Abstract: SA-PO189
Lysozyme Is No Lie! AKI in a Patient with Acute Myeloid Leukemia
Session Information
- Onconephrology: Kidney Outcomes during Cancer Treatment and Nephropathies
October 26, 2024 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Onconephrology
- 1700 Onconephrology
Authors
- Lyu, David, Houston Methodist, Houston, Texas, United States
- Tolani, Renuka, Houston Methodist, Houston, Texas, United States
- Bobart, Shane A., Houston Methodist, Houston, Texas, United States
- Rice, Lawrence, Houston Methodist, Houston, Texas, United States
- Edwards, Angelina, Houston Methodist, Houston, Texas, United States
- Burns, Ethan A., Houston Methodist, Houston, Texas, United States
- Shafi, Tariq, Houston Methodist, Houston, Texas, United States
Group or Team Name
- HMH Nephrology.
Introduction
In patients with leukemia who develop acute kidney injury (AKI) we often suspect tumor lysis syndrome and other common etiologies such as cytokine release syndrome. Lysozyme-induced nephropathy (LyN) is a less recognized cause of AKI. When monocytic cells release lysozyme, a small cation, it is filtered by the glomerulus and reabsorbed by the proximal tubule, resulting in toxic tubular injury. We present a case of a patient who was diagnosed with acute myelomonocytic leukemia (AMML) and had AKI with elevated lysozyme level in the blood that improved with treatment of the underlying leukemia.
Case Description
A 77 year old male with PMH of myelodysplastic syndrome (MDS) was noted to have 0.5 grams of proteinuria and AKI with serum creatinine of 1.9mg/dL from a prior baseline of 1.1 mg/dL. Serological studies and work up for paraproteinemia and thrombotic microangiopathy was negative. CBC showed worsening anemia, increasing leukocytosis (29.4 k/uL) with 18% monocytes and Pelger-Huët neutrophils, as well as thrombocytopenia and the patient was admitted for suspected acute leukemia. Bone marrow biopsy showed AMML, 28% blasts, hypercellular marrow (50%) with trilineage hematopoiesis and monocytosis. Given the severe thrombocytopenia, kidney biopsy was unable to be safely attempted. Given the new diagnosis of AMML, a lysozyme enzyme assay was ordered and the level was greater than 10 ug/mL (normal range < 4.5 ug/mL). Treatment with decitabine infusions commenced and one month after initiation, lysozyme levels decreased to 4.37 ug/mL and creatinine improved to near the patient’s baseline (1.1 mg/dL). The clinical course was consistent with a diagnosis of lysozyme-induced AKI in the setting of AMML.
Discussion
While kidney biopsy remains the gold standard for diagnosis of AKI in the setting of acute leukemia, when unable to be safely performed, clinicians should be aware of the clinical entity of lysozyme-associated AKI. Checking and trending lysozyme enzyme levels can also be a useful tool to guide management of AKI in this setting. In our case, once treatment for AMML was started both lysozyme levels and serum creatinine improved.