from the inner medullary collecting duct to the inner medullary interstitium is thought to be essential for the production of a concentrated urine; however, it has not been possible to test this hypothesis in humans. Recently, a unique combination of genetic abnormalities has been described: absence of Kidd blood group antigens and absence of carrier-mediated urea transport in erythrocytes. Because animal studies indicate a similarity between urea transport in red blood cells and the nephron, it was postulated that patients without the Kidd antigen might lack facilitated urea transport in their kidneys. Hence, their ability to concentrate urine maximally was measured. Current models of nephron function would predict that in the complete absence of urea transport, the maximal concentrating ability would be around 800 to 900 mosM/kg H2O. Two homozygous patients had a moderate decrease in maximal concentrating ability (UosM,max = 819 mosM/kg H2O); a heterozygote also had some limitation. These studies raise the possibility that the erythrocyte urea transporter and the kidney urea transporter are encoded by a single gene (detected by the mutational loss of the Kidd antigen) and that a lack of facilitated urea transport impairs urea recycling in the kidney and, hence, maximal urinary concentrating ability.
A Caucasian French family was investigated including two Jk(a-b-) sibs who had developed anti-JkaJkb. The parents were first cousins. Quantitative study of Kidd antigens using titration scoring and HD50 assay clearly showed the parents and a maternal aunt, phenotypically Jk(a+b-), to have a weak expression of Jka documenting thereby the transmission of the postulated silent gene Jk. Absorption, elution and coagglutination assays revealed the cross reactivity of the antibody developed by the two sibs. Leucocytes and platelets from these two individuals were not shown to absorb anti-JkaJkb.
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11 blood and seric group markers were studied in a case of 46,XX,del(8)(qter yields p22 :) in order to contribute to the exclusion map. MNSs and Jk are informative and could be excluded from the region. The proband is also definitly heterozygous for immunoglobulin Gm groups which were tentatively assigned to the short arm of chromosome 8 or 12.
A haemolytic transfusion incident caused by anti-Jka is reported about. In a 56 year old patient suffering from chronic iron deficiency anaemia an immunization in the Kidd system has taken place within 9 days. In the course of this immunization the fourth incompatible blood transfusion caused a severe transfusion incident. The necessity of serological compatibility testing by the indirect antiglobulin or enzyme test and the significance of making a strict indication for blood transfusions are referred to.
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A case is presented that suggests that intrauterine transfusion carries the risk of sensitization to red cell antigens other than Rho. In this case intrauterine transfusions of JK a-positive red cells were followed by the appearance in the mother's serum of anti-JK a, an antibody known to cause hemolytic disease of the newborn. The use of the mother as a donor of red cells for her fetus will circumvent the problem of further maternal sensitization.
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A case of acute erythroleukaemia is described. The patient's RBC, which at first appeared to be a mixture of groups B and O, were shown in fact to be a mixture of normal B and very weak B.
The A.V.I.S. Blood Transfusion Center of Turin performs the screening of foetomaternal allo-immunizations for the S. Anna Hospital of Turin. This hospital includes 3 hospital departments and 3 obstetrical and gynaecological university departments. The number of births in one year is roughly 13.000, i.e. 50 mother-baby couples, are tested every day. The identification system and the sampling process are described. The program used on the Groupamatic system includes: 1.) First run: Blood typing of mother blood with screening of alloantibodies. Second run: Blood typing control, screening of immune anti-A and anti-B antibodies, syphilis screening. 2.) Washing of cord blood red blood cells: First run: Washed red blood cells ABO and Rhesus typing, direct Coombs test. Second run: Blood typing control. Automatic screening of maternal irregular alloantibodies and automatic indirect Coombs test on washed cordblood red cells are simultaneously controlled with standard manual techniques. Sampling and testing are processed within 24 hours after birth. The set of results concerning mother-baby couples are grouped on one card and sent to the hospital department for a quick MHNN prophylaxy. Results of tests performed on 6.351 pregnancies studied until birth are presented. The automated direct Coombs test was positive with: 1--95% of new borns from mother who have a high immune allo antibody anti-A/B titer (IgG after treatment with two Mercapto etanol greater than I/64). 2--100% of new borns from mother who have irregular allo antibodies in Rh, Kell, Duffy or Kidd systems.
Author deals with the possibility of determination of the biological individuality by serological methods. Determination of HL-A tissue-compatibility antigens and system of MN/Ss and Rh seen to be the most suitable tools. Alloantigens, serum proteins and group of enzymes characterize the biological individual i. e. serological methods can be used as a tool of the identification of a person. Author deals with the possiblity of determination of various razes. For this purpose investigation of the following systems are necessary: ABO-, Rh-, MN/Ss-, Kell-, Duffy-, Lutheran, Kidd, Lewis and Diego. Nevertheless, this problem is not yet solved.
Fifteen polymorphic systems of the blood (ABO, MNSs, Rhesus, P, Kell, Duffy, Kidd, Hp, Gc, Gm, Inv, aP, PGM1, EsD, and 6-PGD) were examined in 191 unrelated male and female patients suffering from malignant melanoma. These polymorphic systems were compared with the corresponding phenotype and gene frequencies of controls from the same geographical area (Rhineland-Palatinate). The only associations discovered were the ABO and Gm polymorphisms: The incidence of O and Gm(-1) phenotypes in patients is obviously higher than in controls. These observations agree with the findings in other population samples from Germany and Bulgaria.