A 78-Year-Old Man with Acute Myeloid Leukemia (AML) and Acute Renal Failure

Abstract

Patient: Male, 78Final Diagnosis: Acute myeloid leukemia (AML)Symptoms: Dyspnea • fatigueMedication: Idarubicin followed by cytarabineClinical Procedure: ChemotherapySpecialty: HematologyObjective:Unusual clinical courseBackground:Renal failure is a common presentation of acute myelomonocytic and monocytic leukemia. It is usually the result of a combined glomerular and tubular dysfunction and is associated with a poor prognosis. No guidelines exist for treatment.Case Report:We herein describe the case of a 78-year-old Caucasian man who presented with acute myeloid leukemia M5, leukostasis with a white count of 340 000/ml, and acute renal failure with a creatinine of 7.7/dL. The patient was initially treated with leukapheresis and 3 days of idarubicin in the setting of continuous renal replacement therapy that resulted in rapid reversal of his renal failure. He then received 7 days of continuous infusion cytarabine and went into a complete remission.Conclusions:Renal failure may complicate the presentation of AML but can be reversible with treatment. Dose adjustment of the chemotherapy is not needed and the treatment can be greatly facilitated with the use of continuous renal replacement therapy, as indicated in our case report. In addition, we emphasize that organ dysfunction, even in elderly patients, is not necessarily a contraindication to aggressive treatment if it is felt to be disease-related and reversible.

Leukostasis in adult acute hyperleukocytic leukemia: a clinician's digest

“…Other potential clinical presentation of leukostasis may include deep venous thrombosis , avascular bone necrosis , acute appendicitis , sudden cardiac death because of right‐sided cardiac mass , splenic rupture , acute kidney injury , retinopathy , and fever.…”

“…Laboratory abnormalities other than marked leukocytosis may include true hypokalemia , pseudo hyperkalemia because of cellular death in vitro (collect heparinized plasma), hyperkalemia, and other laboratory abnormalities due tumor lysis syndrome (hypocalcemia, hyperuricemia, and hyperphosphatemia) . Special attention should be focused on the estimation of platelet counts manually, because automatic cellular counters may overestimate platelet count (some white blood cells will be counted as platelets).…”

The Myeloid-Kidney Interface in Health and Disease

“…Acute myeloid leukemia can present with AKI due to tumor lysis syndrome or thrombotic microangiopathy (61). Less commonly, it can precipitate glomerular phenotypes, such as membranous nephropathy or FSGS (62), or cause direct injury through malignant parenchymal infiltration (63). Chronic myeloid leukemia has been associated with membranous nephropathy, minimal change disease, and membranoproliferative GN (60).…”