Reversal of Severe Diuretic Resistance by Dexmedetomidine Associated Polyuria in Type 1 Cardiorenal Syndrome: A Case Report

Background Dexmedetomidine is a selective α2-adrenergic agonist widely used for sedation in intensive care settings. Although hypotension and bradycardia are well-recognized adverse effects, dexmedetomidine-associated polyuria is a rare and unpredictable adverse effect. Case Summary An 84-year-old man with ischemic dilated cardiomyopathy, permanent atrial fibrillation, type 2 diabetes mellitus, and chronic kidney disease was admitted to the Cardiac Intensive Care Unit with type 1 cardiorenal syndrome, severe systemic and pulmonary congestion, oliguria and acute kidney injury. Despite continuous intravenous furosemide infusion, sequential nephron blockade, and dual vasoactive support with norepinephrine and dobutamine, the patient developed persistent oligo-anuria and worsening congestion. Dexmedetomidine infusion was initiated for psychomotor agitation and disorientation. Shortly thereafter, urine output abruptly increased to approximately 250 mL/h, accompanied by rapid decongestion and improvement in renal function. Following dexmedetomidine withdrawal, oliguria, congestion and renal dysfunction recurred. Rechallenge with dexmedetomidine again induced profound polyuria, with urine output peaking at 650 mL/h and a 10-kg weight loss over 48 hours, allowing de-escalation of diuretic therapy and withdrawal of vasoactive support. The Naranjo score was 6, supporting a probable causal relationship. Discussion This case demonstrates a reproducible temporal association between dexmedetomidine administration and profound polyuria, confirmed by positive rechallenge.