Potassium and survival outcomes in asthma patients: evidence from a retrospective cohort study

Introduction

Asthma is a chronic inflammatory airway disease affecting more than 300 million people worldwide and remains a significant cause of preventable mortality (1). Despite advances in diagnosis and treatment, substantial variability persists in disease severity, frequency of exacerbations, and treatment response among individuals. Identifying key factors that influence asthma progression and patient prognosis is therefore crucial for optimizing clinical management and reducing morbidity and mortality.

Recent studies have highlighted the prevalence of hypokalemia in asthma patients, particularly among those receiving β₂-agonists or corticosteroid therapy. β₂-agonists, such as salbutamol, are widely used to relieve bronchoconstriction, yet they can lower serum potassium levels, increasing the risk of hypokalemia (2). Studies have reported cases of severe hypokalemia following β₂-agonist therapy, with documented electrolyte imbalances and cardiac arrhythmias requiring intensive care intervention (3,4). Corticosteroids, despite their essential role in controlling airway inflammation, may further exacerbate potassium loss through enhanced renal excretion, leading to increased susceptibility to hypokalemia in patients undergoing long-term therapy (5,6).

Potassium is essential for cellular homeostasis, neuromuscular activity, and airway function. Hypokalemia has been associated with worsening asthma symptoms and increased mortality risk through several mechanisms. A reduction in serum potassium may heighten airway hyperresponsiveness, leading to greater bronchial smooth muscle contraction and exacerbation of asthma symptoms (2). The prevalence of hypokalemia is particularly high during acute asthma exacerbations, with more severe cases showing a higher incidence, suggesting a link between potassium imbalance and disease severity (3,5). In addition, potassium depletion can impair respiratory muscle function, including diaphragmatic activity, potentially leading to respiratory failure (7). Hypokalemia has also been implicated in the development of cardiac arrhythmias, further contributing to cardiovascular risks in asthma patients (8).

Dietary potassium intake is a key determinant of serum potassium levels, and inadequate intake may further contribute to hypokalemia, disrupting electrolyte balance and neuromuscular stability. Epidemiological evidence suggests that low potassium intake is associated with decreased serum potassium levels, which may exacerbate hypokalemia in asthma patients (9). In children, insufficient potassium intake has been linked to reduced lung function, as indicated by lower forced expiratory volume in 1 second (FEV₁) and forced vital capacity (FVC), reinforcing the importance of potassium in maintaining airway health (9). Ensuring sufficient potassium intake may therefore be important for preserving electrolyte balance and optimizing respiratory function in asthma patients.

While previous studies have explored the relationship between potassium and asthma, the extent to which potassium status influences asthma-related mortality remains unclear. This study aims to systematically assess the association between potassium and asthma mortality, with the objective of identifying potential preventive and therapeutic strategies to enhance clinical asthma management and reduce asthma-related deaths. We present this article in accordance with the STROBE reporting checklist (available at https://jtd.amegroups.com/article/view/10.21037/jtd-2025-245/rc).

Methods

Study population

This retrospective cohort analysis was based on data obtained from the National Health and Nutrition Examination Survey (NHANES), a nationally representative program administered by the Centers for Disease Control and Prevention (CDC) to evaluate the health and dietary patterns of the U.S. population. Within the NHANES framework, data on dietary patterns, clinical characteristics, and environmental exposures are systematically collected through calibrated interviews, standardized physical examinations, and laboratory-based biochemical assessments. Employing a multistage, probability-based sampling approach, the survey ensures broad representativeness, providing high-quality epidemiological data to track health trends, identify key risk factors, and support evidence-based public health strategies (10,11).

Figure 1 presents the systematic selection of participants from the NHANES database [1999–2018]. The initial cohort comprised 101,316 individuals, from which 87,543 participants without a diagnosis of asthma were excluded. Of the remaining 13,773 individuals with asthma, 5,787 were excluded due to missing mortality data (under 18 years old), resulting in 7,986 participants with verified survival information. An additional 1,707 individuals with incomplete laboratory or dietary data of potassium were excluded, yielding a final study population of 6,279 participants. Within this cohort, 882 were classified as the non-survival group, while 5,397 comprised the survival group.

Figure 1 Flowchart of participant selection and exclusion. NHANES, National Health and Nutrition Examination Survey.

Ethical statement

The study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments.

Assessment of asthma

Asthma in NHANES was identified through participants’ self-reported responses to a standardized survey question. The use of structured instruments and uniform data collection procedures ensures consistency and reliability in classification. Additionally, self-reported physician-diagnosed asthma has been extensively validated in epidemiological research and is recognized as a robust method for large-scale population studies (12-14).

Assessment of potassium

Serum potassium was measured following standardized protocols established by the NCHS to ensure consistency and accuracy across survey cycles. Blood samples collected during the NHANES physical examinations adhered to rigorous quality control standards, as detailed in the NHANES Laboratory Procedure Manual. Comprehensive descriptions of the assay methodologies and instruments are available in publicly accessible documentation and prior studies (15,16). Dietary potassium intake was estimated from two 24-hour recall interviews collected on separate days using standardized data collection procedures (17). Supplement usage over a 24-hour period was also recorded. Average potassium and sodium intake was calculated by combining dietary and supplementary sources across the 2 days.

Assessment of mortality

Among the study population, the median follow-up duration was 104 months, with a maximum follow-up period of 249 months. All-cause mortality was ascertained through record linkage with the National Death Index (NDI), utilizing the 2019 Public-Use Linked Mortality Files provided by the NCHS. Mortality status was determined by matching NHANES participant records with NDI death certificates using unique identifiers such as social security numbers, names, and birth dates. The follow-up period spanned from NHANES enrollment [1999–2018] to December 31, 2019, with causes of death classified according to the International Classification of Diseases, 10^th Revision (ICD-10), ensuring a standardized and comprehensive assessment of mortality outcomes. Mortality data were released on April 28, 2022 (available at: https://www.cdc.gov/nchs/data-linkage/mortality-public.htm).

Assessment of covariables

Age, gender, and race were obtained from the Demographic Data. Body mass index (BMI) was calculated based on measurements recorded in the Examination Data. Dietary intake of potassium and sodium was extracted from the Dietary Data, and serum concentrations of potassium, sodium, and chloride were extracted from the Laboratory Data. Smoking status, glucocorticoid use, asthma exacerbations (within the past 12 months), and comorbidities were collected using standardized questionnaires. Glucocorticoid use was defined based on participants’ responses to medication inventory questions, identifying exposure to either inhaled corticosteroids or systemic steroid agents. Comorbidities were determined based on self-reported physician diagnoses and included renal impairment, hypertension, diabetes, coronary heart disease (CHD), and malignancy. To ensure data validity and reliability, these questionnaires were developed and validated by subject matter experts in accordance with established methodological standards. Trained interviewers administered the surveys according to standardized procedures, with built-in quality control mechanisms designed to minimize measurement error and reporting bias (18-20).

Statistical analysis

Weighted analyses were conducted to ensure that the results accurately reflected the general population. All covariates exhibited no more than 20% missingness and were addressed through multiple imputation, as detailed in Table S1. The distribution of continuous variables was evaluated using the Kolmogorov-Smirnov test. As all continuous variables were non-normally distributed, they were summarized as median with interquartile range (IQR). Categorical variables were reported as counts and percentages. Comparisons of continuous variables were conducted using the Student’s t-test for normally distributed data and the Wilcoxon rank-sum test for non-normally distributed data. Categorical variables were compared using the Chi-squared test.

Cox proportional hazards models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for the association between dietary potassium intake and all-cause mortality. To enhance interpretability and computational stability, daily potassium intake values, expressed in thousands, were scaled by dividing by 1,000. Both serum potassium and potassium intake were assessed as continuous variables and quartiles (analyzed as both categorical and continuous variables). These were incorporated into different models to comprehensively examine potential trends and associations. Model 1 was adjusted for age, gender, and race. Model 2 was additionally adjusted for BMI, smoking status, glucocorticoid use, asthma exacerbation, dietary sodium intake, serum sodium, serum potassium, and serum chloride. Model 3 was further adjusted for renal impairment, hypertension, diabetes, CHD, and malignancy.

Daily potassium intake was categorized into higher and lower intake groups according to the median value, and survival differences between groups were evaluated using Kaplan-Meier survival analysis. The log-rank test evaluated statistical differences in survival distributions. Subgroup and interaction analyses were performed across the following binary variables: age (<60 vs. ≥60 years), gender (male vs. female), race (non-Hispanic White vs. other), BMI (<30 vs. ≥30 kg/m²), smoking history (ever vs. never), and comorbidity status (yes vs. no). Restricted cubic spline (RCS) analysis was applied to investigate non-linear relationships between daily potassium intake and all-cause mortality. Threshold effect analysis identified inflection points in the intake-mortality relationship.

A series of sensitivity analyses was performed to evaluate the robustness of the findings. Potassium intake was analyzed as both a continuous and categorical variable, with tests for linear trend across quartiles. Consistency of associations was assessed using models with stepwise covariate adjustment. Subgroup analyses were further conducted across key covariates.

Statistical analyses were performed using R (version 4.4.2; R Foundation for Statistical Computing, Vienna, Austria) and DecisionLinnc (version 1.1.3; Statsape Co., Ltd., Hangzhou, China). Statistical significance was defined as a two-sided P<0.05.

Results

Patient baseline and clinical characteristics

As shown in Table 1, non-survivors were older (66 vs. 40 years, P<0.001), had a higher proportion of non-Hispanic White individuals (74.65% vs. 68.51%, P=0.01), and a higher BMI (28.76 vs. 28.10 kg/m², P=0.03). Additionally, non-survivors had lower sodium intake (2,722.00 vs. 3,191.00 mg, P<0.001), lower potassium intake (2,317.45 vs. 2,438.50 mg, P<0.001), lower serum chloride (102.70 vs. 104.00 mmol/L, P<0.001), and higher serum potassium (4.10 vs. 3.97 mmol/L, P<0.001).

Non-survivors also had a higher frequency of asthma exacerbation within the past 12 months (56.64% vs. 50.66%, P=0.009), and were more likely to use glucocorticoids (P<0.001). A higher prevalence of smoking history was observed among non-survivors (69.31% vs. 48.83%, P<0.001). Comorbidities were more common in this group, including hypertension (61.18% vs. 28.93%, P<0.001), diabetes (25.42% vs. 7.85%, P<0.001), CHD (15.30% vs. 2.98%, P<0.001), renal impairment (7.90% vs. 2.90%, P<0.001), and malignancy (23.68% vs. 9.46%, P<0.001).

No significant differences were observed in gender distribution (P=0.88) and serum sodium (P=0.44).

Association between serum potassium and all-cause mortality

Table 2 reveals a significant association between serum potassium levels and all-cause mortality in Model 1 (P<0.001); however, the association was no longer statistically significant in Model 2 (P=0.051) and Model 3 (P=0.06) after further adjustment. Similarly, the elevated mortality risk in the highest quartile of serum potassium was attenuated and became non-significant in the fully adjusted models. The trend across quartiles also lost significance after adjustment (P=0.06 in Model 2; P=0.06 in Model 3).

Association between potassium intake and all-cause mortality

Table 3 presents the association between daily potassium intake and all-cause mortality among asthma patients. As a continuous variable, potassium intake was significantly associated with reduced mortality in Model 1 (P<0.001) and Model 2 (P<0.001), and remained significant in Model 3 (P=0.01). In the quartile analysis, HRs for the highest quartile (Q4) compared to the lowest quartile (Q1) were 0.55 (95% CI: 0.40–0.75; P<0.001), 0.55 (95% CI: 0.40–0.70; P=0.001), and 0.64 (95% CI: 0.46–0.89; P=0.008) across Models 1–3, respectively. A significant trend across quartiles was observed in all models (P for trend <0.001, 0.002, and 0.03).

Kaplan-Meier survival curve and subgroup analysis

Kaplan-Meier curves in Figure 2 illustrate survival probabilities across median-stratified dietary potassium intake, adjusted for covariates included in Model 3. Survival probability was greater in the high potassium intake group. The log-rank test indicated a statistically significant difference between the groups (P=0.02; HR =0.85; 95% CI: 0.75–0.98). The subgroup analysis results, presented in Figure 3, show no statistically significant interactions between potassium intake and all-cause mortality across the stratified variables. The P for interaction were non-significant for other subgroups, including age, gender, race, BMI, smoking status, glucocorticoid use, asthma exacerbation, renal impairment, CHD, hypertension, diabetes, and malignancy.

Figure 2 Daily potassium intake and Kaplan-Meier survival curves in asthma patients. The log-rank test indicated a statistically significant difference between the groups (P=0.02; HR =0.85; 95% CI: 0.75–0.98). CI, confidence interval; HPI, higher potassium intake; HR, hazard ratio; LPI, lower potassium intake.

Figure 3 Subgroup analyses of dietary potassium intake and all-cause mortality. HRs were estimated using univariate Cox proportional hazards models within each subgroup. P values for interaction were derived from multiplicative interaction terms to evaluate whether the associations differed significantly between subgroups. BMI, body mass index; CHD, coronary heart disease; CI, confidence interval; HR, hazard ratio.

Non-linear curve fitting and threshold effect analysis

As shown in Figure 4, RCS analysis demonstrated a significant association between dietary potassium intake and all-cause mortality (P for overall <0.001), with evidence of a non-linear dose-response relationship (P for nonlinearity =0.047). The HR decreases with increasing potassium intake at lower levels, followed by a slight upward trend at higher intake levels. Table 4 presents the results of the threshold effect analysis for daily potassium intake and all-cause mortality in asthma patients. A threshold was identified at a daily potassium intake of 3,192 mg/day. Below this threshold (<3,192 mg/day), the HR was 0.78 (95% CI: 0.68–0.89; P<0.001), indicating a protective association. Above the threshold (≥3,192 mg/day), the HR was 1.02 (95% CI: 0.85–1.21; P=0.84), showing no statistically significant association. The log-likelihood ratio test confirmed the presence of a threshold effect (P=0.02).

Figure 4 RCS model depicting the multivariable-adjusted association between dietary potassium intake and all-cause mortality. The solid curve represents the HR, and the shaded area indicates the 95% CI, derived from Cox proportional hazards regression. The background histogram and overlaid kernel density curve (in red) illustrate the distribution of DPI in the analytic sample. P for overall <0.001 indicates a statistically significant association between DPI and mortality; P for nonlinearity =0.047 suggests evidence of a non-linear relationship. CI, confidence interval; DPI, dietary potassium intake; HR, hazard ratio; RCS, restricted cubic spline.

Sensitivity analysis

Potassium intake was modeled as a continuous measure, categorized by quartiles, and evaluated for dose-response trends using an ordinal scale. The association was additionally examined under sequentially adjusted models. Subgroup analyses were conducted by stratifying key covariates. These complementary strategies yielded consistent results, supporting the internal validity of the study.

Discussion

This study investigated the association between potassium and all-cause mortality in asthma patients, with a focus on both dietary potassium intake and serum potassium. The results demonstrated a nonlinear relationship between dietary potassium intake and mortality, indicating a potential threshold effect, where higher potassium intake was associated with a reduced risk of mortality. In contrast, serum potassium levels were not independently associated with mortality. The clinical characteristics of the patients revealed an imbalance between serum potassium levels and dietary potassium intake. This phenomenon may be attributed to multiple factors. While potassium intake was lower, serum potassium levels remained relatively elevated, as shown in Table 1. Compromised renal function affects potassium excretion, leading to hyperkalemia even in cases of reduced dietary intake (21). Additionally, angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers, and potassium-sparing diuretics, which are commonly prescribed for hypertension and heart failure, may further elevate serum potassium (22). Moreover, systemic inflammation or cellular injury-induced potassium release may contribute to worsening hyperkalemia (23).

The systemic benefits of dietary potassium may be mediated through mechanisms beyond serum potassium regulation, such as improved vascular function, reduced oxidative stress, or modulation of inflammatory pathways (22,24). These findings align with previous studies, which suggest that serum potassium levels alone may not fully capture the protective effects of dietary potassium. Therefore, when assessing the health impact of potassium, it is crucial to consider both dietary intake and serum biomarkers to achieve a more comprehensive understanding of its physiological role.

RCS revealed a nonlinear inverse relationship between dietary potassium intake and all-cause mortality. Mortality risk decreased with increasing potassium intake, but after reaching a specific threshold, the protective effect plateaued. This nonlinear trend is consistent with previous research, indicating that moderate potassium intake reduces mortality risk, whereas excessive intake may not provide additional benefits and could pose risks in certain populations. For example, in individuals with impaired renal function or reduced potassium excretion capacity, excessive potassium intake may increase the risk of hyperkalemia (22,25). Further threshold effect analysis confirmed that potassium intake below this threshold was significantly associated with reduced mortality risk, while higher intake levels did not confer additional protective effects (26). These findings highlight the importance of determining optimal potassium intake levels to maximize health benefits while minimizing the potential risks of excessive intake.

Moreover, accumulating evidence from diverse populations supports the potential health benefits of adequate potassium intake. In hemodialysis patients, higher dietary potassium intake was not independently associated with increased mortality, suggesting a more nuanced relationship between potassium and clinical outcomes (27,28). Among U.S. adults, moderate potassium intake (up to approximately 2,300 mg per day) was significantly associated with lower odds of depressive symptoms, indicating a possible mood-stabilizing effect (29). In individuals with type 2 diabetes, low urinary potassium excretion, as an indirect indicator of insufficient dietary intake, was associated with increased all-cause mortality (15). Furthermore, a recent population-based cohort study reported that higher dietary potassium intake was independently associated with reduced all-cause mortality after comprehensive adjustment for potential confounders (30).

This study has limitations. The retrospective design limited medication data to broad categories, without details on specific agents such as bronchodilators. Self-reported asthma and dietary data may introduce recall and misclassification bias. Well-designed prospective studies are warranted to more rigorously control for potential confounding factors. In addition, serum potassium levels were assessed only at baseline, and the lack of longitudinal measurements limited the evaluation of temporal changes and their association with survival outcomes. Finally, this study was based on the nationally representative NHANES dataset, which employs a stratified multistage sampling strategy and incorporates weighting adjustments to enhance generalizability to the U.S. population. The relevance of these findings to other populations requires further validation.

Conclusions

The study found that higher potassium intake was consistently associated with a reduced risk of all-cause mortality in asthma patients, with a nonlinear inverse relationship indicating a protective effect up to a threshold level.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the STROBE reporting checklist. Available at https://jtd.amegroups.com/article/view/10.21037/jtd-2025-245/rc

Peer Review File: Available at https://jtd.amegroups.com/article/view/10.21037/jtd-2025-245/prf

Funding: This study was supported by the Fujian Provincial Health Commission Science and Technology Program, China (No. 2024CX01010061).

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://jtd.amegroups.com/article/view/10.21037/jtd-2025-245/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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