SUN-356 THROMBOPENIA IN A KIDNEY TRANSPLANT PATIENT: A RARE CASE OF LATE-ONSET IMMUNE THROMBOCYTOPENIC PURPURA INDUCED BY TACROLIMUS

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Several long-term hematologic complications are described in kidney transplant patients. While bone marrow toxicity is well known, and in its acute form is often associated with uncontrolled blood levels of antirejection drugs or with the start of new drugs, immune-mediated toxicity is less acknowledged. Diagnosis may be difficult, but is of crucial importance because the identification of a trigger may be the clue for inducing remission. The association with antirejection drugs is increasingly reported, but the diagnosis may be difficult also due to the sudden onset of the disease. We would like to report of an exceptional case of immune thrombocytopenic purpura induced by Tacrolimus at the 8th year of a third kidney transplantation. A 80-year-old man, with a kidney transplant since 2011, for end-stage kidney disease due to IgA nephropathy, was found with asymptomatic thrombocytopenia at 31 G/l, at routine assessment. He had been previously transplanted in 1991 and 2000 (graft loss due to IgA nephropathy recurrence). For his third graft, he received thymoglobulin induction and maintenance therapy with Prednisone, Mycophenolate Mophetil (MMF) and tacrolimus. Kidney function was optimal (creatinine around 100 μmol/l, eGFR CKD-EPI 60-65 ml/min/1.73 m2). At further assessment, the myelogram showed a rich bone marrow without myelodysplasia; coagulation was normal; there was no sign of hemolysis, infection, lupus or antiphospholipid syndrome. Positron Emission Tomography was normal. No precipitating factor was identified. The diagnosis of idiopathic thrombotic purpura (ITP) was retained, and the patient was treated with oral prednisolone (1 mg/kg/day) and high dose intravenous immunoglobulins (2 g/kg). Dapsone treatment was added, but was rapidly discontinued due to abdominal pain. A third line of treatment with Elthrombopag (50 mg/day) allowed partial remission, stabilising the platelet count between 50 and 100 G / l. Due to the incomplete response, in the hypothesis of a cause or con-cause linked to the chronic immunodepressive treatment, MMF was discontinued, without improvement of thrombocytopenia. Subsequently, after resuming MMF, Tacrolimus was discontinued, resulting a rapid and complete remission, with a rise of the platelet count to over 150 G/l within one week. Replacement of Tacrolimus with Cyclosporine A was not followed by a new decrease in platelet count (figure). Thrombocytopenic purpura induced by Tacrolimus is a rare complication of kidney transplantation, which can occur late, be severe and refractory, as in our patient. While the decrease in regulatory T cells on Calcineurin inhibitors, promoting the appearance of autoimmunity, is well known, persistent remission on Cyclosporine A underlines the absence of a “class” effect, and suggest that drug switching may represent a favourable therapeutic strategy.

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