An ASX 72-year-old patient with decreased renal function 3 days after a second renal transplant from a 65-year-old donor. The most likely explanation for the decline in function is what?

An ASX 72-year-old patient with decreased renal function 3 days after a second renal transplant from a 65-year-old donor. The most likely explanation for the decline in function is what?

• A. Hyperacute rejection due to preformed antibodies
• B. Chronic rejection due to alloantibody deposition
• C. Recurrent nephritis
• D. Acute rejection due to failure to suppress class II antigen recognition

Answer: (D)

Acute rejection in the early posttransplant period is a cell‑mediated process where the recipient’s T cells recognize donor MHC antigens, especially MHC class II, presented by donor or host antigen‑presenting cells. If immunosuppressive therapy fails to adequately suppress this T‑cell activation, CD4+ T cells drive an immune attack on the graft, leading to impaired renal function within days. Hyperacute rejection would occur much sooner due to preformed antibodies acting on donor antigens; chronic rejection develops months to years later with vascular changes and alloantibody deposition; recurrent nephritis would reflect disease of the native kidney rather than the transplanted organ. The scenario fits acute cellular rejection driven by inadequate suppression of class II antigen–specific T‑cell responses.

Acute rejection in the early posttransplant period is a cell‑mediated process where the recipient’s T cells recognize donor MHC antigens, especially MHC class II, presented by donor or host antigen‑presenting cells. If immunosuppressive therapy fails to adequately suppress this T‑cell activation, CD4+ T cells drive an immune attack on the graft, leading to impaired renal function within days. Hyperacute rejection would occur much sooner due to preformed antibodies acting on donor antigens; chronic rejection develops months to years later with vascular changes and alloantibody deposition; recurrent nephritis would reflect disease of the native kidney rather than the transplanted organ. The scenario fits acute cellular rejection driven by inadequate suppression of class II antigen–specific T‑cell responses.