A 2010 meta-analysis evaluated the use of intravenous sodium bicarbonate for the prevention of contrast-induced acute kidney injury (CI-AKI), analyzing 18 studies with a total of 3,055 patients. The included studies reported a CI-AKI incidence of 11.6%, which was reduced to 9.6% in the sodium bicarbonate group compared to 13.5% in the control group (p= 0.001). The pooled risk ratio (RR) for CI-AKI prevention using sodium bicarbonate was 0.66 (95% confidence interval [CI] 0.45 to 0.95), suggesting a preventive effect. The effect was more prominent in coronary procedures, particularly in emergency settings, and in patients with chronic kidney disease (CKD). In contrast, studies including both coronary and non-coronary procedures did not demonstrate a significant benefit (RR 0.92; 95% CI 0.50 to 1.70). Among the studies, six prospective trials demonstrated a statistically significant reduction in CI-AKI with sodium bicarbonate administration. Additionally, sodium bicarbonate use was associated with a lower trend in renal replacement therapy (RRT) requirement (0.9% vs. 1.5%; p= 0.259), though the difference was not statistically significant. In-hospital mortality was reported in five trials, with no significant reduction observed (1.7% for sodium bicarbonate vs. 2.1% in controls; p= 0.793). The included studies varied in quality, with only 33% reporting adequate allocation concealment and 61% reporting blinding. Furthermore, there was evidence of publication bias, with full-text manuscripts showing significant effects (n= 1,945 patients; RR 0.66; 95% CI 0.42 to 1.00) compared to abstracts (n= 1,110 patients; RR 0.88; 95% CI 0.56 to 1.39). Subgroup analyses showed no significant effect in diabetic patients (RR 0.80; 95% CI 0.24 to 2.69) or in studies that did not include CKD patients (RR 0.53; 95% CI 0.17 to 1.72; p= 0.29). While the studies demonstrated variability in baseline characteristics, such as serum creatinine levels and contrast type, sodium bicarbonate use was consistently linked to urinary alkalinization. Overall, these findings highlight the need for larger, high-quality trials to clarify the role of sodium bicarbonate in CI-AKI prevention and to explore its impact on RRT and mortality. [1]
A 2012 meta-analysis reviewed data from 19 randomized controlled trials (N= 3,609) to evaluate the efficacy of sodium bicarbonate in preventing CI-AKI. CI-AKI, a common complication defined as an increase in serum creatinine of 25% or at least 0.5 mg/dL within 48 hours of contrast exposure, is associated with significant morbidity and mortality. Clinical studies were included if they compared sodium bicarbonate hydration to sodium chloride (normal saline). Hydration with sodium bicarbonate demonstrated a significant reduction in the incidence of CI-AKI compared to sodium chloride (odds ratio [OR] 0.56; 95% CI 0.36 to 0.86; p= 0.008). Subgroup analysis indicated enhanced efficacy in trials using low-osmolar contrast media (OR 0.40; 95% CI 0.23 to 0.71, p= 0.002) and in emergency procedural settings (OR 0.13, 95% CI 0.05 to 0.35, p<0.001). Additionally, sodium bicarbonate was associated with significant changes in serum bicarbonate (weighted mean difference [WMD] 2.63; 95% CI 1.72 to 3.55; p<0.001) and serum potassium levels (WMD −0.09, 95% CI −0.17 to −0.01, p= 0.03), though no significant differences were observed in post-procedural dialysis requirement (OR 0.94; 95% CI 0.46 to 1.91, p= 0.56) or mortality (OR 0.49; 95% CI 0.23 to 1.04, p= 0.06). While the findings support sodium bicarbonate as an effective prophylactic option for high-risk patients undergoing contrast exposure, the analysis highlights important variability across studies and underscores the need for adequately powered trials to confirm its role in improving clinically relevant outcomes. [2]
A 2015 meta-analysis evaluated the efficacy of perioperative sodium bicarbonate administration in preventing cardiac surgery-associated acute kidney injury (CSA-AKI). Five randomized controlled trials (RCTs; N= 1,092) included cardiac surgery patients requiring cardiopulmonary bypass (CPB) and who were randomized to receive either sodium bicarbonate infusions or sodium chloride (control group). Occurrence of CSA-AKI was defined as increases in serum creatinine of at least 25% or 0.5 mg/dL within five postoperative days. The results demonstrated no statistically significant difference in the rates of CSA-AKI between the sodium bicarbonate and control groups (RR 0.95; 95% CI 0.74 to 1.22; p > 0.05). Mortality outcomes (RR 1.44; 95% CI 0.76 to 2.72) and the requirement for renal replacement therapy (RR 0.90; 95% CI 0.50 to 1.60) similarly showed no significant differences. Parameters measuring intensive care unit stay duration (WMD 2.17 hours; 95% CI −1.15 to 5.49) and mechanical ventilation time (WMD 0.34 hours; 95% CI −0.80 to 1.48) also revealed no meaningful benefits associated with sodium bicarbonate administration. The heterogeneity across studies was moderate for some endpoints, particularly CSA-AKI definitions, but remained low for secondary measures. These findings highlight that the routine use of perioperative sodium bicarbonate for CSA-AKI prevention may lack clinical value and warrant reconsideration. [3]
A 2019 systematic review examined the use of sodium bicarbonate for the treatment and prevention of AKI, with a focus on its role in metabolic acidosis correction. Sodium bicarbonate increases the strong ion difference (SID), simulating renal bicarbonate generation and chloride excretion. Evidence from the BICAR-ICU trial, involving 389 critically ill patients with severe metabolic acidosis (pH <7.2), showed no significant difference in the primary composite outcome of 28-day survival and organ failure (Table 3). However, in patients with moderate to severe AKI (AKI Network stages 2 and 3), sodium bicarbonate reduced the need for renal replacement therapy (RRT) from 52% to 35% (p= 0.0009) and delayed its initiation by approximately 12 hours (p<0.0001). Adverse effects noted in the bicarbonate group included metabolic alkalosis, hypernatremia, and hypocalcemia. A retrospective analysis from the Medical Information Mart for Intensive Care III database evaluated bicarbonate's effects in septic patients. Among 251 individuals with AKI stages 2 and 3, bicarbonate therapy improved survival (hazard ratio, 0.74; 95% CI 0.51 to 0.86; p= 0.021). Despite these findings, the routine use of sodium bicarbonate remains debated due to inconsistent outcomes across studies and concerns about adverse events. The review concluded with a call for larger randomized trials to clarify bicarbonate's role in treating severe acidosis and AKI while addressing its safety and efficacy in various clinical scenarios. [4]
A 2016 meta-analysis assessed the efficacy of sodium bicarbonate compared to sodium chloride in preventing CI-AKI following coronary angiography and/or percutaneous coronary intervention. The study analyzed data from 16 RCTs involving 3,537 patients, with 1,768 allocated to the sodium bicarbonate group and 1,769 to the sodium chloride group. The pooled analysis indicated that sodium bicarbonate significantly reduced the incidence of CI-AKI (RR 0.67; 95% CI 0.47 to 0.96; p= 0.029). Subgroup analyses revealed superior effects of sodium bicarbonate in patients undergoing emergency procedures (RR 0.22; 95% CI 0.08 to 0.60) and with low-osmolar contrast media (RR 0.51; 95% CI 0.31 to 0.84). However, no significant differences were observed for secondary outcomes, including the requirement for dialysis (RR 1.11; 95% CI 0.60 to 2.07; p= 0.729), mortality (RR 0.71; 95% CI 0.41 to 1.21; p= 0.204), or length of hospital stay (mean difference: -1.47 days; 95% CI -4.14 to 1.20; p= 0.279). Sodium bicarbonate also significantly reduced serum creatinine change (mean difference [MD] -0.33; 95% CI -0.55 to -0.12; p= 0.003) and improved urine pH (MD 0.67; 95% CI 0.33 to 1.01; p<0.001). The trial sequential analysis revealed that the required information size (6,614 participants for CI-AKI, 170,510 for dialysis, and 19,516 for mortality) was not achieved. This indicated that the existing data are insufficient to draw definitive conclusions, emphasizing the need for larger, well-designed RCTs to confirm the findings. [5]
A 2012 Cochrane systematic review sought to evaluate the efficacy and safety of sodium bicarbonate administration for the treatment of AKI. This review sought to examine RCTs that investigated sodium bicarbonate use, delivered via any route, among adult patients hospitalized with AKI. AKI was defined using standardized criteria, including acute rises in serum creatinine or reductions in urine output, consistent with the first stage of the Acute Kidney Injury Network (AKIN) definition. Despite identifying 25 potential reports, none met the inclusion criteria due to inappropriate study designs, populations, or interventions. As a result, no eligible studies were available for analysis and the study was unable to draw conclusions regarding the benefits or harms of sodium bicarbonate for AKI treatment. The authors underscored an urgent need for high-quality large scale studies to address the persisting clinical uncertainty surrounding this intervention. [6], [7]
A 2023 narrative review synthesized findings from 27 original research studies and four meta-analyses between 1990 and 2022 to evaluate the role of sodium bicarbonate in various nontoxicologic causes of metabolic acidosis. Comprehensive literature analysis highlighted clinical scenarios such as lactic acidosis, diabetic ketoacidosis (DKA), cardiac arrest, rhabdomyolysis, and non-anion gap metabolic acidosis. The analysis also integrated subgroup data for patients with concomitant AKI, providing nuanced insights into sodium bicarbonate’s effects on outcomes like mortality, hemodynamic stability, and organ support requirements. [8]
Key conclusions from the 2023 review indicate that routine sodium bicarbonate administration does not confer substantial benefits in conditions such as lactic acidosis, where clinical trials like the BICAR-ICU (Table 3) demonstrated no mortality advantage aside from decreased renal replacement therapy in AKI subsets. Ultimately, it was suggested that there may be a role for an infusion of sodium bicarbonate after initial resuscitation in patients with AKI and pH <7.2, although data are limited, and that the emphasis should be placed on treatment of underlying cause of acidosis. [8]