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Antithymocyte globulin is associated with a lower incidence of de novo donor-specific antibodies in moderately sensitized renal transplant recipients. | LitMetric

Antithymocyte globulin is associated with a lower incidence of de novo donor-specific antibodies in moderately sensitized renal transplant recipients.

Transplantation

1 Department of Pharmacy, University of Wisconsin, Madison, WI. 2 Department of Surgery, University of Wisconsin, Madison, WI. 3 Department of Medicine, University of Wisconsin, Madison, WI. 4 Departments of Pathology and Laboratory Medicine, University of Wisconsin, Madison, WI. 5 Address correspondence to: Arjang Djamali, M.D., M.S., F.A.S.N., 5142 MFCB 1685 Highland Avenue, Madison, WI 53705.

Published: March 2014

Background: Recent evidence suggests that de novo donor-specific antibodies (dnDSA) are associated with antibody-mediated rejection (ABMR) and graft failure after kidney transplantation. The effects of induction immunosuppression on dnDSA are unknown.

Methods: The study population comprised 114 consecutive moderately sensitized (positive DSA and negative flow crossmatch) recipients who received deceased donor renal transplants between December 2009 and November 2011. Patients were divided into two groups based on induction immunosuppression: antithymocyte globulin (ATG) (n=85) or basiliximab (n=29) and were followed up for 36 months.

Results: Patients in the ATG group received a mean dose of 4.98 mg/kg ± 7.9 mg/kg, had a significantly higher PRA, and received more plasmapheresis and IVIG at the time of transplant. The incidence of dnDSA (P=0.02, HR=0.33, 95% CI 0.09-1.24) and ABMR (P=0.002, HR=0.2, 95% CI 0.04-0.87) was significantly lower in the ATG group. In multivariate regression analyses, ATG induction was the single most important variable associated with both ABMR and dnDSA.

Conclusions: In moderately sensitized deceased donor renal transplant recipients, induction with ATG is associated with a reduction in the occurrence of dnDSA and ABMR when compared with basiliximab.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4106033PMC
http://dx.doi.org/10.1097/TP.0000000000000031DOI Listing

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