ABO-incompatible Renal Transplantation (abo-incompatible + renal_transplantation)

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Medical Sciences100%

Selected Abstracts

ABO Antibody Titer and Risk of Antibody-Mediated Rejection in ABO-Incompatible Renal Transplantation

AMERICAN JOURNAL OF TRANSPLANTATION, Issue 5 2010
A. A. R. Tobian
Therapeutic plasma exchange (TPE) preconditioning with immunosuppressive therapy reduces ABO antibody titers, permitting engraftment of ABO-incompatible (ABO-I) kidney transplants. The posttransplant predictive role of ABO antibody titers for antibody-mediated rejection (AMR) is unknown. This retrospective study evaluated 46 individuals who received TPE to permit ABO-I kidney transplantation. ABO antibody titers were performed using donor-type indicator red cells. Seven individuals (15.2%) experienced clinical or subclinical AMR. There was no significant difference between recipient blood group, number of pretransplant TPE and baseline titer between those with and without AMR. At 1,2 weeks posttransplant the median titer was 64 (range 4 , 512) among individuals with AMR and 16 (range 2 , 256) among individuals without AMR. Total agglutination reactivity score was significantly higher among individuals with AMR (p = 0.046). The risk of AMR was significantly higher among individuals with an elevated posttransplant titer of ,64 (p = 0.006). The sensitivity of an elevated posttransplant titer was 57.1% with a specificity of 79.5%. The positive predictive value was 33.3% and the negative predictive value was 91.2%. Most individuals with AMR have an elevated titer, however, the positive predictive value of a high titer for AMR is poor. [source]

ABO-incompatible renal transplantation in Epstein syndrome

CLINICAL TRANSPLANTATION, Issue 2010
Masao Ogura
Ogura M, Kikuchi E, Kaito H, Kamei K, Matsuoka K, Tanaka H, Kuroda T, Sekine T, Ito S. ABO-incompatible renal transplantation in Epstein syndrome. Clin Transplant 2010: 24 (Suppl. 22): 31,34. © 2010 John Wiley & Sons A/S. Abstract:, Epstein syndrome (ES) is an autosomal dominant hereditary disease characterized by hereditary nephritis, sensory deafness, and thrombocytopenia. We herein report the case of a 20-yr-old man with ES who underwent ABO blood type-incompatible living-donor kidney transplantation from his mother. He was given platelet transfusion, and his pre-operative number of platelets were 108 × 103/,L. After transplantation, urine output and the decrease in serum creatinine (sCr) were within the acceptable ranges. On the seventh post-operative day (POD), sCr had risen and urine output decreased. Anti-type A antibody rapidly elevated from <2 times (×2) just before transplantation to 64 times (×64), and the patient required hemodialysis again. Resistance index (RI) by ultrasound increased from an average of 0.5 , 0.6 on POD 1 to an average of 0.7 , 0.8 on POD 7. However, several biopsies (POD 4, 7, and 10) showed no obvious findings of acute rejection except for intense C4d deposition. Because acute antibody-mediated rejection was not completely ruled out, he was treated with methyl-prednisolone pulse therapy, plasma exchange, cyclophosphamide, and immunoglobulin. Regardless, his titer of anti-type A antibody was still high, and he still presented oliguria. We performed an emergent splenectomy. Consequently, the levels of anti-type A antibody decreased, the RI also dropped to an average of 0.6. However, on POD 19 and 25 (platelets were 27 × 103/,L and 36 × 103/,L), he developed a massive intraperitoneal hematoma around the graft and region of the removed spleen, which pushed the graft out and caused acute tubular necrosis, resulting in anuria. The RI rose to an average of 0.8 , 1.0 after these episodes. He also experienced bleeding from a duodenal ulcer on POD 21. However, his renal function has fully recovered after acute hemodialysis for 35 d. The latest sCr was 1.5 mg/dL with a recovery in RI to 0.6. Although his platelet count was maintained at a minimum of 50 × 103/,L, he had several severe bleeding episodes, concluding that sufficient platelets are necessary after transplantation in ES. [source]

An ABO-incompatible renal transplant patient who developed severe antibody-mediated vascular rejection 36 days after transplantation

CLINICAL TRANSPLANTATION, Issue 2008
Akiko Fujii
Abstract:, A 44-yr-old man had an ABO-incompatible renal transplantation from his 41-yr-old wife. He was diagnosed with IgA nephropathy at the age of 31 and began hemodialysis to treat chronic renal failure at the age of 39. Preoperative flow panel reactive antibody was negative. An episode biopsy on post-operative day (POD) 18 showed mild infiltrative vasculopathy (v1, g2, ptc1, TMA, PTC+). The serum creatinine (sCr) was 2.26 mg/dL. Anti-A antibody was x32. Double filtration plasmapheresis and plasma exchange were performed. A second episode biopsy was performed on POD 36. The Cr was 3.73 mg/dL. Anti-A antibody was x32. Histologically, antibody-mediated vascular rejection with severe fibrinoid necrosis in the lobular arteries was detected (v3, g2, ptc2, TMA, PTC+). Steroid pulse therapy was performed, and OKT-3 was administered for 10 d. The anti-A antibody titer was x128 on POD 47. A biopsy specimen obtained on POD 55 showed severe vascular rejection with stenosis of the vascular lumen and fibrinoid necrosis (v3, cv2, g1, cg2, ptc1, TMA, PTC+). The sCr was 7.09 mg/dL. Despite double-filtration plasmapheresis, the patient was reintroduced to hemodialysis. Here, we report a case showing the typical histological features of antibody-mediated vascular rejection. [source]