Dasatinib
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Thrombotic microangiopathy and proteinuria: 2 case reports In a report, a 48-year-old woman and a 71-years-old woman were described, who developed thrombotic microangiopathy (TMA) and proteinuria during treatment with dasatinib for chronic myeloid leukaemia (CML) [routes not stated]. Case 1: The 48-year-old woman had been diagnosed with CML in February 2017 and started receiving dasatinib 100 mg/day and showed a good response. She had also developed neutropenia and thrombocytopenia, which normalised afterwards. In August 2018 (at 18 months of follow-up), the dose of dasatinib was increased to 140 mg/day. Subsequently, she complained of worsening hypertension (BP was 180/98mm Hg) and oedema with foamy urine. She started receiving amlodipine, hydrochlorothiazide and labetalol for worsening of hypertension. Her urine analysis showed a significant result for nephrotic-range proteinuria (6208 mg/24 hours) and serum creatinine level was noted as 0.8 mg/dL. In November 2018, trace lower extremity oedema was detected. Her immunological and viral testing were negative. The kidney biopsy was carried out. Pathological findings of kidney biopsy specimen by electron microscopy and light microscopy were consistent with chronic and acute TMA, exhibited by glomerular endothelial cell injury along with capillary wall remodeling, without frank thrombosis. There was a mild chronic damage along with global, focal and segmental glomerulosclerosis and tubulointerstitial scar formation in up-to 20% of the parenchyma. Given the pathological results, a diagnosis of renal-limited TMA secondary to dasatinib was made [duration of treatment to reactions onsets not stated]. Her dasatinib therapy was changed to imatinib in December 2018, which led to improvement in her symptoms. In May 2019, she had a follow-up visit and showed reduction in proteinuria (755 mg/24 hours), her BP was under control (128/89mm Hg) and her anti-hypertensive medications were stopped. Case 2: The 71-year-old woman had been diagnosed with CML and started receiving dasatinib 100 mg/day, which led to clinical remission. She had hypertension over a period of 30 years. After one year of the initiation of dasatinib therapy, she developed proteinuria and haematuria. Urinary protein level was 5.2 g/24 hours and serum-albumin level was noted to be 3.1 g/dL. After five years of the initiation of dasatinib, her lower leg oedema progressed gradually. Her vital sign measurement showed a stable result and had a well-controlled BP. Urinary sediment demonstrated haematuria and fatty cast with oval fat body. Blood immunology and biochemistry tests showed serum creatinine of 0.83 mg/dL, estimated glomerular filtration rate (GFR) of 62.3 mL/min/1.73 m2, blood urea nitrogen of 19 mg/dL, serum albumin of 2.5 g/dL, total cholesterol of 285 mg/dL and low-density lipoprotein cholesterol of 159 mg/dL. Additionally, serum IgG of 415 mg/dL, cystatin GFR of 37.3 mL/min/1.73 m2 and 24 hours creatinine clearance of 42.3 mL/min/1.73 m2. Kidney biopsy findings demonstrated that, the sample of ren
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