Key result
A sodium bicarbonate bolus reduced the unadjusted incidence of contrast-induced nephropathy versus control (1.8% vs 16.4%; P=0.008), but was not significant after multivariable adjustment.
Why the study?
Contrast-induced nephropathy remains an important complication after primary PCI in STEMI patients, and rapid preventive strategies compatible with timely reperfusion are needed.
Does a single preprocedural intravenous bolus of high-concentration sodium bicarbonate reduce the incidence of contrast-induced nephropathy in STEMI patients undergoing primary PCI?
RCT (n=110)
randomized
Yes
Does a single preprocedural intravenous bolus of high-concentration sodium bicarbonate reduce the incidence of contrast-induced nephropathy in STEMI patients undergoing primary PCI?
A single preprocedural bolus of sodium bicarbonate was associated with a lower unadjusted incidence of contrast-induced nephropathy in STEMI patients undergoing primary PCI, but the effect was no longer significant after multivariable adjustment.
Does not support sodium bicarbonate bolus for CIN prevention after adjustment in STEMI PCI; leaves open efficacy in larger trials.
Background Contrast-induced nephropathy (CIN) remains an important complication following primary percutaneous coronary intervention (PPCI) in patients with ST-segment elevation myocardial infarction (STEMI). In emergency settings, preventive strategies must be rapid and compatible with timely reperfusion. This study evaluated whether a single preprocedural bolus of high-concentration sodium bicarbonate was associated with a lower incidence of CIN.Methods In this prospective randomised study, 110 STEMI patients undergoing PPCI at two tertiary centres were enrolled. All patients received standard care, including isotonic saline hydration. Participants were assigned to saline hydration alone or saline plus a single intravenous bolus of 20 mEq of 8.4% sodium bicarbonate administered 5–10 min before contrast exposure. The primary endpoint was CIN within 48 ± 12 h, defined as an increase in serum creatinine ≥0.5 mg/dL or ≥25% from baseline.Results Baseline characteristics were generally comparable, although baseline blood urea nitrogen was higher and estimated glomerular filtration rate lower in the control group. CIN occurred more frequently in controls than in the sodium bicarbonate group (16.4% vs. 1.8%; p = 0.008). Renal function trajectories also favoured sodium bicarbonate. However, sodium bicarbonate did not remain an independent predictor of CIN after multivariable adjustment (OR 0.061, 95% CI 0.003–1.205; p = 0.066).Conclusions Sodium bicarbonate administration was associated with a lower unadjusted incidence of CIN. These findings should be considered hypothesis-generating and require confirmation in larger multicentre studies.
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Zahid et al. (2026) conducted an RCT in ST-segment elevation myocardial infarction (STEMI) (n=110). Sodium bicarbonate vs. Saline hydration alone was evaluated on Contrast-induced nephropathy (CIN) within 48 ± 12 h, defined as an increase in serum creatinine ≥0.5 mg/dL or ≥25% from baseline (OR 0.061, 95% CI 0.003-1.205, p=0.066). A sodium bicarbonate bolus reduced the unadjusted incidence of contrast-induced nephropathy versus control (1.8% vs 16.4%; P=0.008), but was not significant after multivariable adjustment.
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