Key result
Sodium restriction in primary aldosteronism reduces inflammation via sex-specific immune and microbiome shifts.
Why the study?
Patients with primary aldosteronism have increased cardiovascular risk and high dietary sodium intake, but the impact of moderate dietary sodium restriction on their microbiome and immunophenotype is unknown.
Does moderate dietary sodium restriction modulate microbiome composition and immunophenotype in patients with primary aldosteronism?
Does moderate dietary sodium restriction modulate microbiome composition and immunophenotype in patients with primary aldosteronism?
Absolute Event Rate: 0.002309% vs 0.0123%
p-value: p=0.0068
Dietary sodium restriction in patients with primary aldosteronism modulates the peripheral immune cell composition toward a less inflammatory phenotype, suggesting a mechanism for cardiovascular risk reduction.
May attenuate inflammatory phenotype in PA; hypothesis-generating for sex-specific microbiome-immune effects, needing RCTs before practice change.
Background High dietary sodium intake is a major cardiovascular risk factor and adversely affects blood pressure control. Patients with primary aldosteronism (PA) are at increased cardiovascular risk, even after medical treatment, and high dietary sodium intake is common in these patients. Here, we analyze the impact of a moderate dietary sodium restriction on microbiome composition and immunophenotype in patients with PA. Methods Prospective two-stage clinical trial including two subgroups: 15 treatment-naive PA patients compared to matched normotensive controls; and 31 PA patients on mineralocorticoid receptor antagonist treatment before and three months after sodium restriction. Patients underwent blood pressure measurements, laboratory tests, analysis of peripheral blood mononuclear cells via flow cytometry and microbiome analysis. Results We observed a higher percentage of Tregs in treatment-naive PA patients (p = 0.0303), while the abundance of Bacteroides uniformis was higher in PA patients compared to normotensive controls (p = 0.00027) and the abundance of Lactobacillus species however was higher in the subgroup of normotensive controls (p = 0.0290). Sodium restriction was accompanied by a decrease in pro-inflammatory Tc17 cells in male patients (p = 0.0081, females p = 0.3274). Bacteroides uniformis abundance was higher in female patients (0.01230, p = 0.0016) and decreased upon sodium restriction (0.002309, p = 0.0068). Conclusion Dietary sodium restriction in patients with PA modulates the peripheral immune cell composition toward a less inflammatory phenotype. This suggests a potential mechanism by which sodium reduction modulates immune cell composition, leading to blood pressure reduction and positively impacting cardiovascular risk.
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Nowotny et al. (2024) studied Primary aldosteronism (n=49). Dietary sodium restriction vs. Baseline (pre-restriction) and normotensive controls was evaluated on Abundance of Bacteroides uniformis in female patients (p=0.0068). Dietary sodium restriction in patients with primary aldosteronism decreased pro-inflammatory Tc17 cells in males (p=0.0081) and reduced the abundance of Bacteroides uniformis in females (p=0.0068), promoting a less inflammatory phenotype.
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