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Abstract: FR-PO245

Role of Leukapheresis in the Management of AKI Associated with Hyperleukocytosis of Acute Myeloid Leukemia (AML)

Session Information

Category: Onconephrology

  • 1700 Onconephrology


  • Badra, Sherif, University of Florida, Gainesville, Florida, United States
  • Choi, Jusong, University of Florida, Gainesville, Florida, United States
  • Shah, Chintan Vimalkumar, University of Florida, Gainesville, Florida, United States

The rates of AML patients with hyperleukocytosis range from 8–12%. Due to very high early mortality rates, as high as 50% during 30 days after presentation, hyperleukocytosis—especially if complicated by leukostasis—is a hematologic emergency that requires prompt treatment. The role of leukapheresis remains controversial due to the lack of strong data. Hereby, we report a case of acute kidney injury (AKI) that resolved after one session of leukapheresis.

Case Description

A 73-year-old male presented to the hospital with abdominal pain, nausea, vomiting, and generalized fatigue of 2 weeks duration. He was found to have a WBC count of 159,000/µL with 98% peripheral blasts concerning for acute leukemia. On admission, nephrology was consulted for oliguric AKI without evidence of sepsis or hypotension. Urine microscopy revealed a few granular casts suggestive of ATN. The patient did not meet Cairo-bishop criteria for tumor lysis syndrome (TLS). The patient was initiated on hydroxyurea. Due to a lack of improvement in oliguric AKI after four days of presentation and without any other identifiable cause than cytostasis, he underwent one session of leukapheresis (Figure 1). This was followed by two consecutive sessions of dialysis for uremic encephalopathy. Two days later, his urine output increased to about 1.8 L with remarkable kidney function improvement, and he didn’t require further dialysis. Unfortunately, the patient passed away after six weeks of a complicated hospital course and withdrawal of care with comfort measures.


Renal failure can occur due to leukostasis from hyperleukocytosis in acute leukemia as a result of tubular and glomerular dysfunction. The exact mechanism is unknown but possibly due to mechanical obstruction from less deformable leukemic blasts, the release of proinflammatory cytokines, and matrix metalloproteinases that damage endothelial cells. No current guidelines exist for the treatment of renal injury in this setting. Our case suggests leukapheresis should be considered a therapeutic option for such patients.