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Jenea : ali hussein auda d nUU : 3 pnari: D Date:2020/03/25

Report title : Antibody‐mediated rejection

Antibody‐mediated rejection (AMR) is a significant complication following organ transplantation that

contributes toward both short‐ and long‐term injury. three types of AMR exists based on the timing and course
of the rejection event :

 Hyperacute rejection : occurs within minutes to a few hours after transplantation in a presensitized host
and typically is recognized by the surgeon just after the vascular anastomosis is completed. In contrast with
a nonrejecting kidney graft, which regains a normal pink color and tissue turgor and promptly excretes
urine, a hyperacutely rejecting kidney rapidly becomes cyanotic, mottled, and flaccid and may excrete only
a few drops of bloody fluid. The histologic picture is characterized by widespread acute arteritis and
arteriolitis, vessel thrombosis, and ischemic necrosis, all resulting from the binding of preformed antibodies
to graft endothelium.

 J Acute rejection : may occur within days to weeks of transplantation in a nonimmunosuppressed host or
may appear months or even years later, even in the presence of adequate immunosuppression. Acute
rejection is caused by both cellular and humoral immune mechanisms, and in any one patient, one or the
other may predominate, or both may be present. On histologic examination, cellular rejection is marked by
an interstitial mononuclear cell infiltrate with associated edema and parenchymal injury, whereas humoral
rejection is associated with vasculitis.
1. Acute cellular rejection most commonly is seen within the first months after transplantation and typically
is accompanied by clinical signs of renal failure.
2. Acute humoral rejection (rejection vasculitis) caused by antidonor antibodies also may participate in
acute graft rejection.

 Chronic Rejection : Patients present with chronic rejection late after transplantation (months to years) with
a progressive rise in serum creatinine levels over a period of 4 to 6 months. Chronic rejection is dominated
by vascular changes, interstitial fibrosis, and loss of renal parenchyma; there are typically only mild or no
ongoing cellular parenchymal infiltrates.
Treatment:
The current strategy for treating AMR is use of a combination of modalities to address multiple
pathophysiologic pathways.regimens of plasmapheresis or immunoadsorption followed by low‐dose
intravenous immunoglobulin or high‐dose IVIg with or without steroids.