hyperacute rejection

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hy·per·a·cute re·jec·tion

1. a rejection that usually develops immediately after the implantation of a vascular graft; may be caused by preformed, cytotoxic antibodies to the graft;
2. a form of antibody-mediated, usually irreversible damage to a transplanted organ, particularly the kidney, manifested predominantly by diffuse thrombotic lesions, usually confined to the organ itself and only rarely disseminated.


Immunology An immune reaction evoked by allografted organs; the prototypic rejection occurs in renal transplantation, which is subdivided into three clinicopathologic stages. See Cyclosporin A, Graft rejection, Graft-versus-host disease, Second set rejection, Tacrolimus, Transplant rejection.
Rejection types  
Hyperacute rejection Onset within minutes of anastomosis of blood supply, which is caused by circulating immune complexes; the kidneys are soft, cyanotic with stasis of blood in the glomerular capillaries, segmental thrombosis, necrosis, fibrin thrombi in glomerular tufts, interstitial hemorrhage, leukocytosis and sludging of PMNs and platelets, erythrocyte stasis, mesangial cell swelling, deposition of IgG, IgM, C3 in arterial walls
Acute rejection Onset 2-60 days after transplantation, with interstitial vascular endothelial cell swelling, interstitial accumulation of lymphocytes, plasma cells, immunoblasts, macrophages, neutrophils; tubular separation with edema/necrosis of tubular epithelium; swelling and vacuolization of the endothelial cells, vascular edema, bleeding and inflammation, renal tubular necrosis, sclerosed glomeruli, tubular 'thyroidization' Clinical ↓ Creatinine clearance, malaise, fever, HTN, oliguria
Chronic rejection Onset is late–often more than 60 days after transplantation, and frequently accompanied by acute changes superimposed, increased mesangial cells with myointimal proliferation and crescent formation; mesangioproliferative glomerulonephritis, and interstitial fibrosis; there is in general a poor response to corticosteroids

hyperacute rejection

Immediate, intense, and irreversible destruction of grafted material due to preformed antibodies. These antibodies are most common in patients who have rejected a previously transplanted organ or who have received multiple blood transfusions. The risk of hyperacute rejection has been nearly eliminated by testing the recipient's blood for antibodies against donor lymphocytes before surgery.
See also: rejection
References in periodicals archive ?
The most promising approach to vanquishing hyperacute rejection may be not to treat the recipient, but to change the donor organ.
What's more, they fear that overcoming hyperacute rejection isn't the end of their job.
One graft was lost to hyperacute rejection, four to chronic rejection, and the remaining patients died with functioning grafts.
The major strategies used to reduce hyperacute hyperacute rejection such as depletion of anti-Gal antibodies and genetic engineering of swine to express human complement regulatory proteins to decrease complement deposition, might impact host defenses against viral infection (Meije et al.
Reduction of hyperacute rejection and protection of metabolism and function in hearts of human decay accelerating factor (hDAF)-expressing pigs.
The report, published February 8Th by the Department of Health, notes that genetic modification of source animals to knock-out the genes responsible for hyperacute rejection and to add new genes necessary to control later rejection is promising but remains in the very early stages.
vice president of research and development at Nextran, who today is presenting at IBC's Xenotransplantation Conference in San Diego, stated "Through this collaboration with Cytel, we expect to minimize the most significant immunological barrier to transplantation of pig organs -- hyperacute rejection.
PPL says it plans to use cells which have had the gene involved in causing hyperacute rejection "knocked-out" to produce cloned pigs with organs more likely to be accepted by human recipients.
pylori, a second for treating and preventing respiratory infections, and a third for overcoming xenotransplant hyperacute rejection.
The cells are believed to be largely responsible for the phenomenon of hyperacute rejection of animal organs transplanted into human recipients.
In order to develop organs with longer-term survival potential, Alexion is employing a proprietary double-barreled approach to overcome the problem of hyperacute rejection by developing genetically engineered organs that do not express the carbohydrate epitopes and do express proprietary complement inhibitors that act as a shield against the human complement proteins.