Alemtuzumab induction and belatacept maintenance in marginal pathology renal allografts. Issue 6 (11th April 2019)

• Record Type: Journal Article
• Authors: Sparkes, Tracy; Ravichandran, Bharath; Opara, Onumara; Ugarte, Richard; Drachenberg, Cinthia B.; Philosophe, Benjamin; Bromberg, Jonathan S.; Barth, Rolf N.
• Is Part Of: Clinical transplantation. Volume 33:Issue 6(2019)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2019-04-11
• Subjects: donors and donation: extended criteria -- fusion proteins and monoclonal antibodies: alemtuzumab -- fusion proteins and monoclonal antibodies: belatacept -- Immunosuppressant -- kidney (allograft) function/dysfunction; Transplantation of organs, tissues, etc -- Periodicals; 617.95
• DOI: 10.1111/ctr.13531
• Languages: English
• ISSNs: 0902-0063

Abstract

Abstract: We performed a prospective, 12‐month, single‐center, nonrandomized, open‐label pilot study to investigate the use of belatacept therapy combined with alemtuzumab induction in renal allografts with preexisting pathology, as these kidneys may be more susceptible to additional toxicity when exposed to calcineurin inhibitors posttransplant. Nineteen belatacept recipients were matched retrospectively to a cohort of tacrolimus recipients on the basis of preimplantation pathology. The estimated glomerular filtration rate was not significantly different between belatacept and tacrolimus recipients at either 3 or 12 months posttransplant (59 vs 45, P = 0.1 and 56 vs 48 mL/min/1.72/m 2, P = 0.3). Biopsy‐proven acute rejection rates at 12 months were 26% in belatacept recipients and 16% in tacrolimus recipients ( P = 0.7). Graft survival at 1 year was 89% in both groups. Alemtuzumab induction combined with either calcineurin inhibitor or costimulatory blockade therapies resulted in similar acceptable one‐year outcomes in kidneys with preexisting pathologic changes. Longer‐term follow‐up may be necessary to identify preferential strategies to improve outcomes of kidneys at a higher risk for poor function (ClinicalTrials.gov—NCT01496417).