Abstract: FR-PO1222
Tacrolimus-Induced Cardiomyopathy in a Kidney Transplant Recipient: A Reversible Cause of Left Ventricular Hypertrophy
Session Information
- Transplantation: Clinical - Rejection, Biomarkers, and Pharmacology
October 23, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Transplantation
- 2002 Transplantation: Clinical
Authors
- Vanteru, Abinay Siva kumar Reddy, University of Arkansas for Medical Sciences, Little Rock, Arkansas, United States
- Nemalidinne, Krishna Vani, University of Arkansas for Medical Sciences, Little Rock, Arkansas, United States
- Mahmoud, Saad Abdulrahim Talal, University of Arkansas for Medical Sciences, Little Rock, Arkansas, United States
- Alzghoul, Husam Mohammad, University of Arkansas for Medical Sciences, Little Rock, Arkansas, United States
- Khan, Nasir, University of Arkansas for Medical Sciences, Little Rock, Arkansas, United States
Introduction
Tacrolimus, a calcineurin inhibitor commonly used in transplantation, is associated with cardiovascular adverse effects such as hypertension and arrhythmias. Tacrolimus-induced cardiomyopathy is rare and underrecognized, often mimicking infiltrative or hypertrophic cardiomyopathies. Early identification is important, as withdrawal may lead to reversibility.
Case Description
A 71-year-old male with ESRD due to diabetes and hypertension underwent deceased donor kidney transplantation in 2021 (KDPI 22%, CIT 25 hrs, cPRA 39%). Induction included antithymocyte globulin and steroids, followed by tacrolimus and mycophenolate mofetil.
Five months post-transplant, elevated donor-derived cell-free DNA prompted biopsy showing borderline acute cellular rejection and antibody-mediated rejection, treated with steroids, plasmapheresis, and IVIG. Tacrolimus targets were increased.
Three years later, he presented with atrial fibrillation. Echocardiography showed new left ventricular hypertrophy with preserved EF (55–60%) and increased interventricular septal (IVS) thickness from 1.1 cm to 1.6 cm. Cardiac MRI demonstrated asymmetric septal hypertrophy, global hypokinesia, reduced EF (34%), and patchy delayed enhancement suggestive of infiltrative cardiomyopathy.
Evaluation for amyloidosis (SPEP, UPEP, serum free light chains, immunofixation, Tc-PYP scan, genetic testing, fat pad biopsy) was negative. Repeat echocardiogram showed IVS progression to 2.3 cm. Endomyocardial biopsy revealed mild hypertrophy and interstitial fibrosis without amyloid.
Tacrolimus-induced cardiomyopathy was suspected. Tacrolimus was discontinued and replaced with belatacept. At 6 months, IVS thickness improved to 2.1 cm and to 1.8 cm at 1 year.
Discussion
Tacrolimus-induced cardiomyopathy is an uncommon but important diagnosis in transplant recipients with unexplained LV hypertrophy. Proposed mechanisms include altered calcium signaling and myocardial fibrosis.
This case highlights delayed presentation, resemblance to infiltrative disease, and the importance of excluding amyloidosis. Improvement following tacrolimus withdrawal supports reversibility.
Clinicians should consider tacrolimus toxicity in patients with new cardiomyopathy, as early recognition and modification of immunosuppression can improve outcomes.