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Subject: search.filters.subject.Acute cellular rejection

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    A Single-Center Retrospective Clinicopathologic Study of Endomyocardial Biopsies After Heart Transplant at Baskent University Hospital in Ankara, 1993-2014
    (2015) Terzi, Ayen; Sezgin, Atilla; Tunca, Zeynep; Deniz, Ebru; Ayva, Ebru Sebnem; Reyhan, Nihan Haberal; Mulderrisoglu, Haldun; Ozdemir, Binnaz Handan; 0000-0002-2280-8778; 0000-0002-7528-3557; 0000-0002-1225-1320; 0000-0001-9852-9911; 25894188; AAK-1967-2021; X-8540-2019; F-7546-2013; AAK-4587-2021
    Objectives: The purpose of this study was to investigate the frequency and prognostic importance of acute cellular rejection after heart transplant. Materials and Methods: All 84 heart transplant patients at our center from January 1993 to January 2014, including all 576 endomyocardial biopsies, were evaluated with retrospective review of clinical records and endomyocardial biopsies. Routine and clinically indicated endomyocardial biopsies after heart transplant were graded for acute cellular rejection (2005 International Society for Heart and Lung Transplantation Working Formulation). Survival analysis was performed using Kaplan-Meier method. Results: There were 61 male (73%) and 23 female recipients. Median age at heart transplant was 29 years (range, 1-62 y). Posttransplant early mortality rate was 17.9% (15 patients). In the other 69 patients, 23 patients died and 46 patients (66.7%) were alive at mean 69.3 +/- 7.2 months after heart transplant. Mean follow-up was 35.4 +/- 29.8 months (range, 0.07-117.5 mo). Mean 8.4 +/- 4.2 endomyocardial biopsies (range, 1-19 biopsies) were performed per patient. Median first biopsy time was 7 days (range, 1-78 d). The frequency of posttransplant acute cellular rejection was 63.8% (44 of 69 patients) by histopathology; 86% patients experienced the first episode of acute cellular rejection within 6 months after transplant. There were 18 patients with acute cellular rejection >= grade 2R on >= 1 endomyocardial biopsy in 44 patients with acute cellular rejection. No significant difference was observed between survival rates of patients with grade 1R or >= grade 2R acute cellular rejection, or between survival rates of patients with or without diagnosis of any grade of acute cellular rejection. Acute cellular rejection was not related to any prognostic risk factor. Conclusions: Acute cellular rejection had no negative effect on heart recipient long-term survival, but it was a frequent complication after heart transplant, especially within the first 6 months.
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    De Novo Thrombotic Microangiopathy in Renal Transplant Patients
    (2018) Ozdemir, B. Handan; Atilgan, Alev Ok; Akcay, Eda Yilmaz; Ozdemir, Gokce; Soy, Ebru Ayvazoglu; Akdur, Aydincan; Haberal, Mehmet; 0000-0002-7528-3557; 0000-0001-8595-8880; 0000-0001-6831-9585; 0000-0003-2545-0078; 0000-0002-0993-9917; 0000-0002-8726-3369; 0000-0002-3462-7632; 29528010; X-8540-2019; AAK-3333-2021; AAK-1960-2021; AAL-4282-2020; AAC-5566-2019; AAA-3068-2021; AAJ-8097-2021
    Objectives: Thrombotic microangiopathy is a form of renal capillary injury possibly associated with calcineurin inhibitor toxicity, acute humoral rejection, infections, and recurrent diseases. Here, we examined its incidence in patients diagnosed with acute and chronic active humoral rejection, polyomavirus nephropathy, acute cellular rejection, and immunoglobulin A recurrence. Materials and Methods: In total, 272 renal allograft recipients who met the inclusion criteria were reevaluated for presence of renal thrombotic microangiopathy. Thrombotic microangiopathy diagnosis was established by clinical, laboratory, and histologic features. C4d expression in peritubular capillaries was determined. Clinical data were collected from medical records. Results: Of 272 patients (mean age of 42.8 +/- 12.7 years), only 74 patients (27.2%) had de novo thrombotic microangiopathy, which was found in 30/90 patients (33.3%) with acute humoral rejection, 9/51 (17.6%) with acute cellular rejection, 22/53 (41.5%) with chronic active humoral rejection, 10/55 (18.2%) with polyomavirus nephropathy, and 3/23 (13%) with immunoglobulin A nephropathy. Significant differences were shown between therapy type and thrombotic microangiopathy development (P= .02). Patients who received cyclosporine (38.5%) tended to show higher incidence of thrombotic microangiopathy than patients who received tacrolimus (20.7%) or sirolimus (7.7%). Patients with C4d-positive acute humoral (97.6% vs 2.4%) and chronic active humoral rejection (68.2% vs 31.8%) had greater incidence of thrombotic microangiopathy versus those who were C4d-negative. Graft loss was significantly higher in C4d-positive than in C4d-negative thrombotic microangiopathy groups (P < .001). Overall 1-, 3-, and 5-year graft survival was 94%, 85%, and 85% versus 83%, 51%, and 51% in thrombotic microangiopathy-negative versus thrombotic microangiopathy-positive patients (P < .001). Conclusions: Acute humoral rejection and chronic active humoral rejection were the most common and therefore most important causes of de novo thrombotic microangiopathy in renal transplant patients. Its presence in the renal allograft biopsy should arouse suspicion for underlying acute or chronic active humoral rejection.