BACKGROUND: Immune hemolysis secondary to ABO minor incompatibility is a rare graft versus host disease in renal recipients, secondary to anti-ABO antibody produced by lymphocytes of donor origin that reacts against recipient RBCs. METHODS: To investigate the incidence and clinical features of immune hemolysis secondary to ABO minor incompatibility in renal allograft recipients, clinical records of 358 renal transplantation performed in Maryknoll Hospital since 1991 were analyzed retrospectively. RESULTS: Fifty four (15%) of 358 renal transplants were ABO minor incompatible. Immune hemolysis secondary to anti-ABO antibody developed in 5 (9.2%) of 54 ABO minor incompatible renal transplant recipients. Immune hemolysis occurred in 3 (13.6%) patients among 22 allografts from blood type O donor to A recipients and 2 (10%) patients among 20 from blood type O donor to B recipients. All 5 patients received cyclosporin with prednisolone, and MMF was administered to one patient additionally. Immune hemolysis developed on 14+/-3 days after renal transplantation and lasted for about 10+/-3 days. The maximum reduction of hemoglobin was 3.3+/-1.0 g/dL. All patients required donor type (blood type O) washed RBCs transfusion (5.0+/-2.6 units per patient) and plasmapheresis were performed in 3 patients (4.0+/-1.0 per patient). All patients recovered without deterioration of graft function. Age, number of HLA mismatch, creatinine at 1 year after transplantation, frequency of acute rejection and serum cyclosporin level during first 2 weeks were not significantly different between hemolysis group (N=5) and non-hemolysis group (N=49). Living unrelated transplantation is associated with increased incidence of immune hemolysis compared with living related transplantation (p<0.01). CONCLUSION: Although immune hemolysis secondary to ABO minor incompatibility is uncommon, we experienced cases with marked reduction of hemoglobin that required a large amount of transfusion. Therefore, this type of immune hemolysis needs to be considered as a differential diagnosis of posttransplant hemolysis. As our center routinely performs donor specific transfusion (DST), the incidence may be higher than that of other centers where DST is not usually given.
Allografts ; Anemia, Hemolytic* ; Blood Group Incompatibility ; Creatinine ; Cyclosporine ; Diagnosis, Differential ; Graft vs Host Disease ; Hemolysis ; Humans ; Incidence ; Kidney Transplantation ; Lymphocytes ; Plasmapheresis ; Prednisolone ; Retrospective Studies ; Tissue Donors ; Transplantation ; Transplants

Wnt/beta-catenin signaling plays a critical role in bone formation and regeneration. Dentin and cementum share many similarities with bone in their biochemical compositions and biomechanical properties. Whether Wnt/beta-catenin signaling is involved in the dento-alveolar complex formation is unknown. To understand the roles of Wnt/beta-catenin signaling in the dento-alveolar complex formation, we generated conditional beta-catenin activation mice through intercross of Catnb+/lox(ex3) mice with Col1a1-cre mice. In mutant mice, tooth formation and eruption was disturbed. Lower incisors and molars did not erupt. Bone formation was increased in the mandible but tooth formation was severely disturbed. Hypomineralized dentin was deposited in the crown but roots of molars were extremely short and distorted. In the odontoblasts of mutant molars, expression of dentin matrix proteins was obviously downregulated following the activation of beta-catenin whereas that of mineralization inhibitor was increased. Cementum and periodontal ligament were hypoplastic but periodontal space was narrow due to increased alveolar bone formation. While cementum matrix proteins were decreased, bone matrix proteins were increased in the cementum and alveolar bone of mutant mice. These results indicate that local activation of beta-catenin in the osteoblasts and odontoblasts leads to aberrant dento-alveolar complex formation. Therefore, appropriate inhibition of Wnt/beta-catenin signaling is important for the dento-alveolar complex formation.
Animals ; beta Catenin ; Bone Matrix ; Crowns ; Dental Cementum ; Dentin ; Incisor ; Mandible ; Mice ; Molar ; Odontoblasts ; Osteoblasts ; Osteogenesis ; Periodontal Ligament ; Proteins ; Regeneration ; Tooth