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Background In kidney transplantation, immunotherapy with thymoglobulin (rATG) has been used to down-regulate the patient immune system. rATG is a powerful immunobiologic drug used to deplete lymphocytes to prevent early acute rejection. The aim of this research was to evaluate the effects of immunotherapy by rATG on graft suvival during a 9-year period in kidney-transplanted patients with different immunological profiles. Methods A sample of 469 patients were allocated into four groups (G) based on immunological risk of rejection: G1, low risk, not sensitized recipients, solid-phase immunoassay with single antigen beads (SPI-SAB) < 10%; G2, medium risk I, sensitized recipients, SPI-SAB ≥ 10 < 50%; G3, medium risk II sensitized (SPI-SAB ≥50%); and G4, high risk, sensitized recipients, SPI-SAB- donor-specific antibody positive (DSA+). Only patients from G3 and G4 received immunotherapy. Results Of 255 patients who received a kidney from a living donor (LD), 42 (16.47%) from all groups (G) had T-cell–mediated rejection (TCMR) and four (G1) lost their grafts, 8 (3.14%) had antibody-mediated rejection (AMR), and two lost their graft in G1 and G4. Of 214 patients who received a kidney from deceased donors (DD), 37 (17.29%) had TCMR with one lost graft in G1. AMR was shown in 13 (6.07%) patients, with three losses observed in G2. Statistical differences between the groups in the 9-year graft survival rate were found only in the comparison of G1 versus G2 ( P = 0.005) and G2 versus G4 ( P = 0.047) for DD. For LD, no statistical differences were found. Conclusion This clinical retrospective study shows that immunotherapy induction was associated with improvement of outcomes, graft function, and survival in patients treated with immunotherapy in comparison with patients who did not received induction therapy. These findings strongly suggest that immunotherapy should be used for all patients transplanted with kidneys from deceased donors.

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Background: Bacterial infections are a frequent cause of acute morbidity and sometimes mortality in sickle cell disease (SCD). Splenic dysfunction alone does not explain the susceptibility to specific organisms e.g., Staphylococcus aureus and Klebsiella as shown in some studies; suggesting that the splenic dysfunction is not the only explanation and that neutrophil dysfunction may be present. Neutrophils destroy microbes by producing a burst of reactive oxygen species (ROS) (respiratory burst) in response to bacterial components, as well as to phorbol-myristate-acetate (PMA). Some studies have shown that the state of chronic hemolysis in SCD impairs the ability to develop neutrophils to mount a bactericidal oxidative burst, and hence increasing susceptibility to bacterial infections. Aims: to assess the neutrophil oxidative burst in SCD patients and explore the relation to markers of hemolysis. Methods: Twenty-seven hydroxyurea naïve children and adolescents with SCD (mean age 11.1 ± 3.9 years) were enrolled from Pediatric Hematology Clinic at Ain Shams University Children's Hospital. They were compared to 26 age-and sex-matched healthy controls. Patients were studied stressing on transfusion history, chelation therapy, serum ferritin, hematological profile, markers of hemolysis and serum haptoglobin. Neutrophil oxidative burst assay was performed using DHR based flow cytometry. Results: Eleven (40%) out of the 27 patients had HBSS while 16 (60%) patients were sickle thalassemias. Six patients (22.2%) were splenectomized. Severe vaso-occlusive crisis and acute chest syndrome were found in 22.2% and 18.5% of patients, respectively. Four (14.8%) patients had evidence of stroke. Bone fractures and avascular necrosis were found in 5.5% and 11.1 % of patients, respectively. Most of the studied patients were on chelation therapy, either as monotherapy or combined chelation (37% each). White blood cell count and reticulocytic count were significantly higher in SCD patients as compared to healthy controls (P = 0.03 and <0.01 respectively).