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Acute rejection is a category of rejection that occurs on the timescale of weeks to months, with most episodes occurring within the first 3 months to 1 year after transplantation. [ 6 ] [ 8 ] Unlike hyperacute rejection, acute rejection is thought to arise from two distinct immunological mechanisms as lymphocytes , a subset of white blood cells ...
[2] [19] Adults are significantly likely to suffer from hyperacute rejection, [1] thrombosis, or death, but could be considered to be an acceptable risk if the alternative is death. [6] In the case of ABOi renal transplantation, aggressive antibody removal is required, along with supplemental medication, with the resulting condition being ...
[3] An example of complement dependent type II hypersensitivity is an acute hemolytic transfusion reaction following transfusion of ABO incompatible blood. [4] Preformed antibody (predominantly IgM) against donor red cell antigens not found in an individual of a particular blood group (e.g. anti-A IgM in an individual with blood group B), bind to the donor red cell surface and lead to rapid ...
Also known as delayed xenoactive rejection, this type of rejection occurs in discordant xenografts within 2 to 3 days, if hyperacute rejection is prevented. The process is much more complex than hyperacute rejection and is currently not completely understood. Acute vascular rejection requires de novo protein synthesis and is driven by ...
Donor-specific antibodies (DSA) are a concept in transplantation medicine and describe the presence of antibodies specific to the Donor's HLA-Molecules. These antibodies can cause antibody-mediated rejection and are therefore considered a contraindication against transplantation in most cases. [ 1 ]
Kidney transplant rejection can be classified as cellular rejection or antibody-mediated rejection. Antibody-mediated rejection can be classified as hyperacute, acute, or chronic, depending on how long after the transplant it occurs. If rejection is suspected, a kidney biopsy should be obtained. [5]
Rejection mediated by T lymphocytes sensitized by direct allorecognition pathway is predominant in the short period after the transplantation, but usually subsides with depletion of passenger cells while indirect recognition contributes to continuing graft damage and plays role in chronic rejection.
Transplant glomerulopathy (TG) is best recognized histologically by reduplications or "double contours" of the glomerular basement membrane in peripheral glomerular capillary loops; basement membrane stains (methanamine silver and periodic acid-Schiff) work best for this kind of identification. Since it is a focal lesion in the early stages and ...