Hypertension, Primary Aldosteronism, Hypokalemia
Conditions
Keywords
NaMRI, muscle Na+ quantification, K+ supplementation
Brief summary
The study aims to provide quantitative facts on the pathophysiological changes in tissue Na+ content during Na+/K+ redistribution disorders in patients with PA in response to standard therapy. The investigators hypothesize that patients with primary aldosteronism have excessive Na+ storage in the muscle, which can now be quantified non-invasively using 23NaMRI. In analogy to the role of HbA1c as a metabolic long-term marker in diabetes, the quantifiable changes in muscle Na+ content may deliver the data evidence necessary to justify and conduct randomized diagnostic endpoint outcome trials in the future, with the ultimate aim to improve PA detection rate and treatment.
Detailed description
Arterial hypertension is a major modifiable cardiovascular risk factor along with diabetes mellitus. Hypertension due to autonomous elevation in aldosterone production (Primary Aldosteronism; PA) is not responsive to usual antihypertensive medications and is dramatically underdiagnosed in standard clinical routine. Currently, only 0.1% (1,280,000 worldwide and 1,140 Singaporeans) are diagnosed, much lower than the 5-20% (64,000,000-256,000,000 worldwide and 57,000-228,000 Singaporeans) of all patients with arterial hypertension estimated to suffer from PA. Given the high prevalence of PA, low rates of diagnoses, high cardiometabolic morbidity and mortality associated with untreated PA, the detection of more patients with PA is obligatory, and treatment success must be monitored. The investigators hypothesize that patients with primary aldosteronism have excessive Na+ storage in the muscle, which can now be quantified non-invasively using 23NaMRI. This study will be the first to systematically quantify changes in muscle Na+ stores in these patients in response to standard therapy. There is currently no established clinical diagnostic tool to detect or quantify the underlying cellular Na+/K+ redistribution physiology in patients with PA. Seeing and quantifying the Na+ non-invasively with 23NaMRI will provide a fresh look into the pathophysiological principles of solute and fluid homeostasis to evaluate therapy efficacy, and to improve rates of PA diagnoses with an intention to cure. This is a prospective non-randomized multi-centre study with 3 study visits ( pre-potassium treatment, pre- diagnosis and post-treatment) over a study period of 3 years. Approximately 100 participants will be recruited from hospital sites. The purpose of the study is to detect and quantify a hidden pathophysiological Na+/K+ redistribution process at the tissue level, using 23NaMRI, in an effort to provide an alternative to traditional hormone and solute diagnostics in blood and urine.
Interventions
23NaMRI, a non-invasive detection and quantification of hidden tissue Na+ stores in humans.
K+ supplementation intervention is given participants as part of their standard care. In this trial the K+ supplementation dosage is standardized and adjusted based on blood K+ level
Sponsors
Study design
Eligibility
Inclusion criteria
1. Age 21-70 years, with arterial hypertension or suspected to have primary aldosteronism based on Endocrine Society Guidelines. 2. Male and female patients older than 21 years. 3. Willingness to participate and ability to provide informed consent.
Exclusion criteria
1. Patients with
Design outcomes
Primary
| Measure | Time frame | Description |
|---|---|---|
| Patients with primary aldosteronism have a 10-20% higher muscle Na+ content compared to healthy controls | Baseline | Difference in muscle Na+ content as measured with 23NaMRI between patients with PA and healthy controls at baseline. |
Secondary
| Measure | Time frame | Description |
|---|---|---|
| High K+ intake reduces muscle Na+ in patients with primary aldosteronism | Baseline to 3 Months | Change in muscle Na+ content as measured with 23NaMRI, 3 months after initiation of K+ supplementation |
| MR blockade reduces muscle Na+ conten in patients with primary aldosteronism | Baseline to 18 months | Change in muscle Na+ content as measured with 23NaMRI, 12-18 months after initiation of MR blockade treatment |
| Compared to MR blockade, adenoma surgical removal is more efficient in reducing muscle Na+ in patients with primary aldosteronism | 36 Months | Change in muscle Na+ content as measured with 23NaMRI after adenoma surgical removal compared to MR blockade treatment. |
Countries
Singapore