Abstract: SA-PO1190
When the ACE Turns Against You: A Rare Case of Lisinopril-Induced Leukopenia After Transplantation
Session Information
- Transplantation: Clinical - Complications, Pediatrics, and Multi-Organ Considerations
October 24, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Transplantation
- 2002 Transplantation: Clinical
Authors
- Aamir, Nawal, University of Massachusetts Chan Medical School, Worcester, Massachusetts, United States
- Aulakh, Gagan, University of Massachusetts Chan Medical School, Worcester, Massachusetts, United States
- Choi, Moonyoung, University of Massachusetts Chan Medical School, Worcester, Massachusetts, United States
- Fan, Pang-Yen, University of Massachusetts Chan Medical School, Worcester, Massachusetts, United States
Introduction
Angiotensin-converting enzyme inhibitors (ACEi) are widely used in nephrology for hypertension and proteinuria control, including in kidney transplant recipients. Leukopenia in this setting is usually attributed to other drugs or viral infection, and ACEi are rarely considered. We report severe leukopenia with marked absolute lymphocytopenia temporally linked to lisinopril dose escalation, highlighting an underrecognized hematologic complication of a common agent.
Case Description
A 51-year-old woman with IgA nephropathy–related CKD V underwent preemptive living donor kidney transplantation and was maintained on tacrolimus, mycophenolate, prednisone, valganciclovir, and trimethoprim-sulfamethoxazole with excellent allograft function. Two months post-transplant, lisinopril was started at 10 mg daily, after which her WBC fell from 5.5 ×10^3/µL to a nadir of 0.9 ×10^3/µL with profound absolute lymphocytopenia despite stopping valganciclovir and mycophenolate. CMV PCR was negative and tacrolimus levels were therapeutic. Given the strong temporal association, lisinopril was discontinued, leading to rapid leukocyte recovery and allowing reintroduction of mycophenolate and valganciclovir without recurrent severe leukopenia.
Discussion
Post-transplant leukopenia is common and usually attributed to mycophenolate, valganciclovir, or infection, often leading to reduction of essential immunosuppression. ACE inhibitors are a lesser-known cause of hematologic toxicity; case reports describe severe cytopenias, including lisinopril-associated pancytopenia, suggesting idiosyncratic marrow suppression. A proposed mechanism is increased N-acetyl-seryl-aspartyl-lysyl-proline, a peptide that inhibits hematopoiesis. In our patient, leukopenia developed and progressed after lisinopril up-titration, persisted despite withdrawal of more typical culprits, and improved promptly with ACE inhibitor discontinuation, with subsequent safe reintroduction of mycophenolate and valganciclovir. The marked absolute lymphocytopenia adds novelty, as most ACE inhibitor–related cytopenias are reported as neutropenia. This case supports ACE inhibitors as a reversible cause of leukopenia with prominent lymphocyte involvement and emphasizes considering ACE inhibitor exposure or dose escalation before reducing critical immunosuppressive therapy.