Will transplantation of kidneys from donors with blood group A2 into recipients with blood group B help British Indo-Asian patients with renal failure?

Despite a high incidence of renal failure, disproportionately fewer Indo-Asians in the United Kingdom receive a renal transplant, in part because of the high prevalence of blood group B. It is now clear that it is possible to safely transplant kidneys from donors with blood group A of the subtype A2 into recipients with blood group B if the latter have low titers of anti-A antibodies. We measured the anti-A titers in 25 Indo-Asian patients on dialysis being considered for transplantation and found stably low titers in all. Titers were comparable to those found in a control white population with blood group B. In addition, in a complement-dependent cytotoxicity crossmatch against group A lymphocytes, the only positive results were obtained in those with high preexisting panel reactivity (i.e., because of the presence of preformed anti-human leukocyte antigen antibodies). We conclude that there are grounds for investigating this approach further to solve the ethnic disparity in rates of transplantation.

Anaphylactic reaction with prothrombin complex concentrate in a patient with IgA deficiency and anti-IgA antibodies.

Immunoglobulin A (IgA) deficiency with anti-IgA antibodies is not listed as an absolute or relative contraindication for the use of prothrombin complex concentrates (PCCs). We discuss a patient who developed an anaphylactic reaction to PCC on a background of selective IgA deficiency with anti-IgA antibodies and with a history of anaphylactic reaction to other blood products. Further analysis of PCCs revealed the presence of variable quantities of immunoglobulins of all classes, including IgA. Although the summary of product characteristics for PCCs from various manufacturers does not list IgA deficiency with anti-IgA antibodies as an absolute or relative contraindication, our findings suggest that PCCs are not devoid of IgA and great caution must be exercised with their use in patients with IgA deficiency with anti-IgA antibodies and with previously documented reactions.

Erythroid urea transporter deficiency due to novel JKnull alleles.

BACKGROUND: The Kidd blood group antigens Jka and Jkb are encoded by the red blood cell (RBC) urea transporter gene. Homozygosity for silent JK alleles results in the rare Jk(a-b-) phenotype. To date, seven JKnull alleles have been identified, and of these, two are more frequent in the Polynesians and Finns. This study reports the identification of other JKnull alleles in Jk(a-b-) individuals of different ethnic or geographic origins. STUDY DESIGN AND METHODS: Nine Jk(a-b-) samples and a sample from a Jk(a-b+) mother of a Jk(a+b-) baby were investigated. Polymerase chain reaction amplification and sequence analysis of the JK gene was performed. Western blotting and urea lysis were used to confirm Jk(a-b-) RBCs. RESULTS: Four novel alleles were identified: two different nonsense mutations, 202C>T (Gln68Stop) and 723delA (Ile262Stop) were identified on otherwise consensus JK*1 and JK*2 alleles, respectively. A missense mutation, 956C>T (Thr319Met), was identified in a JK*1 allele from an African-American and a JK*2 allele in two people of subcontinental Indian descent. Immunoblotting and urea lysis confirmed absence of JK glycoprotein in RBC membranes from a sample carrying the 956C>T mutation. Other previously described JKnull mutations were found in samples of origins other than in which they were first identified. CONCLUSION: The molecular bases of the Jk(a-b-) phenotype are diverse and this is the first report of JKnull alleles in individuals of African and subcontinental Indian descent. Although rare, these alleles should be taken into consideration when planning genotyping strategies for blood donors and patients.

ABO incompatible living renal transplantation with a steroid sparing protocol.

BACKGROUND: ABO incompatible (ABOi) live-donor renal transplantation is a successful and accepted form of treatment for patients with renal failure. Although there is significant controversy as to how antiblood group antibodies should be removed and their resynthesis prevented, subsequent immunosuppressive regimes have all involved steroids. We and other groups have successfully used steroid sparing regimes for conventional ABO compatible transplantation and this study describes the use of our steroid sparing protocol in ABOi transplantation. METHODS: We have transplanted 10 ABOi patients using 1 week of steroids (prednisolone 1 mg/kg for 4 days, 0.5 mg/kg for 3 days and then stopped), tacrolimus and mycophenolate mofetil. Steroids were reintroduced in the event of rejection. RESULTS: Patient- and allograft-survival 1 year posttransplantation is 100%. Three patients experienced antibody-mediated rejection within 2 weeks of transplantation, which was successfully reversed. There has been no late rejection. Allograft function was similar to our live-donor ABO compatible transplant patients receiving a similar steroid sparing regime (12-month mean creatinine 131+/-15 micromol/L vs. 138+/-48 micromol/L; mean CrCl 63.2+/-22 mL/min vs. 56.7+/-20 mL/min). CONCLUSIONS: This study shows that ABOi live-donor transplantation can be successfully accomplished using a steroid-sparing protocol.

RBC T activation and hemolysis in a neonatal intensive care population: implications for transfusion practice.

BACKGROUND: Reports of transfusion-associated hemolysis in infants with T-activated RBCs have led to the suggestion that infants should be screened and provided with low-titer anti-T blood components. T-activated RBCs react with the lectins Arachis hypogea and Glycine soja; variants of T (Th and Tx) and Tk also react with A. hypogea, but not G. soja. Although Tk is not a true variant of T, for the purposes of this study, all RBCs that are reactive with A. hypogea but are not reactive with G. soja are called "T variants." STUDY DESIGN AND METHODS: A prospective study was carried out to examine T and T variant activation and transfusion-associated hemolysis in a neonatal intensive care population and to determine if antibodies to T and T variant are detectable in donor plasma. A total of 2041 samples from 375 infants were tested for T and T variant activation utilizing a lectin panel. Three hundred donor plasma samples were tested for antibodies to T and T variant. RESULTS: Forty-eight of 375 infants (12.8%) had T- and T-variant-activated RBCs. Of these, 13 of 48 (27%) developed at least one episode of sepsis and 9 of 48 (19%) developed necrotizing enterocolitis (NEC) at some point during their inpatient stay. T activation was not always temporally associated with the onset of NEC or sepsis. The remaining 26 of 48 (54%) were healthy infants receiving convalescent care in the neonatal intensive care units and showed no evidence of either NEC or sepsis. Twelve (of 375) additional infants (3.2%) who developed NEC and 100 (27%) who developed sepsis showed no RBC T activation. Twenty-three of 48 (48%) infants with T-activated RBCs received standard blood components, but no transfusion-associated hemolysis occurred. Donor plasma samples contained T but not T variant antibodies. CONCLUSION: T variant activation of RBCs occurs in healthy neonates as well as in infants with NEC and sepsis, but T activation appears rare. Transfusion- associated hemolysis was not seen. The provision of specially prepared blood components for infants with NEC is unnecessary.