Improving precision in predicting alloreactivity is an important unmet need and may
require individualized consideration of non-HLA antibodies. We report a 21-year-old
man with kidney failure from immunoglobulin A nephropathy who met all traditional
criteria for a “low-risk” transplant for immune memory. He was unsensitized and received
a haplotype-matched living donor kidney transplant from his mother. There were no
anti-HLA donor-specific antibodies and flow cross-match was negative. After immediate
function, he developed delayed graft function on postoperative day 2. The transplant
biopsy specimen was suggestive of antibody-mediated rejection and acute tubular injury
with increased vimentin proximal tubular expression compared to the implantation biopsy
specimen. He had a history of juvenile idiopathic arthritis, and non-HLA antibody
screening demonstrated preformed anti-vimentin antibody. He was successfully treated
with plasmapheresis, intravenous immunoglobulin, antithymocyte globulin, and methylprednisolone,
with renal recovery. The follow-up biopsy specimen demonstrated decreased vimentin
expression with decreased alloinflammation, and graft function remains stable at 1
year posttransplantation (estimated glomerular filtration rate, 62 mL/min/1.73 m2). We postulate that preformed anti-vimentin autoantibodies bound to vimentin expressed
on apoptotic tubular epithelial cells induced by ischemia-reperfusion injury and to
constitutively expressed vimentin on peritubular capillaries and podocytes. Our case
is suggestive of the involvement of anti-vimentin antibody, for which the pathogenic
epitopes may be exposed during ischemia-reperfusion injury.
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Article Info
Publication History
Published online: September 09, 2019
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© 2019 by the National Kidney Foundation, Inc.

