Sodium bicarbonate therapy for metabolic acidosis in children stratified by acute kidney injury status and chloride levels: a retrospective cohort study
Original Article

Sodium bicarbonate therapy for metabolic acidosis in children stratified by acute kidney injury status and chloride levels: a retrospective cohort study

Xiangying Meng1#, Conglian Qiu1#, He Huang2#, Yi Hong3, Rongzhou Xiao1, Meilin Han1, Zhenjiang Bai1, Yuanyuan Xu4, Huaqing Liu5, Shuiyan Wu1

1Pediatric Intensive Care Unit, Children’s Hospital of Soochow University, Suzhou, China; 2Department of Pediatric, Xuzhou Hospital of Traditional Chinese Medicine, Xuzhou, China; 3Department of Pediatrics, Changshu Hospital Affiliated to Nanjing University of Chinese Medicine, Suzhou, China; 4Department of Pediatric Intensive Care Unit, Anhui Provincial Children’s Hospital, Hefei, China; 5Health Supervision Institute of Gusu District, Suzhou, China

Contributions: (I) Conception and design: H Liu, Y Xu, S Wu; (II) Administrative support: S Wu, Y Xu; (III) Provision of study materials or patients: H Liu, X Meng, C Qiu, H Huang; (IV) Collection and assembly of data: H Liu, Y Hong, R Xiao, M Han; (V) Data analysis and interpretation: H Liu, Y Hong, R Xiao, M Han; (VI) Manuscript writing: All authors; (VII) Final approval of manuscript: All authors.

#These authors contributed equally to this work.

Correspondence to: Shuiyan Wu, MD, PhD. Pediatric Intensive Care Unit, Children’s Hospital of Soochow University, No. 92 Zhongnan Street, Suzhou 215000, China. Email: wushuiyany@163.com; Huaqing Liu, MD. Health Supervision Institute of Gusu District, No. 28 Nanhuan East Road, Suzhou 215000, China. Email: rendanruju0872@163.com; Yuanyuan Xu, MD. Department of Pediatric Intensive Care Unit, Anhui Provincial Children’s Hospital, No. 39 Wangjiang East Road, Hefei 230051, China. Email: xuyuanyuan@ahmu.edu.cn.

Background: The efficacy of sodium bicarbonate in treating metabolic acidosis remains debated. Prior research indicated potential benefits for hyperchloremic patients and those with acute kidney injury (AKI). This study explored its effectiveness in children with or without AKI at diverse baseline chloride levels.

Methods: A retrospective cohort of children with metabolic acidosis was selected from the Paediatric Intensive Care (PIC) database. Intensive care unit (ICU)-related data on diagnosis, laboratory tests, treatment, and outcomes were retrieved. Sub-grouping was done based on AKI status and baseline chloride levels. In-hospital and 28-day mortality were compared between children receiving and not receiving sodium bicarbonate, with adjustment for confounding factors.

Results: Sodium bicarbonate therapy did not decrease in-hospital or 28-day mortality in overall AKI or in overall non-AKI children. Among stage 2–3 AKI [pediatric reference change value optimized for AKI (pROCK)] children, those on therapy had lower in-hospital (19.43% vs. 35.40%, P=0.002) and 28-day (17.43% vs. 32.74%, P=0.002) mortality, but this was not significant after adjustment. Stratification by baseline chloride level revealed a divergent association: when chloride was ≥113 mmol/L, sodium bicarbonate therapy was associated with lower mortality in both AKI and non-AKI children; conversely, when chloride was <107 mmol/L, it was associated with increased mortality.

Conclusions: The association between sodium bicarbonate therapy and mortality in children with metabolic acidosis critically depends on baseline chloride levels. Its use was associated with increased mortality in those with hypochloremia (chloride <107 mmol/L) but reduced mortality in those with hyperchloremia (chloride ≥113 mmol/L), regardless of AKI status. Without considering baseline chloride, sodium bicarbonate therapy was not associated with a mortality benefit in patients with moderate to severe AKI.

Keywords: Sodium bicarbonate; acute kidney injury (AKI); hyperchloremia; mortality

Submitted Jan 01, 2026. Accepted for publication Feb 25, 2026. Published online Mar 23, 2026.

doi: 10.21037/tp-2025-1-943

Highlight box

Key findings

• Sodium bicarbonate therapy is associated with reduced mortality in children with metabolic acidosis and hyperchloremia (chloride ≥113 mmol/L), regardless of acute kidney injury (AKI) status. Conversely, it was associated with increased mortality in children with hypochloremia (chloride <107 mmol/L). The association with reduced mortality in stage 2–3 AKI patients was not significant after multivariate adjustment.

What is known and what is new?

• The efficacy of sodium bicarbonate for treating metabolic acidosis is debated. Prior research suggests that it may not improve survival overall but could benefit patients with moderate-to-severe AKI. Emerging evidence also suggests that chloride levels may serve as a useful indicator to guide treatment decisions regarding sodium bicarbonate use.

• This study specifically suggests that the survival benefit associated with sodium bicarbonate is linked to hyperchloremia (chloride ≥113 mmol/L), and this association applies to children with or without AKI. Crucially, it demonstrates that without considering baseline chloride, sodium bicarbonate was not associated with a reduction in mortality in patients with moderate-to-severe AKI, highlighting chloride as one relevant stratification factor.

What is the implication, and what should change now?

• The implication is that clinical practice should shift from a one-size-fits-all approach to a chloride-stratified strategy; now, serum chloride levels should be measured to guide sodium bicarbonate use in metabolic acidosis, reserving it primarily for patients with hyperchloremia.

Introduction

Metabolic acidosis is a common and serious complication that severely affects the prognosis of patients. It is manifested as a decrease in the concentration of bicarbonate in the serum, leading to a decrease in blood pH (pH <7.35), accompanied by a secondary decrease in arterial partial pressure of carbon dioxide (PaCO2) (1). It can cause hemodynamic instability, reduced myocardial contractility and arterial vasodilation, decreased cellular oxygen supply and mitochondrial oxygen consumption, weakened catecholamine reactivity, and induce insulin resistance (2,3). In addition, it can also cause immunosuppression and impaired leukocyte function (4,5). On the basis of treating the primary cause, the use of sodium bicarbonate to correct acidosis is a commonly used clinical treatment method, but its clinical efficacy is controversial. Because clinical studies, including randomized controlled trials, suggest that sodium bicarbonate treatment cannot improve the survival status of overall patients (6), nor can it improve the renal function of kidney transplant recipients with metabolic acidosis (7). However, several studies have observed in the results of subgroup analyses that sodium bicarbonate can or has a tendency to improve the prognosis of patients with moderate to severe acute kidney injury (AKI) (6,8).

AKI is also a common complication with poor prognosis in the intensive care unit (ICU) (9,10). Many etiologies that lead to metabolic acidosis can also lead to AKI, such as infections and trauma. Metabolic acidosis is not only a result of renal dysfunction but also a factor in the progression of renal dysfunction (11). AKI combined with metabolic acidosis may indicate a more severe course of the disease and a worse outcome, including a high mortality rate, increased length of hospital stay and ICU stay (12). Recently, Liu et al. conducted a real-world data study based on a large sample of children and found that the chloride level affects the efficacy of sodium bicarbonate (13). Similarly, in adult patients, it has also been found that patients with hyperchloremic metabolic acidosis may potentially benefit from sodium bicarbonate therapy (14). Both the patient’s chloride level and AKI may affect the efficacy of sodium bicarbonate therapy for metabolic acidosis. To further explore the patients who may potentially benefit from sodium bicarbonate therapy for metabolic acidosis, this study analyzed the efficacy of sodium bicarbonate therapy in children with and without AKI at different baseline chloride levels. We present this article in accordance with the TRIPOD reporting checklist (available at https://tp.amegroups.com/article/view/10.21037/tp-2025-1-943/rc).

Methods

Source and selection of subjects

This study is a retrospective cohort study design. Children with metabolic acidosis during their admission to the pediatric ICU (PICU) were screened from the Paediatric Intensive Care (PIC) database. The PIC database is a public database established by the Children’s Hospital Affiliated to Zhejiang University. The database includes information on the treatment, examination, outcomes, etc. of all children admitted to the PICU in this institution from 2010 to 2018 (15). Data collation, patient inclusion, and exclusion were carried out according to the method of Liu et al. (13). The establishment of the database has been approved by the Institutional Review Board of Zhejiang Children’s Hospital. The study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. This is retrospective cohort data. Since it does not involve intervening in patients and does not disclose patient information, it is exempt from obtaining informed consent from patients.

Definitions

The diagnostic definition of metabolic acidosis is arterial blood pH <7.35 and bicarbonate less than 22 mmol/L (13,16). Two methods, pediatric reference change value optimized for AKI (pROCK) and modified Risk, Injury, Failure, Loss, and End-Stage Kidney Disease (mRIFLE) criteria, were used to diagnose AKI. The pROCK defined AKI by an increase in serum creatinine (SCr) of both ≥20 µmol/L and ≥30% within 7 days (17). The mRIFLE diagnostic criteria: An abrupt (within 48 hours) reduction in kidney function currently defined as an absolute increase in SCr of more than or equal to 0.3 mg/dL (≥26.4 µmol/L), a percentage increase in SCr of more than or equal to 50% (1.5-fold from baseline), or a reduction in urine output (documented oliguria of less than 0.5 mL/kg per hour for more than 6 hours) (18,19). The classifications of AKI and metabolic acidosis were defined according to the above literature.

Grouping and outcome

According to the medication records of whether patients in the database received intravenous infusion of 5% sodium bicarbonate treatment, the patients were divided into the sodium bicarbonate therapy group and the group without sodium bicarbonate therapy. The frequency and dose of sodium bicarbonate administration were determined by each treating doctor according to their own experience, the patient’s body weight, and the assessment of the patient’s condition. According to whether the patients were diagnosed with AKI, the patients were divided into the AKI subgroup and the non-AKI subgroup. According to the chloride level of the patients at the time of diagnosis of metabolic acidosis, they were divided into subgroups of <107, 107–<113, and ≥113 mmol/L (13,14). These specific cut-offs were derived from a prior study using the same database. In that analysis, the interaction between chloride levels and sodium bicarbonate treatment on mortality was assessed, and mortality curves suggested a transition point around 110 mmol/L. The cut-offs of 107 and 113 mmol/L were chosen to create clinically meaningful subgroups based on this inflection point and for consistency with previous research (13,14).

Statistical analysis

SAS 9.4 was used to clean and statistically analyze the data. Measurement variables were described using the median (interquartile range) or mean ± standard deviation. When the comparison between the two groups conformed to the normal distribution, the Student’s t-test was used, and when it did not conform to the normal distribution, the Wilcoxon two-sample test was used. Categorical variables were described using frequency (%), and the Chi-squared test or Fisher’s exact probability method was used for comparison between groups. Using in-hospital death or 28-day death as the dependent variable, the logistic multivariate regression method was used to correct potential confounding factors (age, sepsis, pneumonia, meningoencephalitis, disease diagnosis, grade of metabolic acidosis, bicarbonate, Ca2+, K+, Cl− , Na+, PaCO2, AKI stage, lactate, total bilirubin, triglyceride total protein hemoglobin, red blood cell and white blood cell), and the risk of death associated with the use of sodium bicarbonate was calculated. A two-sided test was used, and when P<0.05, a statistical difference was considered to exist.

Results

Risk of death in patients receiving sodium bicarbonate therapy classified by the AKI and non-AKI

According to the diagnostic criteria of mRIFLE and pROCK, 324 and 596 children with AKI were screened, respectively, and the screening flowchart is shown in Figure 1. Regardless of whether the mRIFLE or pROCK diagnostic criteria were used, the administration of sodium bicarbonate could not reduce the in-hospital death and 28-day death risks of overall AKI children and overall non-AKI children (Figure 2 and Figure S1). The baseline characteristics of children with or without AKI and with or without sodium bicarbonate administration are shown in Tables S1-S4.

Figure 1 Screening flow chart. AKI, acute kidney injury; mRIFLE, modified RIFLE; pROCK, pediatric reference change value optimized for AKI; RIFLE, Risk, Injury, Failure, Loss, and End-Stage Kidney Disease.
Figure 2 Risk of in-hospital death for children with sodium bicarbonate therapy stratified by AKI. *, a binary logistic multivariate regression model was used with death as the dependent variable, adjusted for factors such as age, sepsis, pneumonia, meningoencephalitis, disease diagnosis, grade of metabolic acidosis, HCO3−, Ca2+, K+, Cl−, Na+, PaCO2, lactate, total bilirubin, triglyceride, total protein, hemoglobin, red blood cell, and white blood cell, as applicable. AKI, acute kidney injury; CI, confidence interval; HCO3−, bicarbonate; mRIFLE, modified RIFLE; NaHCO3, sodium bicarbonate; OR, odds ratio; PaCO2, arterial partial pressure of carbon dioxide; pROCK, pediatric reference change value optimized for AKI; RIFLE, Risk, Injury, Failure, Loss, and End-Stage Kidney Disease.

According to the pROCK diagnostic criteria, the in-hospital mortality (19.43% vs. 35.40%, P=0.002) and 28-day mortality (17.43% vs. 32.74%, P=0.002) of children with grade 2–3 AKI treated with sodium bicarbonate were lower than those of children who did not receive it. The patients who did not receive sodium bicarbonate had more severe metabolic acidosis and lower chloride levels (Table S5). After correcting the above confounding factors, there was no statistically significant difference in the risk of death between the two groups (Figure 2 and Figure S1).

Risk of death for AKI children stratified by chloride level

When the chloride <107 mmol/L, sodium bicarbonate therapy increased the in-hospital death and 28-day death risks of children with AKI (pROCK criteria), and the adjusted odds ratios (ORs) were 1.931 [95% confidence interval (CI): 1.015–3.672] and 1.978 (95% CI: 1.007–3.888), respectively. When the chloride ≥113 mmol/L, sodium bicarbonate therapy reduced the in-hospital death risk (adjusted OR =0.413; 95% CI: 0.174–0.981). Although sodium bicarbonate therapy had a lower 28-day mortality rate (10.84% vs. 20.69%), the difference was not statistically significant (Figure 3 and Figure S2). In addition, according to the mRIFLE diagnostic criteria, when the chloride ≥113 mmol/L, sodium bicarbonate therapy reduced both the in-hospital death and 28-day death risks, and the adjusted ORs were 0.154 (95% CI: 0.031–0.779) and 0.185 (95% CI: 0.036–0.949), respectively. Regardless of whether the mRIFLE or pROCK diagnostic criteria were used, when 107≤ chloride <113 mmol/L, sodium bicarbonate therapy could not reduce the in-hospital death risk or 28-day death risk of children.

Figure 3 Risk of in-hospital death for AKI children with sodium bicarbonate therapy stratified by chloride level. AKI, acute kidney injury. *, a binary logistic multivariate regression model was used with death as the dependent variable, adjusted for factors such as age, sepsis, pneumonia, meningoencephalitis, disease diagnosis, grade of metabolic acidosis, HCO3−, Ca2+, K+, Cl−, Na+, PaCO2, lactate, total bilirubin, triglyceride, total protein, hemoglobin, red blood cell, and white blood cell, as applicable. AKI, acute kidney injury; CI, confidence interval; HCO3−, bicarbonate; mRIFLE, modified RIFLE; NaHCO3, sodium bicarbonate; OR, odds ratio; PaCO2, arterial partial pressure of carbon dioxide; pROCK, pediatric reference change value optimized for AKI; RIFLE, Risk, Injury, Failure, Loss, and End-Stage Kidney Disease.

Risk of death for non-AKI children stratified by chloride level

After stratification by chloride level, when the chloride <107 mmol/L, sodium bicarbonate therapy increased the in-hospital and 28-day death risks of non-AKI children (mRIFLE or pROCK criteria). Conversely, when the chloride ≥113 mmol/L, sodium bicarbonate therapy reduced the in-hospital and 28-day death risks. When 107≤ chloride <113 mmol/L, sodium bicarbonate therapy could not change the in-hospital death risk or 28-day death risk (Figure 4 and Figure S3).

Figure 4 Risk of in-hospital death for non-AKI children with sodium bicarbonate therapy stratified by chloride level. *, a binary logistic multivariate regression model was used with death as the dependent variable, adjusted for factors such as age, sepsis, pneumonia, meningoencephalitis, disease diagnosis, grade of metabolic acidosis, HCO3−, Ca2+, K+, Cl−, Na+, PaCO2, lactate, total bilirubin, triglyceride, total protein, hemoglobin, red blood cell, and white blood cell, as applicable. AKI, acute kidney injury; CI, confidence interval; HCO3−, bicarbonate; mRIFLE, modified RIFLE; NaHCO3, sodium bicarbonate; OR, odds ratio; PaCO2, arterial partial pressure of carbon dioxide; pROCK, pediatric reference change value optimized for AKI; RIFLE, Risk, Injury, Failure, Loss, and End-Stage Kidney Disease.

Discussion

This study found that the association between sodium bicarbonate therapy and mortality in children with metabolic acidosis is strongly modified by baseline serum chloride levels. Specifically, therapy was associated with improved survival in patients with hyperchloremia (chloride ≥113 mmol/L) but with increased mortality risk in those with hypochloremia (chloride <107 mmol/L), regardless of the presence or absence of AKI. This suggests that the chloride level may be a more decisive factor in predicting treatment response than AKI status alone.

When examining the role of AKI status, our findings align with and extend prior research. Sodium bicarbonate therapy did not improve survival in the overall AKI or non-AKI cohorts. Among children with stage 2–3 AKI (by pROCK criteria), unadjusted analysis showed lower mortality with therapy, consistent with some adult studies suggesting benefit in moderate-to-severe AKI (6,8). However, after adjustment for confounders, including baseline chloride, potassium, and acidosis severity, this association was no longer significant. The larger sample size and more comprehensive adjustment in our study may explain this difference from earlier reports and provide a more robust estimate.

The biological plausibility for chloride-guided therapy is well-founded. Chloride is pivotal in maintaining acid-base homeostasis. The kidneys regulate serum bicarbonate and chloride in a reciprocal manner (20-22). In hyperchloremic metabolic acidosis, bicarbonate deficiency and chloride excess represent two facets of the same disorder. Supplementing bicarbonate directly addresses this deficit and may mitigate the adverse effects of hyperchloremia, potentially improving hemodynamic response to vasopressors and normalizing the strong ion difference (23-25). Conversely, in metabolic acidosis with low chloride levels, endogenous bicarbonate may be relatively preserved. Administering exogenous bicarbonate in this context risks exacerbating electrolyte imbalances, potentially explaining the worsened outcomes we observed.

It should be noted that in this study, AKI was defined according to two different diagnostic criteria, pROCK and mRIFLE, leading to some variation in results. While adult criteria like RIFLE, Acute Kidney Injury Network (AKIN), and Kidney Disease: Improving Global Outcomes (KDIGO) are often referenced in pediatrics (26-29), the pROCK criteria were developed to account for age-related variations in SCr and may offer better prognostic accuracy in children (17,30).

Study limitations

This study has several limitations. The retrospective observational design precludes causal inference, and despite multivariate adjustments, unmeasured confounding and confounding by indication remain concerns. Detailed data on sodium bicarbonate exposure (timing, cumulative dose) were unavailable. The chloride level thresholds, though empirically derived, are somewhat arbitrary and were not tested with alternative cut-offs; variability in laboratory methods may affect their generalizability. Finally, findings from this single-center PICU cohort in China require external validation.

Conclusions

In conclusion, this study suggests that sodium bicarbonate therapy may improve survival outcomes in children with hyperchloremic metabolic acidosis (chloride ≥113 mmol/L), irrespective of AKI status. However, when baseline chloride is not considered, it does not significantly reduce mortality in patients with moderate to severe AKI. These findings support the measurement of serum chloride as one useful criterion to guide bicarbonate therapy in metabolic acidosis.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the TRIPOD reporting checklist. Available at https://tp.amegroups.com/article/view/10.21037/tp-2025-1-943/rc

Peer Review File: Available at https://tp.amegroups.com/article/view/10.21037/tp-2025-1-943/prf

Funding: This study was supported by the Suzhou Science and Technology Development Project for the study design and collection, analysis, and interpretation of data (No. SYW2025015).

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://tp.amegroups.com/article/view/10.21037/tp-2025-1-943/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. The study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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Cite this article as: Meng X, Qiu C, Huang H, Hong Y, Xiao R, Han M, Bai Z, Xu Y, Liu H, Wu S. Sodium bicarbonate therapy for metabolic acidosis in children stratified by acute kidney injury status and chloride levels: a retrospective cohort study. Transl Pediatr 2026;15(4):136. doi: 10.21037/tp-2025-1-943

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