An Unusual Case of AKI in a Kidney Allograft

Introduction: Post-transplant lymphoproliferative disorder (PTLD) is the third most common malignancy following transplantation, after skin cancer and renal cell carcinoma. Here, we present a case of chronic lymphocytic leukemia (CLL), a type of PTLD, and discuss its impact on kidney graft survival. Case Description: A 64-year-old female status post kidney transplant in (2016), was evaluated for acute kidney injury. She received thymoglobulin (4 mg/kg) and was maintained on FK, mycophenolic acid (MPA), and prednisone. She experienced combined cellular (ACR 2B) and antibody-mediated rejection (ABMR) in 2017, treated with thymoglobulin (6 mg/kg), plasmapheresis, IVIg, and rituximab, with subsequent ABMR recurrences in 2018 and 2019 managed similarly. 2 years ago, she was diagnosed with (CLL), primarily presenting with lymphadenopathy, lymphocytosis, and abnormal smear; her Rai stage remained < 3, prompting hematology surveillance and discontinuation of MPA. Given elevated cell-free DNA, a kidney biopsy was performed, revealing moderate glomerulitis (g2), severe peritubular capillaritis (ptc3), mild tubulitis (t1), and severe interstitial inflammation (i3). She received IV steroids & IVIg. With CLL history, IHC revealed lymphoma cells + for PAX-5 and CD20 (B-cell markers) with aberrant CD5 expression, along with kappa light-chain restriction, consistent with her known CLL. Discussion: CLL is the most common leukemia in adults: 25–30% of cases. Clinically extranodal involvement occurs in approximately 10% of patients; however, autopsy studies suggest renal lymphocytic infiltration in 60–90% of patients. Histologically, renal involvement is characterized by diffuse infiltration of mature lymphocytes affecting the interstitium, tubules, and peritubular capillaries, with glomerular involvement being less common. In this case, the occurrence of AKI and elevated cell-free DNA prompted further diagnostic evaluation. Notably, the presence of renal involvement altered treatment plan from "watch and wait" strategy to active treatment using a Bruton's tyrosine kinase (BTK) inhibitor.