Reactions 1680, p136 - 2 Dec 2017 immunosuppression with corticosteroids, tacrolimus 0.15 mg/kg and mycophenolic acid. His prophylactic medications included ganciclovir and cotrimoxazole. His creatinine levels on POD 4 was 125.53 µmol/L. Subsequently Various toxicities: 3 case reports he showed an increase in his creatinine levels and a biopsy on In a series, a 55-year-old woman developed thrombotic POD 8 showed Banff Ia cellular rejection. He received microangiopathy (TMA), graft loss, acute tubular necrosis methylprednisolone for his graft rejection. A control biopsy (ATN) and interstitial fibrosis and tubular atrophy (IFTA) and a conduced on POD 13 showed mesangiolysis and double 44-year-old man developed TMA, mesangiolysis and graft loss contours. He showed no signs of capillaritis or glomerulitis during treatment with tacrolimus. Additionally, a 33-year-old and C4d was negative. Other possibilities of TMA were ruled man developed TMA, IFTA and mesangiolysis during treatment out, and drug related TMA was suspected. At the time of TMA with everolimus and tacrolimus [routes not stated; not all diagnosis, his laboratory tests showed creatinine of dosages stated]. 178.57 µmol/L, haemoglobin of 88 g/L and platelet counts of Patient 1: A 33-year-old man with a history of atypical 218000 /mm . His trough level of tacrolimus was 6.9 ng/dL haemolytic uraemic syndrome (HUS), underwent a renal and schistocytes were negative. His tacrolimus was stopped transplant. His induction therapy consisted of basiliximab and and belatacept was initiated. His creatinine level decreased; antithymocyte globulin. His maintenance therapy consisted of however, on POD 31, a control biopsy showed Bnaff IIa tacrolimus, mycophenolic acid and prednisone. On post- cellular rejection, which was treated with antithymocyte operative day 150 (POD), his tacrolimus was switched to globulin. Belatacept was continued; a repeat biopsy on everolimus to prevent calcineurin inhibitor induced toxicity. POD 40 showed no signs of TMA or rejection and normalised He was undergoing treatment with everolimus 1.50mg daily creatinine levels. along with mycophenolic acid 1440mg daily. His creatinine Author comment: "We report three cases of de novo drug- level on POD 240 was 154.7 µmol/L. He became intolerant to induced TMA in renal transplant patients who were managed mycophenolic acid and developed diarrhoea on POD 330; his by replacing calcineurin inhibitors or proliferation signal mycophenolic acid was withdrawn and prolong-release inhibitors with belatacept". "If TMA is not treated, it can lead tacrolimus was initiated. On POD 740, he was admitted with a to graft loss or renal cortical necrosis." deteriorating renal function and creatinine level of 291 µmol/L. A biopsy was conducted, which confirmed the presence of Cicora F, et al. Use of belatacept as alternative immunosuppression in three renal mesangiolysis and grade 1 interstitial fibrosis and tubular transplant patients with de novo drug-induced thrombotic microangiopathy. Case Reports in Medicine 2013: 2013. Available from: URL: http:// atrophy (IFTA). He had no signs of capillaritis or glomerulitis doi.org/10.1155/2013/260254 - Argentina 803284091 and C4d was negative. He was subsequently diagnosed with TMA and his laboratory tests showed creatinine levels of 247.52 µmol/L, haemoglobin 141 g/L and platelet count of 145000 /mm . Schistocytes were absent. His trough levels of tacrolimus and everolimus were 10.4 ng/mL and 7.6 ng/mL respectively. Other possible causes of TMA were ruled out, and drug-induced TMA was suspected. Tacrolimus and everolimus treatment was discontinued. He was initiated on belatacept and immunosuppression with prednisone and mycophenolic acid. His creatinine levels decreased to 194 48 µmol/L on POD 800, 60 days after TMA diagnosis and a repeat biopsy did not reveal TMA. Patient 2: A 55-year-old woman with unknown renal disease, who had been undergoing haemodialysis for five years, underwent a renal transplant. Her induction therapy consisted of basiliximab. She was also receiving immunosuppressive therapy with unspecified corticosteroids, tacrolimus 0.15 mg/kg and mycophenolic acid. Her prophylactic medications consisted of ganciclovir and cotrimoxazole [trimethoprim/sulfamethoxazole]. Her creatinine levels on POD 5 were 137.02 µmol/L. However, her creatinine levels were elevated up to 300.56 µmol/L on POD 15. A biopsy showed Banff Ia cellular rejection. She was treated with methylprednisolone and her creatinine levels decreased. Between POD 15 and POD 30 she developed deep vein thrombosis, urinary fistula and haematoma on the abdominal wall. On POD 20, she was admitted with elevated creatinine levels and pain in graft area; Banff IIa rejection was observed. She was treated with antithymocyte globulin; however, her creatinine increased again. A biopsy confirmed the presence of TMA in the initial phase along with mild ATN and grade 1 IFTA. She showed no signs of capillaritis or glomerulitis and C4d was negative. Her laboratory tests at the time of TMA diagnosis were creatinine 548 µmol/L, haemoglobin of 91 g/L and platelet counts were 55000 /mm . Schistocytes were absent. Her trough level of tacrolimus was 15.7 ng/mL. Other possible causes of TMA were ruled out, and drug-induced TMA was suspected. Belatacept was initiated and her prednisone with mycophenolic acid was continued. By POD 90, biopsy showed no signs of TMA and graft rejection. Her creatinine had also normalised to 90.17 µmol/L. Patient 3: A 44-year-old man with unknown renal disease had been undergoing haemodialysis for two years and underwent a renal transplant. He was initiated on induction therapy which consisted of antithymocyte globulin and 0114-9954/17/1680-0001/$14.95 Adis © 2017 Springer International Publishing AG. All rights reserved Reactions 2 Dec 2017 No. 1680
Reactions Weekly – Springer Journals
Published: Dec 2, 2017
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