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Abstract: FR-PO212

Thrombotic Microangiopathy Associated With Use of Liposomal Doxorubicin

Session Information

Category: Onconephrology

  • 1600 Onconephrology


  • Brauer Ornelas, Claudia Michelle, Weill Cornell Medicine, New York, New York, United States
  • Kelly, Ciara M., Memorial Sloan Kettering Cancer Center, New York, New York, United States
  • Salvatore, Steven, Weill Cornell Medicine, New York, New York, United States
  • Glezerman, Ilya, Memorial Sloan Kettering Cancer Center, New York, New York, United States

TMA is rare with liposomal doxorubicin and its presentation and prognosis is not well defined in this setting. We report a patient on single agent liposomal doxorubicin who developed TMA.

Case Description

72-year-old female with history of well controlled hypertension (HTN) and retroperitoneal liposarcoma referred to renal service for elevated serum creatinine (SCr) and edema. She underwent resection and left nephrectomy at the time of diagnosis of liposarcoma. Patient was started on liposomal doxorubicin at 40mg/m2 per cycle (cumulative dose 1240mg/m2) 18 months prior to presentation. Her baseline SCr was 1 (0.6-1.1) mg/dL but it has been slowly rising for the past 7 months. She was taking alendronate, amlodipine and levothyroxine. Hydrochlorothiazide was added recently for worsening HTN. Patient appeared comfortable. BP was 166/86 but vital signs otherwise were stable. Exam was unremarkable except for lower extremity edema. Laboratory data revealed SCr of 2mg/dL and nephrotic range proteinuria (4g/day). Urinalysis showed five RBC/ HPF. Initial work up showed normal complement level, haptoglobin and urine and serum protein electrophoresis. Hepatitis B and C serologies as well as ANA and ANCA were negative. Lactate dehydrogenase level was elevated 317 (130-250) U/L. aHUS complement panel showed no serologic evidence of complement abnormalities. CT scan of abdomen and pelvis showed unchanged multifocal recurrent disease and well no evidence of right hydronephrosis. Patient underwent kidney biopsy which showed chronic endothelial injury suggestive of chronic thrombotic microangiopathy involving glomeruli. Liposomal doxorubicin was stopped and SCr peaked at 5.4mg/dl four months after biopsy but gradually improved to a trough of 3.4 mg/dL at last follow up. Nephrotic range proteinuria and edema resolved.


Liposomal doxorubicin associated TMA is not a well-known potential side effect. There have been two cases of biopsy proven TMA in ovarian cancer patients on single agent liposomal doxorubicin after prolonged exposure. In another case report a patient with liposarcoma of kidney had a prolonged exposure to liposomal doxorubicin and developed TMA leading to hemodialysis. Our patient also had large cumulative exposure indicating that TMA may be dose dependent.