Abstract :
[en] Acute rejection after kidney transplantation is a major cause
of allograft dysfunction and can lead to rapid loss of graft
function despite anti-rejection therapy. Even when kidney
function initially recovers, acute rejection is associated with
an increased risk of long-term graft failure (1). Acute
rejection is, accordingly, a well-established surrogate
endpoint for long-term outcomes. High-quality evidence
has shown that induction therapy with a biological agent
lowers the risk of acute rejection, and it is therefore widely
administered as part of the early immunosuppressive
regimen (2,3). In recipients at low immunological risk (i.e.
patients with no previous exposure to human leukocyte
antigens [HLA]) either lymphocyte-depleting polyclonal
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