Kidney Week

Abstract: FR-PO1225

When the Cure Causes Pain: Calcineurin Inhibitor Pain Syndrome Masquerading as Fibromyalgia After Kidney Transplantation

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

• Rodriguez Gomez, Gloria Paulina, Beth Israel Deaconess Medical Center, Boston, Massachusetts, United States

Gloria Paulina Rodriguez Gomez, MD

• Kudlapur, Nathan, Beth Israel Deaconess Medical Center, Boston, Massachusetts, United States

Nathan Kudlapur, MD

• Pavlakis, Martha, Beth Israel Deaconess Medical Center, Boston, Massachusetts, United States

Martha Pavlakis, MD, FASN

• Dale, Leigh-Anne, Beth Israel Deaconess Medical Center, Boston, Massachusetts, United States

Leigh-Anne Dale, MD

Introduction

Calcineurin inhibitor pain syndrome (CIPS) is a rare but underrecognized complication of CNI-based immunosuppression with significant impact on quality of life in transplant recipients. Timely recognition is essential, as the definitive treatment is CNI reduction or transition to alternative immunosuppression.

Case Description

A 55-year-old woman with ESKD secondary to hypertension underwent deceased-donor kidney transplantation in May 2024, maintained on tacrolimus, mycophenolate, and prednisone. She had a prior diagnosis of fibromyalgia with chronic bilateral lower extremity pain. In March 2026, she presented with acute-on-chronic right lower extremity pain radiating from hip to foot, rated 10/10 despite IV opioids. Exam revealed tenderness over the right lower extremity and allograft and inability to ambulate independently due to pain. Tacrolimus trough remained historically at goal 5-7. Allograft function was at baseline (creatinine 1.4 mg/dL). MRI of bilateral tibiae demonstrated patchy bone marrow edema in the proximal third bilaterally with low T1 signal, without fracture or avascular necrosis—radiographically symmetric despite clinically unilateral symptoms. Infectious and vascular workup was unremarkable. Pain improved with IV fluids and gabapentin, and strength normalized to 5/5 prior to discharge. Immunosuppression was transitioned to belatacept inpatient, and the patient reported meaningful improvement in lower extremity pain at 2-month follow-up.

Discussion

CIPS is an underdiagnosed cause of functional impairment in CNI-exposed transplant recipients, with reported incidence of 1-17% across transplant populations. The proposed mechanism involves CNI-mediated sympathetic vasoconstriction causing intraosseous hypertension and bone marrow edema, analogous to avascular necrosis. This case illustrates that CIPS should be considered in any transplant recipient on CNI presenting with new or worsening diffuse pain, even when an alternative pain diagnosis exists. Notably, symptoms were unilateral despite bilateral MRI findings, highlighting that asymmetry does not exclude the diagnosis. Recognition of CIPS as a CNI-mediated toxicity—rather than a pain management problem—is critical, as CNI reduction or withdrawal is the primary intervention.