Browsing by Author "Celebi, Zeynep Kendi"
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Item ANALYSIS OF INTRA-PATIENT VARIABILITY OF TACROLIMUS IN TRANSPLANT PATIENTS WITH DATA MINING(2020) Topcu, Deniz Ilhan; Turgut, Didem; Celebi, Zeynep Kendi; Haberal, Mehmet A.Item CLINICAL FEATURES AND SENSITIZATION RISK FACTORS IN PATIENTS AWAITING KIDNEY TRANSPLANTATION: A SINGLE CENTER EXPERIENCE(2020) Erdogmus, Siyar; Celebi, Zeynep Kendi; Sayin, Burak; Acar, F. Nurhan Ozdemir; Karakaya, Emre; Haberal, Mehmet A.Item HOW CALCINEURIN INHIBITOR DOSAGE AND BLOOD TROUGH LEVELS AFFECT KIDNEY ALLOGRAFT SURVIVAL?(2020) Turgut, Didem; Celebi, Zeynep Kendi; Ozdemir, B. Handan; Colak, Turan; Soy, Ebru H. Ayvazoglu; Haberal, Mehmet A.Item The Mutation Identified in TWEAK-Fn14 Pathway May Affect the Clinical Course of IgA Nephropathy/Henoch-Schonlein Purpura Nephritis: A Case Report(2021) Celebi, Zeynep Kendi; Turgut, Didem; Erdogmus, Siyar; Avsaroglu, Ezgi; Musabak, Haci Ugur; Colak, TuranThe TNF-like weak inducer of apoptosis (TWEAK) gene was first discovered in 1997 and its receptor Fn14 in 2001. TWEAK can be protective or damaging, depending on the status of the tissue. While basal TWEAK and Fn14 concentrations were found to be low in the kidney under normal conditions, TWEAK levels and tissue receptor expression were found to be increased in the presence of an acute injury.We report here the first case with persistent microscopic hematuria since infancy with TWEAK gene mutation, who was diagnosed with IgA Nephropathy/Henoch-Schonlein Purpura Nephritis at the age of 18 during a kidney biopsy. The genetic mutation in this patient may have caused a better course of the disease.Item PARAMETERS AFFECTING ESTIMATED GLOMERULAR FILTRATION RATE AND DEVELOPING HYPERTENSION AFTER DONOR NEPHRECTOMY(2020) Celebi, Zeynep Kendi; Turgut, Didem; Sayin, Cihad Burak; Colak, Turhan; Kirnap, Mahir; Haberal, Mehmet A.Item Rapidly Progressive Renal Failure in AA Amyloidosis: A New Clinical and Histopathological Entity for an Old Disease(2020) Celebi, Zeynep Kendi; Kiremitci, Saba; Sadioglu, Rezzan Eren; Keven, Kenan; 0000-0003-3279-9796; ABB-9570-2020Objective: Secondary renal AA amyloidosis (RAAA) presents with proteinuria and/or as nephrotic syndrome and progresses to end stage renal disease (ESRD) insidiously. However, some patients with secondary amyloidosis show a more rapid renal disease progression than the usual course. In this study, we aimed to investigate the underlying cause of the rapidly progressive renal disease in the patients with secondary amyloidosis. Materials and Methods: Patients with kidney biopsy proven secondary RAAA were divided into 2 groups: the rapidly progressive group (estimated glomerular filtration rate >60 mL/min, who needed renal replacement therapy within one year of diagnosis) and the control group. Biopsy specimens were reevaluated for glomerular-vascular amyloid load, tubular atrophy, interstitial fibrosis, and interstitial inflammation. The biopsy characteristics and biochemical parameters were compared between the groups. Results: Histopathological examination showed global amyloid deposition, vascular pole involvement, peritubular capillary amyloid deposition, and severe interstitial inflammation associated with rapidly progressive disease. Estimated glomerular filtration rate was lower and proteinuria was higher in the rapidly progressive group than in the control group. Vascular pole amyloid deposition was found to be a predictor of ESRD in multivariate analysis. Conclusion: This study shows that higher amyloid deposition and severe inflammation revealed in in kidney biopsy of secondary RAAA cases can be risk factors for rapidly progressive renal failure.Item Sensitization Status of Patients on the Deceased Donor Kidney Transplant Waiting List: A Single-Center Experience(2022) Erdogmus, Siyar; Celebi, Zeynep Kendi; Turgut, Didem; Sayin, Burak; Ozdemir, Fatma Nurhan; Colak, Turan; Haberal, Mehmet; 0000-0002-3462-7632; AAJ-8097-2021Objectives: This study aimed to analyze the features of patients on the deceased donor kidney transplant waiting list and risk factors associated with sensitization that affect panel reactive antibody status in our center. Methods: Patients' data were collected retrospectively. Panel reactive antibody screening and definition tests were studied for class I (A, B, and C) and class II (DR, DP, DQ) antigens with Luminex every 6 months. Patients with panel reactive antibody >5% and antibody strength >1000 median fluorescence intensity were considered panel reactive antibody-positive. Based on the panel reactive antibody status, the patients were divided into 2 groups: the panel reactive antibody-positive group and -negative group. Results: A total of 338 patients (60% male, mean age: 52.6 +/- 14.6 years) were included in the analysis. Panel reactive antibody positivity was detected in 117 (34.6) patients on the waiting list. Compared with the panel reactive antibody-negative patient group, the panel reactive antibody-positive patient group had higher rate of women and lower age (P <.001 and P <.001, respectively). The patients in the panel reactive antibody-positive group also had longer dialysis vintage (P =.027), higher rate of blood transfusion history (P <.001), organ transplant (P <.001), and higher number of blood transfusion (P <.001). Female gender (odd ratio:4.094, 95% CI:2.275-7.368, P <.001), history of blood transfusion (odds ratio:2.027, 95% CI:1.131-3.633, P =.018), and organ transplant (odds ratio:16.894, 95% CI:7.212-39.578, P <.001) were independent risk factors associated with panel reactive antibody positivity. Conclusion: Updates of the organ allocation system to consider sensitized patients and new strategies to expand the donor pool and donation rates are needed in Turkiye.Item WHY CAN'T I HAVE A KIDNEY TRANSPLANT? LIMITATIONS TO DONATE KIDNEY OR TO HAVE ALLOGRAFT(2020) Celebi, Zeynep Kendi; Erdogmus, Siyar; Acar, Nurhan Ozdemir; Soy, Ebru H. Ayvazoglu; Haberal, Mehmet A.