A Hidden Risk in the Loop: Furosemide-Triggered Hemolysis in Glucose-6-Phosphate Dehydrogenase Deficiency

Introduction: Glucose-6-phosphate dehydrogenase (G6PD) deficiency is the most common enzymatic disorder of red blood cells worldwide, predisposing patients to oxidative stress-induced hemolysis. While classic triggers include infections, fava beans, and known oxidative medications, furosemide is not commonly recognized as a cause of hemolysis in G6PD-deficient patients. Case Description: A 62-year-old woman with a history of diabetes mellitus type 2, hypertension, hyperlipidemia, chronic kidney disease (CKD) stage 3b, and anemia was admitted for hypertensive urgency. She was noted to have worsening anemia during admission. Laboratory workup revealed findings consistent with hemolysis; low haptoglobin (<10 mg/dL), elevated reticulocyte count, and elevated indirect bilirubin. Peripheral smear showed schistocytes, burr cells, and target cells. A direct Coombs test was negative, and G6PD enzyme levels were significantly reduced (85 U/red cells). The patient had recently been started on furosemide for lower extremity edema. Furosemide was suspected to be the oxidative trigger for hemolysis and was discontinued, after which her hemoglobin stabilized without further transfusion or recurrence of hemolysis. She was later transitioned to torsemide without complication. Discussion: This case highlights an unusual but significant adverse reaction to furosemide in the context of G6PD deficiency. Although furosemide is not routinely classified among oxidative stressors in G6PD deficiency, this report adds to the limited but growing body of evidence suggesting a potential hemolytic risk. Given the widespread use of furosemide, especially in patients with CKD, heightened awareness and cautious use in G6PD-deficient individuals are warranted. Clinicians should consider G6PD deficiency in the differential diagnosis of unexplained hemolysis and remain vigilant regarding the potential oxidative risks of commonly used medications such as furosemide. When loop diuretic therapy is necessary, switching to a chemically related but structurally distinct agent like torsemide may offer a safer alternative in G6PD-deficient patients.