Hyperacute rejection of living related kidney graft caused by IgG endothelial specific antibodies with a negative monocyte cross-match.

We present a case report of a 30-year-old man, who hyperacutely rejected a blood group identical, HLA-haploidentical living related kidney graft in spite of the fact that he had never been immunized. Anti-endothelial IgG antibodies that did not react with monocytes were detected with flow cytometry, on a panel of human umbilical cord cells in his serum retrospectively. On the basis of this experience we put for consideration the possibility of regular examination of non-HLA antibodies in potential living graft recipients.

[Von Willebrand disease--type 2N (case report)].

Isolated reduced coagulation activity of FVIII may be a manifestation of haemophilia A, carriership of haemophilia A, haemophilia A in a woman, acquired haemophilia A and type 2N of von Willebrand's disease. The authors were concerned with the cause of isolated reduction of the coagulation activity of factor VIII (19 IU/dl) in a 40-year-old woman with a history of excessive haemorrhage of the type of mild haemophilia A with a negative family history. The personal history, family history and laboratory examination suggested type (variant) 2N of von Willebrand's disease.

[A homozygous quantitative defect of alpha 2-antiplasmin in a family from central Slovakia].

Alpha2-antiplasmin is the main inhibitor of plasma fibrinolytic system. An inborn defect of alpha2-antiplasmin was first described by Koie et al. in 1978 in connection with severe haemorrhage syndrome.

[Dominant beta-thalassemia alleles in the Czech and Slovak population (beta-thalassemia mutations in 112(T-A) and 121(G-T) codons and the unstable Hradec Králové hemoglobin or alpha 2 beta 2 115 (G17) Ala-Asp)].

In four unrelated families of Czech and Slovak origin two nonsense dominant beta-thalassaemic alleles (CD 121 (G-T); CD 112 (T-A)) and in one family simple substitution in codon 115 (GCC-GAC) or alpha 2 beta 2 115 (G17) Ala-Asp HB-Hradec Králové were identified. Mutations in codons 112 and 115 were described for the first time. Phenotypic manifestation of beta-thal.