Abstract: SA-PO0899
Hypoglycemia with Elevated C-Peptide After Initiation of High-Dose Torsemide
Session Information
- Health Maintenance, Nutrition, and Metabolism
October 24, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Health Maintenance, Nutrition, and Metabolism
- 1500 Health Maintenance, Nutrition, and Metabolism
Authors
- Perez, Aubriana C., The University of Texas Southwestern Medical Center, Dallas, Texas, United States
- Sambandam, Kamalanathan Kolandavelu, The University of Texas Southwestern Medical Center, Dallas, Texas, United States
Introduction
Loop diuretics, such as torsemide, are ubiquitous among patients with advanced CKD for volume management. Torsemide is not commonly known to cause glycemic abnormalities in this population.
Case Description
We discuss a case of a 72-year old female with ESKD on peritoneal dialysis admitted for refractory hypoglycemia which corrected after discontinuation of torsemide. The patient presented after an episode of dizziness and unresponsiveness, with measured blood glucose of 35 mg/dl. There was no known history of diabetes (A1C 5.2%) or surreptitious insulin use. Despite dietary and IV repletion, hospitalization was complicated by recurrent hypoglycemia. Workup revealed negative sulfonylurea screening and normal AM cortisol. Notably, there was evidence of elevated C-peptide (107 ng/ml; Ref: 1.1-4.4 ng/ml), elevated proinsulin (>700 pmol/L; Ref: 3.6-22 pmol/L), and inappropriately low beta-hydroxybutyrate (<0.1 mmol/L), consistent with an endogenous hyper-insulinemic process. The patient had been started on high-dose torsemide (150 mg twice daily) a week prior to admission, when the concern was raised that torsemide may be contributing to hypoglycemia due to structural similarity with sulfonylureas. Following withdrawal of torsemide, the patient's blood glucose remained >100 mg/dl off of glucose supplementation.
Discussion
Torsemide possesses a sulfonylurea-pyridine moiety that is analogous to the sulfonylurea-benzene functional group on sulfonylureas, which targets ATP-sensitive K channels (K-ATP) on pancreatic beta cells to facilitate insulin release. Other sulfa-based medications, such as trimethoprim-sulfamethoxazole, have been associated with hypoglycemia independent of co-administration of sulfonylureas in rare cases, raising the question of structural cross-reactivity with other sulfonylurea-based medications, such as torsemide.1 Notably, no prior cases of hypoglycemia have been documented specifically in the context of torsemide use. Only one in-vitro study has demonstrated the capability of torsemide to exert extra-renal effects at supratherapeutic doses, in particular, inhibition of K-ATP channels in rat aortic vasculature - a process which was not observed in other loop diuretics such as furosemide.2 This case underscores the potential for torsemide to inadvertently affect non-target processes such as insulin metabolism at high doses in advanced CKD.