Recently, ABO-ILKT has been recognized as a useful alternative therapy for end-stage kidney disease with ABO-incompatibility, and its outcome is comparable to that of ABO-CLKT.
Blood sample mixtures were divided into four groups: group M, cross-matched blood type mixing; group O, donor type O with other blood type mixing (A, B, or AB); group S, ABO type-specific uncross-matched blood mixing; and group I, ABO incompatibility mixing.
The blood mixtures were divided into three groups: group M, cross-matched blood-type mixing (n = 20); group S, ABO type-specific uncross-matched blood (n = 20); and group I, ABO incompatibility (not ABO type-specific blood and not process cross-matched) mixing (n = 20).
The cases were further subdivided into unexplained hyperbilirubinemia (n = 50), ABO(+) hyperbilirubinemia (n = 50), ABO(-) control (n = 50), and ABO(+) control (n = 50) groups on the basis of the presence or absence of DC(-) ABO incompatibility.
The ABO incompatibility between the couples is likely to be a risk factor for early spontaneous abortions and also the heterozygote selection of ABO blood group genotypes.
HIV vectors derived from cells expressing ABO antigens displayed sensitivity to fresh human serum analogous to ABO incompatibility, and ABO histo-blood group sugars were detected on the viral envelope protein, glycoprotein 120 (gp120).
UGT1A1 gene promoter polymorphism and G71R mutation are possible risk factors for Turkish neonates with DC(-) ABO incompatibility and unexplained hyperbilirubinemia.
The most common genetic variant was short heme oxygenase (HO)-1 promoter GT-allele (<24 repeats) (39.4 %), followed by GA at nt388 in hepatic solute carrier organic anion transporter 1B1 (SLCO1B1) (31.1 %), GA at nt211 in UDP-glucuronosyltransferase 1A1 (UGT1A1) (29.3 %), ABO incompatibility (16.2 %), alpha thalassemia (5.0 %), and G6PD deficiency (3.2 %).
The use of anti-CD38 therapy with daratumumab to target residual host plasma cells is safe and effective, and it can be considered in refractory recipients with PRCA after allo-HSCT secondary to ABO incompatibility.
The major causes of severe hyperbilirubinaemia were idiopathic (33.3%), sepsis (35.3%), ABO incompatibility (17.6%) and glucose-6-phosphate dehydrogenase (G6PD) deficiency (11.8%).
The most common genetic variant was short heme oxygenase (HO)-1 promoter GT-allele (<24 repeats) (39.4 %), followed by GA at nt388 in hepatic solute carrier organic anion transporter 1B1 (SLCO1B1) (31.1 %), GA at nt211 in UDP-glucuronosyltransferase 1A1 (UGT1A1) (29.3 %), ABO incompatibility (16.2 %), alpha thalassemia (5.0 %), and G6PD deficiency (3.2 %).
The most common genetic variant was short heme oxygenase (HO)-1 promoter GT-allele (<24 repeats) (39.4 %), followed by GA at nt388 in hepatic solute carrier organic anion transporter 1B1 (SLCO1B1) (31.1 %), GA at nt211 in UDP-glucuronosyltransferase 1A1 (UGT1A1) (29.3 %), ABO incompatibility (16.2 %), alpha thalassemia (5.0 %), and G6PD deficiency (3.2 %).
The most common genetic variant was short heme oxygenase (HO)-1 promoter GT-allele (<24 repeats) (39.4 %), followed by GA at nt388 in hepatic solute carrier organic anion transporter 1B1 (SLCO1B1) (31.1 %), GA at nt211 in UDP-glucuronosyltransferase 1A1 (UGT1A1) (29.3 %), ABO incompatibility (16.2 %), alpha thalassemia (5.0 %), and G6PD deficiency (3.2 %).
The most common genetic variant was short heme oxygenase (HO)-1 promoter GT-allele (<24 repeats) (39.4 %), followed by GA at nt388 in hepatic solute carrier organic anion transporter 1B1 (SLCO1B1) (31.1 %), GA at nt211 in UDP-glucuronosyltransferase 1A1 (UGT1A1) (29.3 %), ABO incompatibility (16.2 %), alpha thalassemia (5.0 %), and G6PD deficiency (3.2 %).
The most common genetic variant was short heme oxygenase (HO)-1 promoter GT-allele (<24 repeats) (39.4 %), followed by GA at nt388 in hepatic solute carrier organic anion transporter 1B1 (SLCO1B1) (31.1 %), GA at nt211 in UDP-glucuronosyltransferase 1A1 (UGT1A1) (29.3 %), ABO incompatibility (16.2 %), alpha thalassemia (5.0 %), and G6PD deficiency (3.2 %).
The most common genetic variant was short heme oxygenase (HO)-1 promoter GT-allele (<24 repeats) (39.4 %), followed by GA at nt388 in hepatic solute carrier organic anion transporter 1B1 (SLCO1B1) (31.1 %), GA at nt211 in UDP-glucuronosyltransferase 1A1 (UGT1A1) (29.3 %), ABO incompatibility (16.2 %), alpha thalassemia (5.0 %), and G6PD deficiency (3.2 %).