Abstract: SA-PO239
Dripping Clues: Unveiling Diabetes Insipidus (DI), a Sneaky Presentation of Acute Myeloid Leukemia (AML)
Session Information
- Onconephrology: Immunological Cross-Talk
November 04, 2023 | Location: Exhibit Hall, Pennsylvania Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Onconephrology
- 1700 Onconephrology
Authors
- Rathi, Naveen, University of Cincinnati College of Medicine, Cincinnati, Ohio, United States
- Kim, Isaac Inhwak, University of Cincinnati College of Medicine, Cincinnati, Ohio, United States
- Gudsoorkar, Prakash Shashikant, University of Cincinnati College of Medicine, Cincinnati, Ohio, United States
Introduction
DI is a rare complication of AML seen with cytogenetic defects especially monosomy 7 & inversion 3. It can occur before or after diagnosis of AML, with or without brain imaging abnormalities. Here, we report a case of hypernatremia from DI in a patient with AML.
Case Description
A 68-year-old male with no medical history presented to ICU with altered mental status & polyuria (urine output > 5L/day), noted to have hemoglobin 6.8 g/dL. Led to AML diagnosis based on blood and bone marrow tests (Fig1). Karyotyping revealed inversion 3 [inv(3)(q21q26)] & monosomy 7. His serum sodium (SNa) was high on admission at 168 mEq/L. Over the past 3-4 weeks, he had increased urination. Further evaluations, including an MRI of the brain, showed no abnormalities. Urine osmolality was 168 mOSm/L (other metabolic tests were normal). Treatment with diamino D-arginine vasopressin (ddAVP) (2- 4 mcg/day) & free water boluses improved SNa (Fig2) and urine osmolality. Diagnosis of probable central DI based on the response to ddAVP, was made. With his mental status improving, he was switched to oral desmopressin (0.05 mg BID) and maintained stable SNa (140-145 mEq/L) upon discharge. Unfortunately, due to the non-response to his therapy for AML (decitabine), he was transitioned to hospice.
Discussion
The pathogenesis of DI associated with AML (DI-AML) is not well understood. A possible mechanism is due to hypothalamic-pituitary infiltration of the leukemic cells or dysregulation of ADH due to dysthrombopoesis. Since approximately 90% of circulating ADH is associated with platelets, dysthrombopoesis in AML could lead to decreased levels and function of ADH. The 2 most common cytogenetic defects associated with DI-AML are monosomy 7 (80%) and inv-3 (46%). Patients with inv-3 and 50% involving monosomy 7 demonstrate activation of the MECOM [(MDS1 and EVI1 (ectopic virus integration site 1 protein homolog) complex] gene, leading to an increase in EVI-1 (a protein product). This disrupts the hypothalamic ADH secretion. We need more studies to prove an association between DI & AML. Our patient had features of CDI based on the evaluation & treatment response.