Abstract: FR-PO0882
When Treatment Floods the System: A Case of Medication-Induced Mixed Polyuria in an Immunocompromised Host
Session Information
- Fluid, Electrolyte, and Acid-Base Disorders: Case Reports - 1
October 23, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Fluid, Electrolytes, and Acid-Base Disorders
- 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Authors
- Adams Chahin, Juan J., VA Caribbean Healthcare System, San Juan, Puerto Rico
- Asencio-Torres, Gabriela M., VA Caribbean Healthcare System, San Juan, Puerto Rico
- Rodriguez, William, VA Caribbean Healthcare System, San Juan, Puerto Rico
Introduction
Polyuria is frequently attributed to excess fluid administration, diuretics, and/or arginine vasopressin deficiency. However, medication-induced etiologies are often underrecognized. In immunocompromised patients receiving multiple antimicrobials, overlapping drug effects can disrupt renal sodium and water handling. Trimethoprim-Sulfamethoxazole (TMP/SMX) may cause renal salt wasting, while intravenous Voriconazole—formulated with sulfobutylether beta-cyclodextrin—can promote free water diuresis. We present a case of severe mixed polyuria due to concurrent drug effects, complicating diagnosis and management.
Case Description
A 41-year-old man with a history of allogeneic stem cell transplant for 1 year due to adult T-cell leukemia/lymphoma presented with five days of fever, chills, sore throat, and dyspnea. He was admitted with sepsis under workup for opportunistic infection and initiated on broad spectrum antimicrobials. On the following days, patient became hypotensive with laboratories demonstrating hypotonic hyponatremia (133 mEq/L) and marked polyruiria (~6.5L/day) requiring aggressive fluid replacement. Urine studies (osmolarity 145 mOsm/kg, sodium 48 mEq/L, and osmolar excretion 940 mOsm/day) were consistent with mixed polyuria. Despite low cortisol (1.5 ug/dL), he was on high-dose prednisone due to suspected chronic graft vs host disease. Polyuria worsened with fluid resuscitation at ~1000ml/hr prompting Desmopressin with partial response (< 50% increase in urine osmolarity). After discontinuation of TMP/SMX, urine sodium drop (<20), but water diuresis persisted ensuing hypernatremia requiring repeated Desmopressin. Polyuria ultimately resolved after switching Voriconazole from intravenous to oral formulation.
Discussion
This case highlights the diagnostic complexity of polyuria in critically ill patients, where overlapping mechanisms may obscure the underlying physiology. TMP/SMX–induced renal salt wasting and intravenous Voriconazole–associated free water diuresis led to severe polyuria and electrolyte disturbances. Rapid resolution after discontinuing these agents—particularly switching to oral voriconazole—highlights the importance of recognizing medication effects and formulations. Early identification and adjustment of pharmacologic contributors are key to reducing morbidity and improving outcomes.