Journal List > J Korean Soc Transplant > v.30(1) > 1034502

Yun, Lee, Oh, Kim, Sin, Kim, and Kim: Overcome of Drug Induced Thrombotic Microangiopathy after Kidney Transplantation by Using Belatacept for Maintenance Immunosuppression

Abstract

Thrombotic microangiopathy (TMA) is a serious complication of solid organ transplantation. Drug-induced TMA is typically caused by immunosuppressants, particularly calcineurin inhibitors. Withdrawing the causative drug can be one of the treatments for TMA. However, the more immunosuppressants are reduced, the more risk of rejection increases. Even if TMA is successfully resolved, the outcomes of patient and graft survival would be worse than expected. Therefore, it is necessary to maintain efficient and safe immunosuppression therapy. We report on a case of de novo TMA after kidney transplantation triggered by tacrolimus and reactivated by sirolimus. Belatacept, a novel CTLA4 Ig fusion protein, was administered for maintenance immunosuppressant with mycophenolate mofetil and prednisolon. The patient had excellent early graft outcome, and there have been no adverse events so far.

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Fig. 1.
Changes in treatment progresses. (A) Platelet count and lactate dehydrogenase (LDH). (B) Creatinine and hemoglobin. (A, B) Period with the treatment: tacrolimus (1st), postoperative day (POD) 1∼2; thymoglobulin (1st), POD 3∼7; tacrolimus (2nd), POD 7∼9; sirolimus, POD 9∼ 10; thymoglobulin (2nd), POD 10∼ 17; cyclophosphamide, POD 19∼47; belatacept, POD 60≥; mycophenolate mofetil, POD 1∼; prednisolon, POD 1∼; plasmapheresis, POD 13; ureterocystostomy, POD 14; biopsy (1st), POD 26; biopsy (2nd), POD 111.
jkstn-30-38f1.tif
Fig. 2.
The first biopsy revealed microthrombi (arrows) in glomerular capillary lumina (trichrome stain, ×400).
jkstn-30-38f2.tif
Fig. 3.
The third biopsy showed no inflammatory cell infiltration both in glomeruli and interstitium. Focal mesangial cell proliferation (arrow) was noted as the sequel of thrombotic microangiopathy (PAS stain, ×200).
jkstn-30-38f3.tif
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