Abstract: SA-PO0218
Severe Syndrome of Inappropriate Antidiuretic Hormone Secretion Following a Single Infusion of AVD Chemotherapy in a Patient with Hodgkin Lymphoma
Session Information
- Onconephrology: MGRS, HSCT, Electrolytes, RCC, and More
November 08, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Onconephrology
- 1700 Onconephrology
Authors
- Brahmajosyula, Anagha, Kempegowda Institute of Medical Sciences, Bengaluru, KA, India
- Altamirano, Fabian Andres, University of Miami Miller School of Medicine, Miami, Florida, United States
- Drexler, Yelena, University of Miami Miller School of Medicine, Miami, Florida, United States
Introduction
The syndrome of inappropriate antidiuretic hormone (SIADH) is a well-recognized adverse
effect of certain chemotherapeutic agents, such as vincristine and cyclophosphamide. Severe
SIADH following a single infusion of AVD chemotherapy – doxorubicin, vinblastine, and
dacarbazine – is unusual. There is limited evidence implicating vinblastine as a cause of SIADH.
Case Description
A 55-year-old female with biopsy-confirmed classical Hodgkin’s lymphoma (cHL) presented with
an enlarging neck mass and was started on AVD. Extensive lymphadenopathy had been noted
14 months earlier, but the patient had only received treatment with dexamethasone. Five days
after AVD initiation, her serum sodium decreased from 134 to 125 mEq/L. After 1L of normal
saline, her serum sodium further declined to 118 mEq/L. Serum osmolality was 247 mOsm/kg,
urine osmolality was 730 mOsm/kg, and urine sodium was 152 mEq/L. Given long-term steroid
use, adrenal insufficiency was considered. However, this was ruled out by a morning cortisol
level of 25.9 mcg/dL. The Furst ratio of urine cations to serum cations was >1, consistent with
SIADH and indicating negative electrolyte-free water excretion. Due to worsening hyponatremia
and altered mental status, 3% hypertonic saline was started, and serum sodium improved to
125 mEq/L. Subsequent management included fluid restriction, increased dietary protein intake,
and oral urea 30 grams twice daily. Serum sodium ultimately normalized 3 weeks post-AVD.
Although a second cycle of AVD was planned, the patient’s clinical status worsened due to
refractory cHL, and she transitioned to hospice.
Discussion
This case highlights a rare but serious complication of AVD chemotherapy – severe SIADH
potentially triggered by vinblastine. Although vinblastine-induced SIADH is rarely reported, its
structural similarity to vincristine suggests a shared mechanism, namely direct renal and
neurohypophyseal toxicity leading to disrupted osmoreceptor control of ADH secretion. Prompt
recognition and treatment are essential. Management involves fluid restriction, pharmacologic
therapy such as oral urea, and cautious correction with hypertonic saline to avoid osmotic
demyelination. Clinicians should maintain a high index of suspicion and monitor electrolytes
closely in patients receiving vinca alkaloids.