Kidney Week

Abstract: FR-PO0489

Empagliflozin in Patients with Moderate-to-Advanced CKD, Acutely Decompensated Heart Failure, and Diuretic Resistance: The DRIP-AHF Clinical Trial

Session Information

• CKM: Clinical - Trials, Epidemiology, and Biomarkers
  October 23, 2026 | Location: Exhibit Hall A, Convention Center
  Abstract Time: 10:00 AM - 12:00 PM

Category: Cardiovascular-Kidney-Metabolic Health

• 602 Cardiovascular-Kidney-Metabolic Health: Clinical

Authors

• Mavrakanas, Thomas A., McGill University Health Centre, Montreal, Quebec, Canada

Thomas A. Mavrakanas, MD, MS, FASN

• Marques, Pedro, McGill University Health Centre, Montreal, Quebec, Canada

Pedro Marques, MD, MS, MSc

• Travlos, Christoforos K., Research Institute of the McGill University Health Centre, Montreal, Quebec, Canada

Christoforos K. Travlos, MD

• Baroz, Frederic, Research Institute of the McGill University Health Centre, Montreal, Quebec, Canada

Frederic Baroz, MD, MS, MSc

• Elenjickal, Elias John, Research Institute of the McGill University Health Centre, Montreal, Quebec, Canada

Elias John Elenjickal, MD, FASN

• Cherney, David, Toronto General Hospital, Toronto, Ontario, Canada

David Cherney, MD, PhD

• Sharma, Abhinav, McGill University Health Centre, Montreal, Quebec, Canada

Abhinav Sharma, DrMed, PhD

Background

Loop diuretic resistance in patients with acutely decompensated heart failure is associated with elevated risk of 60-day mortality and is more common in the setting of CKD. While SGLT-2 inhibitors are effective in patients with acute heart failure, the potential combinatory impact of this class of drugs with loop diuretics in patients with acute heart failure and diuretic resistance remains unknown.

Methods

DRIP-AHF was a prospective, interventional, single arm clinical trial (NCT05305495). Patients with baseline eGFR of 15-45 ml/min/1.73m², acutely decompensated heart failure, and evidence of inadequate response to loop diuretics were enrolled. All patients received an intravenous bolus of 1.5 mg/kg of furosemide. Those with a urine output <300 ml in the first two hours were confirmed to have diuretic resistance. Three hours after the first furosemide bolus, patients with diuretic resistance received 25 mg of empagliflozin, followed by a second furosemide bolus of 1.5 mg/kg two hours later. The primary outcome was the diuretic effect of empagliflozin in association with furosemide, compared with furosemide alone, as identified by the 3-hour urine output after each furosemide dose.

Results

A total of 25 patients with diuretic resistance were recruited. Mean age was 71±15 years, 72% were male, mean eGFR was 27 ± 9 ml/min/1.73m², and median NT-proBNP was 23876 pg/ml. Mean urine output at 3 hours increased from 205 ± 29 ml with furosemide to 314 ± 51 ml with empagliflozin plus furosemide (mean difference of 109 ml, 95% CI from 40 to 177 ml, p< 0.01). Mean sodium excretion also increased from 16 mmol/3h to 26 mmol/3h (mean difference of 10 mmol, 95% CI from 3 to 17 ml, p< 0.01). Fractional excretion of sodium increased from 4% to 6% (mean difference of 2%, 95% CI from 1 to 3%, p< 0.001). In 15 patients, empagliflozin was continued for at least 5 days during hospitalization. There was no increase in beta-hydroxybutyrate levels in these participants.

Conclusion

Empagliflozin when given in combination with intravenous furosemide was associated with a modest but significant increase in urine output in patients with acutely decompensated heart failure and objectively identified diuretic resistance. Our results support early initiation of SGLT-2 inhibitors in patients with acutely decompensated heart failure in the inpatient setting.