Risk Factors of Antibody-Mediated Rejection and Predictors of Outcome in Kidney Transplant Recipients.

OBJECTIVES: Kidney transplant is the treatment of choice for patients with end-stage renal disease. Antibody-mediated rejection is associated with higher rates of graft loss in kidney transplant recipients. Determining the risk factors of antibody-mediated rejection is vital for its prevention, early diagnosis, and appropriate treatment, as these factors may be important in maintaining long-term graft survival in transplant recipients. In our study, we analyzed the risk factors of antibody-mediated rejection in kidney transplant recipients and the negative impact of antibody-mediated rejection on graft function. MATERIALS AND METHODS: We analyzed demographic and clinical data of 124 kidney transplant recipients (37 female [30%] and 87 male [70%] patients) who were diagnosed with antibody-mediated rejection at transplant biopsy. We compared graft outcomes of this patient cohort versus 75 kidney transplant recipients (24 female [32%] and 51 male [68%] patients) who were not diagnosed with antibody-mediated rejection. RESULTS: Mean ages of patients with and without antibody-mediated rejection were 38.2 ± 13.6 and 34.4 ± 13.0 years, respectively. Mean ages of donors for patients with antibody-mediated rejection was significantly higher (48.0 ± 13.2 y) than for donors of patients without antibody-mediated rejection (47.1 ± 11.4 y; P < .05). Rate of graft loss was 15.3% in patients with antibody-mediated rejection; patients without antibody-mediated rejection had no graft loss (P < .05). Positive panel reactive antibody levels and blood transfusion before transplant were found to be risk factors of antibody-mediated rejection in kidney transplant recipients. However, recipients who received tacrolimus had less antibody-mediated rejection episodes than recipients who received sirolimus or cyclophosphamide. CONCLUSIONS: Antibody-mediated rejection is associated with high rates of graft loss in kidney transplant recipients. Avoiding blood transfusion, lowering panel reactive antibody levels, choosing younger donors, and using tacrolimus in high-risk kidney transplant recipients may reduce antibody-mediated rejection rates and provide better graft survival.

Do Antithymocyte Globulin-Free Acute Rejection Therapies Increase the Risk of Polyoma Nephropathy in Renal Transplant Recipients?

INTRODUCTION: BK virus nephropathy is a serious complication that can lead to allograft kidney loss. Excessive immunosuppression increases the risk. We aimed to evaluate whether there is an increased risk of BK viremia and nephropathy in patients who underwent high-dose immunosuppression because of the development of acute rejection in the early period after kidney transplantation. METHODS: This retrospective cohort study was performed between April 2015 and March 2016. Twenty-nine patients who had biopsy-proven acute rejection in the first 3 months were evaluated for BK viremia and nephropathy. Thirty patients who had transplantations at the same period were the control group. Plasma BK-DNA values were examined at 1, 2, 3, 6, 9, and 12 months after the rejection treatment and at 3, 6, 9, and 12 months in the control group. Presence of polyoma nephropathy was examined with surveillance biopsies at the 6 and 12 months. RESULTS: Acute rejection treatment was started on the 12th day after transplantation (2-37 days). Seventeen cellular rejections and 12 humoral rejections were reported by biopsy. Two of the 12 humoral rejections were suspicious. Only pulse steroid (PS) (n = 18); PS, plasmapheresis, and intravenous immunoglobulin (n = 8); PS and intravenous immunoglobulin (n = 2); and PS and plasmapheresis (n = 1) treatments were performed. In 21 patients in the rejection group and 25 patients in the control group, BK-DNA was not positive at all. Two patients had graft loss at 11 and 36 months in the rejection group. Graft losses were secondary to rejection. CONCLUSIONS: Treatment with antithymocyte globulin-free regimens after acute rejection episodes did not lead to an increase in BK viremia.