Decitabine
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Acute kidney injury, thrombotic microangiopathy with glomerular crescents formation and tubular necrosis: case report A 47-year-old man developed acute kidney injury (AKI) and thrombotic microangiopathy (TMA) with glomerular crescents formation and tubular necrosis following chemotherapy with decitabine for membranous nephropathy (MN). The man presented with due to aggravated oedema for 10 days. His medical history was notable for nephrotic syndrome for about 2 years, which had been managed with supportive therapy until 4 months earlier, when he was diagnosed with typical MN. He had received prednisone along with IV cyclophosphamide 0.8g every 2 weeks until 6 weeks earlier, when he developed petechiae on his body. Cyclophosphamide was discontinued after receiving a cumulative dose of about 5g. Thereafter, he achieved partial remission despite no alternative agent for cyclophosphamide. Laboratory analyses revealed a drop in platelet count from 60 × 103/µL to 10 × 103/µL over 2 weeks. Bone marrow smear showed impaired megakaryocyte maturation and platelet production, and immune thrombocytopenic purpura was suspected. He received one platelet transfusion and started receiving low-dose infusions of decitabine injections 10mg for 3 days. However, he developed recurrent oedema with a weight gain of about 15kg over 10 days. Meanwhile, his serum creatinine increased from a baseline of 89 µmol/L to 392 µmol/L. Subsequently, his platelet count returned to 69 × 103/µL. He was hospitalised for investigation and treatment. On admission, physical examination revealed a moon face and severe anasarca with a BP of 168/105mm Hg. Laboratory data collected on admission revealed the following: serum creatinine 256 µmol/L, platelet count 194 × 103/µL, serum LDH 460 IU/mL, urine protein 11.9 g/d, sediments RBCs 8–10/HP, antiphospholipase A2 receptor (PLA2R) antibody 107 RU/mL, normal complement-3 (C3), C4, and factor-H concentrations, negative anti-factor-H, antiglomerular basement membrane (GBM) and anti-neutrophil cytoplasmic antibodies, absence of monoclonal immunoglobulin in serum and urine samples during immune fixation electrophoresis, negative Coombs’ test and absence of schistocytes. Hyperchloraemia, hypokalaemia, hypouricaemia and renal glycosuria were suggestive of tubular injury. Ultrasound examination showed no signs of renal venous thrombosis. Therefore, a diagnosis of new-onset AKI with haematuria after exposure to decitabine, superimposed on a pre-existing but non-remission MN was made. The development of severe thrombocytopenia was attributed to the treatment with cyclophosphamide, since thrombocytopenia developed 4 weeks before the increase of serum creatinine and started to recover about 4 weeks after the discontinuation of cyclophosphamide. Renal biopsy revealed fifty glomeruli; seven of them demonstrated ischaemic sclerosis. All the glomeruli exhibited an MN pattern as diffuse glomerular basement membrane (GBM) thickening, with subepithelial immune complex deposits and foot process effacement. Twelve glomeruli ex
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