acute rejection


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a·cute cel·lu·lar re·jec·tion

graft rejection that usually begins within 10 days after a graft has been transplanted into a genetically dissimilar host. Lesions at the site of the graft characteristically are infiltrated with large numbers of lymphocytes and macrophages that cause tissue damage. See: primary rejection.
Synonym(s): acute rejection

rejection

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

acute rejection

The early destruction of grafted or transplanted material, usually beginning a week after implantation. Acute rejection is identified clinically by decreased function of the transplanted organ. High-dose corticosteroids are the first treatment of acute rejection; they are typically quite effective. Antilymphocyte globulin (ALG), the monoclonal antibody OKT 3, mycophenolate mofetil, and tacrolimus are used when corticosteroids are not effective. See: suppressive immunotherapy; macrophage processing; major histocompatibility complex; T cell
See also: rejection
References in periodicals archive ?
Posttransplant kidney complications Perinephric fluid Renal collecting Vascular complications collections system New students Hematoma Obstructive Renal artery thrombosis hydronephrosis or stenosis Seroma Nonobstructive Renal vein thrombosis hydronephrosis or stenosis Urinoma Urinary leak Segmental infarction Lymphocele Nephrolithiasis Graft torsion Abscess Renal abscess Arteriovenous fistula Hematoma Fungal infections Transitional cell cancer Parenchymal abnormalities Focal: Tumors (urethral and bladder tumors) Posttransplant lymphoproliferative syndrome Focal infarction Pyelonephritis/renal abscess Cysts Nephrocalcinosis Diffuse: Acute tubular necrosis Hyperacute rejection Acute rejection
All 8 episodes of acute rejection presented increased expression of one or both genes.
There have been no acute rejection episodes, opportunistic infections, or renal complications in the first 24 months after transplant.
Three variables for monitoring graft loss were identified from the primary aim of this study: medication nonadherence, acute rejection, and change in kidney function.
While higher-grade acute rejection can usually be readily noted on low-power view, grade A1 rejection might only be detected at higher-power analysis, especially in specimens with procedural artifacts and atelectasis.
Kim et al., "Pretransplant soluble CD30 level has limited effect on acute rejection, but affects graft function in living donor kidney transplantation," Transplantation, vol.
Of the 55 R+ patients who received induction therapy 38 (69%) developed CMV infection/disease before any treatment for acute rejection. Out of 37 patients treated for acute rejection (11 received induction therapy) 17 (46%) developed CMV infection/disease, seven after treatment with methylprednisolone and 10 after treatment with methylprednisolone and r-ATG.
Postoperative complications were recorded and included acute rejection, posttransplant hemodialysis, posttransplant diabetes mellitus, or cytomegalovirus infection.
Patients were divided into two groups; acute rejection group (AR group) (79 patients) and non acute rejection group (non-AR group) (161 patients).
The patient experienced acute rejection and underwent amputation 3 weeks post-transplant.
In addition to that, it has been shown that activated protein C resistance and Factor V mutation are associated with an increased incidence of acute rejection and graft loss in kidney transplant recipients [5-7].
But even when seemingly necessary, many biopsies find that a patient isn't having an acute rejection episode, says Peter Heeger, a transplant nephrologist at Mount Sinai Hospital in New York City.

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