K. Parker
East Carolina University
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Featured researches published by K. Parker.
Transplantation | 2013
Matthew J. Everly; Lorita M. Rebellato; Carl E. Haisch; Miyuki Ozawa; K. Parker; Kimberly P. Briley; Paul G. Catrou; Paul Bolin; W. Kendrick; S. Kendrick; Robert C. Harland; Paul I. Terasaki
Background To date, limited information is available describing the incidence and impact of de novo donor-specific anti–human leukocyte antigen (HLA) antibodies (dnDSA) in the primary renal transplant patient. This report details the dnDSA incidence and actual 3-year post-dnDSA graft outcomes. Methods The study includes 189 consecutive nonsensitized, non-HLA-identical patients who received a primary kidney transplant between March 1999 and March 2006. Protocol testing for DSA via LABScreen single antigen beads (One Lambda) was done before transplantation and at 1, 3, 6, 9, and 12 months after transplantation then annually and when clinically indicated. Results Of 189 patients, 47 (25%) developed dnDSA within 10 years. The 5-year posttransplantation cumulative incidence was 20%, with the largest proportion of patients developing dnDSA in the first posttransplantation year (11%). Young patients (18–35 years old at transplantation), deceased-donor transplant recipients, pretransplantation HLA (non-DSA)–positive patients, and patients with a DQ mismatch were the most likely to develop dnDSA. From DSA appearance, 9% of patients lost their graft at 1 year. Actual 3-year death-censored post-dnDSA graft loss was 24%. Conclusion We conclude that 11% of the patients without detectable DSA at transplantation will have detectable DSA at 1 year, and over the next 4 years, the incidence of dnDSA will increase to 20%. After dnDSA development, 24% of the patients will fail within 3 years. Given these findings, future trials are warranted to determine if treatment of dnDSA-positive patients can prevent allograft failure.
Transplantation | 2013
Maria Cecilia S. Freitas; Lorita M. Rebellato; Miyuki Ozawa; Anh Nguyen; Nori Sasaki; Matthew J. Everly; Kimberly P. Briley; Carl E. Haisch; Paul Bolin; K. Parker; W. Kendrick; S. Kendrick; Robert C. Harland; Paul I. Terasaki
Background Anti–HLA-DQ antibodies are the predominant HLA class II donor-specific antibodies (DSAs) after transplantation. Recently, de novo DQ DSA has been associated with worse allograft outcomes. The aim of this study was to determine the further complement-binding characteristics of the most harmful DQ DSA. Methods Single-antigen bead technology was used to screen 284 primary kidney transplant recipients for the presence of posttransplantation DQ DSA. Peak DSA sera of 34 recipients with only de novo DQ DSA and of 20 recipients with de novo DQ plus other DSAs were further analyzed by a modified single-antigen bead assay using immunoglobulin (Ig)-G subclass-specific reporter antibodies and a C1q-binding assay. Results Compared with recipients who did not have DSA, those with de novo persistent DQ-only DSA and with de novo DQ plus other DSAs had more acute rejection (AR) episodes (22%, P=0.005; and 36%, P=0.0009), increased risk of allograft loss (hazards ratio, 3.7, P=0.03; and hazards ratio, 11.4, P=0.001), and a lower 5-year allograft survival. De novo DQ-only recipients with AR had more IgG1/IgG3 combination and C1q-binding antibodies (51%, P=0.01; and 63%, P=0.001) than patients with no AR. Furthermore, the presence of C1q-binding de novo DQ DSA was associated with a 30% lower 5-year allograft survival (P=0.003). Conclusions The presence of de novo persistent, complement-binding DQ DSA negatively impacts kidney allograft outcomes. Therefore, early posttransplantation detection, monitoring, and removal of complement-binding DQ might be crucial for improving long-term kidney transplantation outcomes.
American Journal of Transplantation | 2013
M. Taniguchi; Lorita M. Rebellato; Junchao Cai; J. Hopfield; Kimberly P. Briley; Carl E. Haisch; Paul G. Catrou; Paul Bolin; K. Parker; W. Kendrick; S. Kendrick; Robert C. Harland; Paul I. Terasaki
Reports have associated non‐HLA antibodies, specifically those against angiotensin II type‐1 receptor (AT1R), with antibody‐mediated kidney graft rejection. However, association of anti‐AT1R with graft failure had not been demonstrated. We tested anti‐AT1R and donor‐specific HLA antibodies (DSA) in pre‐ and posttransplant sera from 351 consecutive kidney recipients: 134 with biopsy‐proven rejection and/or lesions (abnormal biopsy group [ABG]) and 217 control group (CG) patients. The ABGs rate of anti‐AT1R was significantly higher than the CGs (18% vs. 6%, p < 0.001). Moreover, 79% of ABG patients with anti‐AT1R lost their grafts (vs. 0%, CG), anti‐AT1R levels in 58% of those failed grafts increasing posttransplant. With anti‐AT1R detectable before DSA, time to graft failure was 31 months—but 63 months with DSA detectable before anti‐AT1R. Patients with both anti‐AT1R and DSA had lower graft survival than those with DSA alone (log‐rank p = 0.007). Multivariate analysis showed that de novo anti‐AT1R was an independent predictor of graft failure in the ABG, alone (HR: 6.6), and in the entire population (HR: 5.4). In conclusion, this study found significant association of anti‐AT1R with graft failure. Further study is needed to establish causality between anti‐AT1R and graft failure and, thus, the importance of routine anti‐AT1R monitoring and therapeutic targeting.
Transplantation | 1972
K. Parker; Dina M. Schreinemachers; Hilaire J. Meuwissen
Clinical Transplantation | 2011
Lorita M. Rebellato; Matthew J. Everly; Carl E. Haisch; Miyuki Ozawa; Kimberly P. Briley; K. Parker; Paul G. Catrou; Paul Bolin; W. Kendrick; S. Kendrick; Robert C. Harland
Clinical Transplantation | 2014
Lorita M. Rebellato; K. Parker; Matthew J. Everly; Kimberly P. Briley; W. Kendrick; S. Kendrick; Carl E. Haisch; Paul I. Terasaki; Paul Bolin
Open Access Journal of Science and Technology | 2015
K. Parker; Bryant Winifred; Connie Garris-Sutton; Fatima Rana; Paul Bolin
Transplantation | 2012
Matthew J. Everly; L. M. Rebellato-deVente; Carl E. Haisch; Miyuki Ozawa; K. Parker; Kimberly P. Briley; Paul G. Catrou; Paul Bolin; W. Kendrick; S. Kendrick; Robert C. Harland; Paul I. Terasaki
Transplantation | 2012
Matthew J. Everly; L. M. Rebellato-deVente; Pingping Wu; Miyuki Ozawa; K. Parker; Kimberly P. Briley; Paul G. Catrou; Paul Bolin; W. Kendrick; S. Kendrick; Carl E. Haisch; Robert C. Harland; Paul I. Terasaki
Transplantation | 2012
Lorita M. Rebellato; Paul Bolin; K. Parker; C. Winborne; K. Bringolf; S. Kendrick; W. Kendrick; Robert C. Harland; Carl E. Haisch; Matthew J. Everly; Paul I. Terasaki