Antineoplastics/mycophenolate mofetil/tacrolimus

  • PDF / 171,223 Bytes
  • 1 Pages / 595.245 x 841.846 pts (A4) Page_size
  • 89 Downloads / 151 Views

DOWNLOAD

REPORT


1 XS

Proteinuria and other toxicities: case report A 67-year-old man showed worsening of hypertension due to bevacizumab for colorectal cancer, severe proteinuria and renal dysfunction during treatment with bevacizumab, oxaliplatin, fluorouracil and levofolinic acid for colorectal cancer and immunosuppressive therapy with tacrolimus and myophenolate mofetil. Additionally, he developed thrombotic microangiopathy due to an interaction between tacrolimus and bevacizumab, and thrombocytopenia as a result of oxaliplatin [routes and duration of treatments to reaction onsets not stated; not all dosages and outcomes stated]. The man, who had a history of hypertension and diabetes, underwent kidney transplantation for chronic kidney failure 14 years prior. He had been receiving immunosuppressive therapy with tacrolimus 3 mg/day and mycophenolate mofetil. He was also treated with amlodipine and candesartan for high blood pressure. However, 11 years following kidney transplant, he developed colorectal cancer with multiple lung and liver metastases. Therefore, he started receiving mFOLFOX6 regimen comprising fluorouracil [5-fluorouracil], levofolinic acid [levofolinate] and oxaliplatin. Two weeks following initiation of the mFOLFOX6 regimen, bevacizumab 5 mg/kg/day was added to the treatment regimen. In addition, he received amlodipine for the management of BP; however, he developed a rapid increase in systolic blood pressure following initiation of bevacizumab. The man was treated with candesartan cilexetil [candesartan]. Thereafter, his urine protein creatinine ratio (UPCR) and the urine protein concentration increased to 3.5 g/gCr and 300 mg/dL, respectively, following treatment with 5 cycles of combined treatment regimen (bevacizumab and mFOLFOX6). A rise in serum concentration of tacrolimus (aetilogy unspecified) was noted during the initial 4 cycles of chemotherapy; however, no correlation between serum tacrolimus concentration and proteinuria was observed. The dose of tacrolimus was tapered to 2 mg/day. Subsequently, he again experienced a rise in his BP, which was controlled by increasing the dose of amlodipine. Serum albumin concentration also increased (aetiology unspecified) during chemotherapy; however, hypoalbuminemia was not observed. The concentration of urinary protein continued to increase and the UPCR and urinary protein concentration further increased to 7.1 g/gCr and 1000 mg/dL, respectively, after 16 cycles of the chemotherapy. Thereafter, he also developed renal dysfunction (estimated GFR 48.6 mL/min/1.73m2). The diagnosis of severe proteinuria and renal dysfunction secondary to the chemotherapy and immunosuppression therapy was confirmed. In addition, he also developed thrombotic microangiopathy (TMA) secondary to pharmacodynamic drug interaction (additive or synergistic effect) between bevacizumab and tacrolimus leading to tissue damage. Consequently, bevacizumab was discontinued resulting in decrease in urinary protein concentration; however, UPCR continued to worsen. Subsequently, UPCR also improved

Data Loading...