Sodium bicarbonate did not protect the kidneys in acidosis and shock
In a 500-patient ICU trial across seven countries, bicarbonate infusions for metabolic acidosis in patients on vasopressors did not lower major kidney events or death at 30 days.
| Group | Value (%) |
|---|---|
| Sodium bicarbonate | 40.2 |
| Placebo | 39.4 |
Giving intravenous sodium bicarbonate to critically ill patients whose blood has turned too acidic is one of intensive care's long-running instincts: the acid is dangerous, bicarbonate neutralises it, so correcting the number ought to help the patient. The SODa-BIC trial tested that instinct where it matters most — in patients who were also in shock — and found that correcting the chemistry did not translate into better outcomes for the kidneys or survival [s1].
Metabolic acidosis is common in the sickest ICU patients and is linked to worse outcomes, but whether treating the acidosis itself changes anything, or merely papers over the underlying problem driving it, has stayed unresolved for decades. SODa-BIC is among the largest randomised attempts to answer it [s1][s2].
What the trial did
SODa-BIC was a pragmatic, adaptive, double-blind, randomised trial [s1]. It enrolled adults with metabolic acidosis — defined by a blood pH below 7.30, a base excess no higher than −4 mmol per litre, and an arterial carbon-dioxide level at or below 45 mm Hg without a breathing tube (or at or below 50 mm Hg with one) — who were receiving vasopressors, the drugs used to hold up blood pressure in shock [s1]. Participants were assigned to receive either sodium bicarbonate or a placebo of 5% dextrose [s1].
The infusion ran for up to five hours, with the rate adjusted toward a target pH of at least 7.30 and a base excess of at least 0 mmol per litre — that is, the bicarbonate group's chemistry was actively steered back toward normal [s1]. The primary outcome was a major adverse kidney event within 30 days, a composite of death, the use of renal-replacement therapy (dialysis or its equivalents), or persistent kidney dysfunction [s1].
In all, 500 patients were enrolled across 55 ICUs in seven countries, with 245 assigned to sodium bicarbonate and 255 to placebo [s1]. The trial was funded by Australia's National Health and Medical Research Council and sponsored by an academic critical-care research centre — not by a manufacturer — and registered as SODa-BIC [s1][s2].
What it found
The correction of the acid did not carry through to the outcomes.
A major adverse kidney event within 30 days occurred in 98 of 244 patients (40.2%) in the sodium bicarbonate group and in 100 of 254 patients (39.4%) in the placebo group — an adjusted difference of 1.2 percentage points (95% confidence interval −7.1 to 9.4; P = 0.78) [s1]. The confidence interval spans zero comfortably in both directions, which is the statistical signature of a genuine null: the data are compatible with a small benefit, a small harm, or nothing at all.
The component outcomes told the same story. Renal-replacement therapy was used within 30 days in 16.8% of the bicarbonate group and 20.9% of the placebo group (adjusted difference −3.9 percentage points; 95% CI −10.6 to 2.7) [s1]. In-hospital mortality by day 30 was 25.4% with bicarbonate and 24.0% with placebo (adjusted difference 1.8 percentage points; 95% CI −5.6 to 9.2) [s1]. None of these differences was statistically distinguishable from chance.
How to read it
The authors' conclusion is that sodium bicarbonate in critically ill patients with metabolic acidosis who are receiving vasopressors "did not lead to a lower risk of major adverse kidney events within 30 days than placebo" [s1]. The signal to take from that is not that the acid does not matter, but that treating the number does not fix the patient — the acidosis is a readout of how sick someone is, and neutralising it does not undo the shock, infection or organ injury generating it.
Two honest caveats. This trial targeted a broad group of patients in shock; a much-discussed earlier trial suggested a possible benefit in the narrower subgroup with severe acidosis and existing kidney injury, and SODa-BIC's abstract does not settle every such subgroup question [s1]. And the primary outcome was measured at 30 days, so it speaks to early outcomes rather than long-run kidney recovery [s1]. But for the routine, reflex use of bicarbonate to "correct the pH," this is a clear neutral result from an independent, publicly funded trial.
The finding sits alongside a broader pattern in critical care of long-standing habits failing controlled tests. Related coverage has examined a null trial of two mucoactive drugs in ventilated patients, bicarbonate in in-hospital cardiac arrest, and the global burden of sepsis.
What to watch
The open questions are whether any subgroup — for instance, patients with the most severe acidosis and established kidney injury — still benefits, and whether guidelines move from "consider bicarbonate" toward reserving it for narrow, specific indications [s1].
This article describes trial results and is not medical advice. Treatment decisions in intensive care rest with the clinicians responsible for a patient.
Sources
- Sodium Bicarbonate for Critically Ill Adults with Metabolic Acidosis and Shock — New England Journal of Medicine, 12 June 2026
- SODa-BIC trial record, NCT05697770 — ClinicalTrials.gov
Sources
- Sodium Bicarbonate for Critically Ill Adults with Metabolic Acidosis and Shock — New England Journal of Medicine , June 12, 2026
- SODa-BIC: SODium BICarbonate for Metabolic Acidosis in the ICU (NCT05697770) — ClinicalTrials.gov
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