{"id":10976,"date":"2026-04-13T06:04:07","date_gmt":"2026-04-13T06:04:07","guid":{"rendered":"https:\/\/www.kauveryhospital.com\/ima-journal\/?p=10976"},"modified":"2026-04-13T06:15:57","modified_gmt":"2026-04-13T06:15:57","slug":"when-the-silent-graft-speaks-acute-t-cell-mediated-rejection-presenting-as-subtle-allograft-dysfunction","status":"publish","type":"post","link":"https:\/\/www.kauveryhospital.com\/ima-journal\/ima-journal-april-2026\/when-the-silent-graft-speaks-acute-t-cell-mediated-rejection-presenting-as-subtle-allograft-dysfunction\/","title":{"rendered":"When the Silent Graft Speaks: Acute T-Cell Mediated Rejection Presenting as Subtle Allograft Dysfunction"},"content":{"rendered":"

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Abstract<\/h2>\n

Acute rejection remains a formidable impediment to long-term renal allograft survival despite significant therapeutic advancements. We report a case of a 36-year-old female, post ABO-compatible living-related renal transplantation, who presented with insidious graft dysfunction. Histopathological evaluation revealed features consistent with acute T-cell mediated rejection (TCMR) Grade 1B, accompanied by moderate acute tubular injury. The patient was managed with pulse corticosteroids followed by anti-thymocyte globulin (ATG). This case underscores the deceptive subtlety of clinical presentation and emphasizes the indispensable role of early biopsy and prompt immunosuppressive escalation in preserving graft integrity.<\/p>\n

Introduction<\/h2>\n

Renal transplantation is widely regarded as the definitive therapeutic modality for end-stage renal disease; however, acute rejection episodes continue to jeopardize graft longevity. Among these, T-cell mediated rejection (TCMR) represents a predominant immunological insult characterized by cellular infiltration and tubulointerstitial injury. Contemporary guidelines proposed by KDIGO advocate for early recognition and decisive intervention to mitigate irreversible allograft damage. Notably, clinical manifestations may often be muted, rendering histopathological evaluation indispensable.<\/p>\n

Case Presentation<\/h2>\n

A 36-year-old female, with a history of hypertension for one year, underwent an ABO-compatible living-related renal transplant in December 2022 and maintained stable graft function until the present episode. She presented with a biochemical profile suggestive of graft dysfunction, with serum creatinine elevated to 2.24 mg\/dL and blood urea of 66 mg\/dL. Hematological evaluation revealed hemoglobin of 12.3 g\/dL, leukocytosis (12,800\/\u00b5L), and platelet count of 3.55 lakh\/\u00b5L. There were no clinical or laboratory indicators of infection, drug toxicity, or post-renal obstruction, thereby warranting further evaluation with a renal allograft biopsy.<\/p>\n

Histopathological Findings<\/h2>\n

Light Microscopy<\/h2>\n

Examination of the allograft biopsy demonstrated an adequate core comprising both cortex and medulla with six glomeruli. The glomeruli were unremarkable, with no evidence of mesangial expansion, glomerulitis, or transplant glomerulopathy. However, there was conspicuous peritubular capillaritis (ptc2), accompanied by marked interstitial inflammation (i3) and severe tubulitis (t3). Tubular epithelial vacuolations and features consistent with moderate acute tubular injury were noted. The vasculature revealed mild arteriolar hyalinosis (ah1) without evidence of vasculitis (v0).<\/p>\n

Immunohistochemistry<\/h2>\n