Description
Whilst dichotomous thresholds are currently used to diagnose primary aldosteronism (PA), emerging data support the concept of a continuum of aldosterone excess. A robust cellular marker of aldosterone excess that correlates strongly with clinical outcomes following mineralocorticoid receptor (MR) antagonist treatment or adrenalectomy will complement the aldosterone-renin ratio (ARR) and confirmatory tests in the diagnostic algorithm for PA. As peripheral blood monocytes highly express the MR, they represent an accessible MR-responsive tissue to study aldosterone-induced changes in gene transcription. A number of genes identified by previous students will be characterised in vitro using RT-PCR and cell culture to confirm a change in their expression in response to MR activation or antagonism. These may then be validated in larger patient cohorts as robust biomarkers of aldosterone excess and inappropriate MR activation.
Essential criteria:
Minimum entry requirements can be found here: https://www.monash.edu/admissions/entry-requirements/minimum
Keywords
primary aldosteronism, biomarker, hypertension, endocrine hypertension, aldosterone
School
School of Clinical Sciences at Monash Health / Hudson Institute of Medical Research » Molecular and Translational Sciences
Available options
PhD/Doctorate
Honours
BMedSc(Hons)
Time commitment
Full-time
Top-up scholarship funding available
No
Physical location
Monash Health Translation Precinct (Monash Medical Centre)
Co-supervisors
Prof
Peter Fuller