Browsing by Author "Ghafari, Ali"

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    Effect of Active Vitamin D on Expression of Co-Stimulatory Molecules and HLA-DR in Renal Transplant Recipients
    (Başkent Üniversitesi, 2009-06) Ahmadpoor, Pedram; Ghafari, Ali; Makhdoomi, Khadije; Ghasemmahdi, Laila; Ilkhanizadeh, Behrooz
    Objectives: Full activation of T cells requires 2 distinct but synergistic signals. The first is the T-cell antigen receptor, which is antigen specific, and the second is activation of co-stimulatory signals. Active vitamin D (1, 25-dihydroxyvitamin D3) decreases T-cell activation and proliferation, inhibits differentiation and maturation of dendritic cells, and induces tolerogenic dendritic cells. These immunoregulatory effects may be due, at least in part, to changes in cytokine secretion and expression of co-stimulatory molecules. The use of active vitamin D has been reported to improve allograft survival, decelerate loss of allograft function, and prevent acute rejection. This study was conducted to assess the effect of active vitamin D on the expression of co-stimulatory molecules and HLA-DR in renal transplant recipients. Materials and Methods: In this prospective study, we enrolled 24 renal transplant recipients who had undergone a transplant 6 to 18 months earlier, had stable allograft function, and were without episodes of allograft dysfunction or febrile illness in the previous 2 months. Participants were administered oral calcitriol 0.5 μg daily for 4 weeks. Expression of HLA-DR, CD28, CD86, and CD40 in peripheral blood leukocytes was assessed by flow cytometry before and after calcitriol administration. Results: Compared to baseline levels, expression of HLA-DR decreased by 16.8%; expression of CD28, by 30%; of CD40, by 31.2%; and of CD86, by 36.7%. Conclusions: In renal transplant recipients, decreased expression of co-stimulatory and HLA-DR molecules occurred after treatment with active vitamin D. Such changes may be involved in increasing allograft survival.
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    Risk Factors of Long-Term Graft Loss in Renal Transplant Recipients with Chronic Allograft Dysfunction
    (Başkent Üniversitesi, 2010-12) Khalkhali, Hamid Reza; Kazemnejad, Anoushirvan; Hajizadeh, Ebrahim; Ghafari, Ali
    Background: Graft loss owing to chronic allograft dysfunction is a major concern in renal transplant recipients. We assessed the affect of immune and nonimmune risk factors on death-censored graft loss in renal transplant recipients with chronic allograft dysfunction. Materials and Methods: We performed a retrospective, single-center study on 214 renal transplant recipients with chronic allograft dysfunction among 1534 renal transplant recipients at the Urmia University Hospital from 1997 to 2005. Data registry includes details from all renal transplants. The renal transplant recipient information is regularly updated to determine current graft function, graft loss, or renal transplant recipient’s death. The selection criteria were a functional renal allograft for at least 1 year and a progressive decline in allograft function. Results: Increasing donor age (RR=1.066; P < .001), recipient age (RR=1.021, P = .0), recipient weight (RR=1.024; P = .029), and waiting time on dialysis to transplant. (RR=1.047; P = .006), pretransplant hypertension (RR=3.126; P < .001), pretransplant diabetes (RR=5.787; P < .001), delayed graft function (RR=6.087; P < .001), proteinuria (RR=2.663; P = .001), posttransplant diabetes (RR=2.285; P = .015), posttransplant hypertension (RR=2.047; P = .017), and AR (RR=3.125; P < .001). Patients in stage 2 at the beginning of chronic allograft dysfunction relative to stage 1 (RR=4.823; P < .001) and patients in stage 3 at the beginning of chronic allograft dysfunction relative to stage 1 (RR=123.06; P < .001) were significant risk factors for death-censored graft loss. Using mycophenolate mofetil versus azathioprine reduced death-censored graft loss (RR=0.499; P ≤ .001). Conclusion: We found that age of donor, pretransplant hypertension, pretransplant diabetes, type of immunosuppression (mycophenolate mofetil vs azathioprine), delayed graft function, proteinuria, and stage of allograft dysfunction at the start of chronic allograft dysfunction are the major risk factors for late renal allograft dysfunction.