Kidney Week

Abstract: FR-PO1170

Who Is the Culprit? Tacrolimus vs. Thymoglobulin, A Rare Case of Thrombotic Microangiopathy After a Second Deceased Donor Kidney Transplant (DDKT)

Session Information

• Transplantation: Clinical - Transplant Access, Recipient Evaluation, Living Donors, Pregnancy, and More
  October 23, 2026 | Location: Exhibit Hall A, Convention Center
  Abstract Time: 10:00 AM - 12:00 PM

Category: Transplantation

• 2002 Transplantation: Clinical

Authors

• Pervez, Aqsa, Henry Ford Hospital, Detroit, Michigan, United States

Aqsa Pervez, MD

• Farouji, Abdelhadi, Henry Ford Hospital, Detroit, Michigan, United States

Abdelhadi Farouji, MD

• Ansari, Rehan, Henry Ford Hospital, Detroit, Michigan, United States

Rehan Ansari, MD

• Patel, Anita K., Henry Ford Hospital, Detroit, Michigan, United States

Anita K. Patel, MD

• Metwally, Sherif, Henry Ford Hospital, Detroit, Michigan, United States

Sherif Metwally, MD

• Shrivastava, Pritika, Henry Ford Hospital, Detroit, Michigan, United States

Pritika Shrivastava, MD

• Prashar, Rohini, Henry Ford Hospital, Detroit, Michigan, United States

Rohini Prashar, MD, FASN

Introduction

In recent years, Tacrolimus is synonymous with immunosuppression post transplant. Often associated with tremors and nephrotoxicity, tacrolimus has rarely been implicated in TMA, particularly immediately post-transplant. TMA is mostly associated with elevated levels of the drug, but can occur in the therapeutic range. We present a case of early TMA following a second DDKT in a patient with chronic tacrolimus immunosuppression.

Case Description

A 33 y/o/ F with CKD V, congenital atrophic kidneys received a DDKT seven years after a living unrelated kidney transplant. Her first transplant course consisted of alemtuzumab induction and complicated by membranous nephropathy and chronic antibody mediated rejection treated with rituximab leading to graft failure and CKD V. She was maintained on a triple tacrolimus/mycophenolate/prednisone regimen with taco levels around 5 heading into second transplant.

She received thymoglobulin induction for her second transplant (46 y/o DCD, KDPI 52%, cPRA 96%, 5 AgMM). Her immediate post transplant period was characterized by slow graft function, hematuria, and labs reflective of microangiopathic hemolysis with hemolytic anemia, low haptoglobin (<30mg/dL), new onset thrombocytopenia and presence of schistocytes on peripheral smear. Given improvement of graft function after discontinuation of Tacrolimus and negative workup with normal complement and ADAMTS 13 levels, it was determined that tacrolimus was likely the offending agent. As thrombocytopenia and anemia improved, tacrolimus was re-introduced at POD # 8 to her immunosuppression regimen with improvement and stabilization of graft function.

Discussion

This case adds to limited but relevant evidence of tacrolimus as a potential cause of de novo thrombotic microangiopathy in the early post-transplant period. Prompt recognition and exclusion of alternative etiologies can facilitate hematological recovery and stabilization of graft function. Our case also highlights the potential confounding and inciting role thymoglobulin may play in endothelial injury which along with complement activation are primary pathways leading to de novo post-transplant TMA. Successful re-introduction of tacrolimus with close monitoring of renal function underscores the importance of individualizing immunosuppression in patients with high immune risk to preserve allograft function.