Abstract: TH-PO0743
Intravenous Sodium Bicarbonate and Kidney Replacement Therapy Use in Critically Ill Patients with Severe Metabolic Acidemia and AKI: A Systematic Review
Session Information
- AKI: Critical Care, CKRT, Cardiorenal Syndromes, and Clinical Outcomes
October 22, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 102 AKI: Clinical, Outcomes, and Trials
Authors
- Nwachukwu, Kelechi, NYC Health + Hospitals, New York, New York, United States
- Buadu, Maame Araba E., NYC Health + Hospitals, New York, New York, United States
- Aye, Chawmay, NYU Langone Health, New York, New York, United States
- Milla, Cristian A., NYU Langone Health, New York, New York, United States
Background
Severe metabolic acidemia in critically ill patients with acute kidney injury (AKI) is associated with increased mortality, hemodynamic instability, vasopressor requirement, and frequent initiation of kidney replacement therapy (KRT). Intravenous sodium bicarbonate is commonly administered to correct acidemia and potentially delay KRT initiation; however, its benefit remains controversial. We performed a systematic review evaluating the effect of intravenous sodium bicarbonate on KRT utilization and clinical outcomes in critically ill patients with severe metabolic acidemia and AKI.
Methods
A focused systematic review of PubMed and major peer-reviewed nephrology and critical care studies evaluating intravenous sodium bicarbonate therapy in adult ICU patients with severe metabolic acidemia and AKI was performed. Randomized trials, observational studies, and contemporary reviews were evaluated. Primary outcome was KRT utilization. Secondary outcomes included mortality, acid-base correction, ICU outcomes, and adverse events. Particular emphasis was placed on the BICAR-ICU and BICARICU-2 trials.
Results
Intravenous sodium bicarbonate therapy consistently improved serum bicarbonate concentration and arterial pH. In BICAR-ICU, bicarbonate therapy did not improve the primary composite outcome overall; however, patients with AKI stage 2–3 demonstrated reduced KRT utilization and improved survival. BICARICU-2 similarly failed to demonstrate a mortality benefit but showed lower KRT utilization among bicarbonate-treated patients. Across studies, reduced dialysis utilization appeared primarily related to correction of severe acidemia and avoidance of acidosis-triggered dialysis initiation rather than direct reversal of kidney injury. Reported adverse events included hypernatremia, metabolic alkalosis, hypocalcemia, hypercapnia, and volume overload, although major complications were uncommon.
Conclusion
Current evidence does not support intravenous sodium bicarbonate therapy as a definitive mortality-reducing intervention in critically ill patients with severe metabolic acidemia and AKI. However, randomized data suggest bicarbonate therapy may reduce or delay KRT utilization in selected patients with moderate-to-severe AKI and severe acidemia, supporting a potential role as a temporizing or KRT-sparing strategy.