Cell-mediated, acute allograft rejection occurs when cytotoxic T lymphocytes react against foreign MHCs. It is marked histologically by lymphocytic infiltrate of the tubules and interstitium.
Acute, cell-mediated rejection can occur from a few weeks to 6 months following kidney transplantation. Lymphatic infiltrate in the tubules and interstitium is seen upon renal biopsy. This process often results in parenchymal cell damage and/or graft vasculitis. A quick way to differentiate acute transplant rejection from hyperacute and chronic rejection is by a time-line approach: hyperacute occurs within minutes of transplant, acute occurs within weeks, and chronic occurs months to years after transplant.
Nickeleit and Andreoni review the role of inflammatory cells in renal allografts. They state that immunohistochemical detection of C4d, a complement degradation product, can be utilized in the investigation of the molecular signaling cascades involved in graft rejection mechanisms.
Akoh and Mathuram Thiyagarajan discuss the risks associated with renal transplantation from elderly living donors. In comparison to younger donors, kidney transplants from living donors over age 65 are at greater risk of delayed graft function, acute rejection, and graft failure.
Illustration A depicts the mechanism of acute graft rejection. Illustration B summarizes the 3 different types of rejection: hyperacute, acute, and chronic. Illustration C demonstrates an example of acute rejection at lower magnification; note how the glomerulus is relatively unaffected in this case but there is dense lymphocytic infiltration around the tubules and within the interstitium (most notable at upper right portion of slide).
Answer 1: Gross sloughing of tubular epithelial cells can be seen in acute tubular necrosis.
Answer 3: Medications that may cause crystal nephropathy include sulfadiazine, acyclovir, indinavir, triamterene, and methotrexate among others.
Answer 4: Granular deposition within the GBM is suggestive of Goodpasture's syndrome (anti-GBM antibody disease).
Answer 5: This is consistent with crescentic glomerulonephritis, a potential sequela of many different forms of inflammatory glomerular injury.
Nickeleit V, Andreoni K. Inflammatory cells in renal allografts. Front Biosci. 2008 May 1;13:6202-13. Review
PMID:18508654 (Link to Abstract)
Akoh JA, Mathuram Thiyagarajan U. Renal Transplantation from Elderly Living Donors. J Transplant. 2013;2013:475964. Epub 2013 Sep 12. Review.
PMID:24163758 (Link to Abstract)