Question

*The answer is C.* Transplant rejection reactions have been traditionally categorized into hyperacute, acute, and chronic rejection based on the clinical tempo of the response and on the mechanisms involved. Acute rejection is characterized by an abrupt onset of azotemia and oliguria, which may be associated with fever and graft tenderness. A needle biopsy would be expected to show (1) interstitial infiltrates of lymphocytes and macrophages, (2) edema, (3) lymphocytic tubulitis, and (4) tubular necrosis. Neutrophilic vasculitis and fibrinoid necrosis (choice D) are seen in hyperacute rejection. Arterial intimal thickening (choice A), glomerulosclerosis (choice B), and tubular atrophy (choice E) are seen in chronic graft rejection.

Diagnosis: Acute graft rejection

Answer 1

Transplant rejection is an immune response triggered by MHC molecule mismatches, leading to acute graft rejection, which is characterized by lymphocyte infiltration and tubular necrosis in biopsies.

Step-by-step explanation:

Transplant rejection occurs when a recipient's immune system recognizes a transplanted organ or tissue as foreign and mounts an immune response against it. The most critical factor in transplant rejection is the mismatch of major histocompatibility complex (MHC) molecules, also known as human leukocyte antigens (HLAs), between the donor and the recipient. In cases of acute graft rejection, a biopsy would typically show pathological features such as interstitial infiltrates of lymphocytes and macrophages, edema, lymphocytic tubulitis, and tubular necrosis. These are symptoms of the body's cytotoxic T cells responding to the donor organ as if it were a pathogen, despite the transplant's intention to provide medical benefit.