Screening for De Novo Anti-Human Leukocyte Antigen Antibodies in Nonsensitized Kidney Transplant Recipients Does Not Predict Acute Rejection
Gill JS, Landsberg D, Johnston O, Shapiro RJ, Magil AB, Wu V, Tinckam K, Keown P. Transplantation. 2010 Jan 27;89(2):178-84
Several studies have shown the development of anti-donor HLA-antibodies after transplantation is a risk factor for graft loss, suggesting that antibodies should be monitored to identify patients at risk of immunologic events. In this study, patients were prospectively studied for the development of antibodies during the first year post-transplant. Anti-HLA antibodies developed at the same time or after episodes of acute rejection, and was therefore not predictive of acute rejection.
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Abstract:
BACKGROUND: The purpose of this study was to determine whether screening for anti-human leukocyte antigen (HLA) antibodies (Abs) could predict development of acute rejection (AR) before clinical evidence of kidney allograft dysfunction in nonsensitized recipients. METHODS: Eighty-four non-HLA identical kidney transplant recipients were prospectively tested for anti-HLA Abs (FlowPRA analysis and anti-HLA Ab specificity determination) at 0, 10, 20, 30, 60, 90, 180 and 365 posttransplantation, and at the time of clinical suspicion of AR. Allograft biopsies were performed at the time of engraftment, 3 and 12 months posttransplantation, when patients developed new anti-HLA Abs, or when clinically indicated. RESULTS: Among the 70 patients without preformed anti-HLA Abs, 11 developed de novo anti-HLA Abs (8 donor-specific Abs) at a median of 30 days (q1-q3=10-180 days) after transplantation. Patients with de novo anti-HLA Abs had a shorter time to AR than patients without de novo anti-HLA Abs, P=0.06. However, in all cases, de novo anti-HLA Abs developed concomitantly or after a clinically evident AR. CONCLUSIONS: Although de novo anti-HLA Abs were associated with AR, routine screening for anti-HLA Abs was not useful in identifying patients at risk for AR before clinical evidence of allograft dysfunction.
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