7-T 39K MRI showed that primary aldosteronism causes muscle K+ depletion (72.7 vs 79.1 mmol/L, P=0.02) and Na+ increase, reversed after treatment.
Does combined 7-T 39K and 23Na MRI detect alterations in skeletal muscle K+ and Na+ distribution in participants with primary aldosteronism?
42 participants including 21 with primary aldosteronism (mean age 52, 11 female) and 21 age- and sex-matched controls (mean age 53, 11 female). Additionally, 55 male mice were used for translational validation.
7-T 39K and 23Na MRI of the calf muscle before and approximately 4 months after standard therapy (mineralocorticoid receptor antagonists or adrenalectomy)
Age- and sex-matched control participants undergoing a single MRI scan
Apparent tissue K+ concentrations (aTPCs) and apparent tissue Na+ concentrations (aTSCs)surrogate
Combined 7-T 39K and 23Na MRI can noninvasively detect aldosterone-mediated tissue electrolyte shifts and their reversal following treatment in patients with primary aldosteronism.
Background Although 98% of potassium (K+) resides intracellularly, current clinical diagnostics assess only extracellular K+ concentrations. Noninvasive imaging of tissue K+ distribution could provide novel insights into pathophysiologic processes in diseases such as primary aldosteronism (PA). PA is characterized by excessive aldosterone production, which leads to electrolyte imbalances, hypertension, and increased cardiovascular risk. Purpose To determine whether potassium 39 (39K) MRI combined with sodium 23 (23Na) MRI can help detect alterations in skeletal muscle K+ and Na+ distribution in participants with PA. Materials and Methods A prospective pre-post study in participants with PA and a cross-sectional case-control study in participants with PA and age- and sex-matched control participants were conducted between January 2019 and April 2024. Participants underwent 7-T 39K and 23Na MRI of the calf muscle before treatment and approximately 4 months after standard therapy (mineralocorticoid receptor antagonists or adrenalectomy). Control participants underwent a single scan. Apparent tissue K+ concentrations (aTPCs) and apparent tissue Na+ concentrations (aTSCs) were quantified; serum aldosterone and K+ were measured and correlated with imaging. Fifty-five male mice underwent sham surgery or deoxycorticosterone acetate-pellet implantation for translational chemical muscle K+ validation. Statistical tests included the Student t test or Mann-Whitney U test (between-group), Wilcoxon signed-rank test (within-participant), and Spearman correlation (two-sided α = .05). Results Forty-two participants were evaluated, including 21 participants with PA (mean age, 52 years ± 9 SD; 11 female participants) and 21 control participants (mean age, 53 years ± 9; 11 female participants). Participants with PA showed lower aTPC and higher aTSC than control participants (mean aTPC: 72.7 mmol/L ± 6.8 vs 79.1 mmol/L ± 10.0, P = .02; mean aTSC: 23.9 mmol/L ± 5.3 vs 19.0 mmol/L ± 3.0, P P = .001) but decreased aTSC (25.2 mmol/L ± 4.8 to 18.9 mmol/L ± 3.4; P + (r2 = .02, P = .54). Mouse muscle chemistry mirrored MRI-based K+ depletion. Conclusion Combined 39K and 23Na MRI enabled noninvasive detection of aldosterone-mediated tissue electrolyte shifts. ClinicalTrials.gov Identifier: NCT04251780 © RSNA, 2026 Supplemental material is available for this article. See also the editorial by Ellermann in this issue.
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Christoph Kopp
Anke Dahlmann
Lena V. Gast
Radiology
Heidelberg University
Johannes Gutenberg University Mainz
Friedrich-Alexander-Universität Erlangen-Nürnberg
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Kopp et al. (Sun,) reported a other. 7-T 39K MRI showed that primary aldosteronism causes muscle K+ depletion (72.7 vs 79.1 mmol/L, P=0.02) and Na+ increase, reversed after treatment.
www.synapsesocial.com/papers/69a91cbed6127c7a504bfa06 — DOI: https://doi.org/10.1148/radiol.252004