The Joint Annual Scientific Meetings of the Endocrine Society of Australia and the Society for Reproductive Biology 2018

Twenty-four-hour urinary sodium and aldosterone excretion in hypertensive patients may indicate underlying primary aldosteronism (#292)

Jenny Sung Won Yun 1 2 3 , Kay Weng Choi 4 , StellaMay Gwini 5 , Jun Yang 1 6 7 , Peter Fuller 1 2
  1. Centre for Endocrinology and Metabolism, Hudson Institute of Medical Research, Melbourne, Victoria, Australia
  2. Department of Endocrinology, Monash Health, Melbourne, Victoria, Australia
  3. The University of Melbourne, Melbourne, Victoria, Australia
  4. Pathology, Monash Health, Melbourne, Victoria, Australia
  5. Department of Epidemiology and Preventive Medicine, School of Public Health and Preventive Medicine, Monash University, Melbourne, Victoria, Australia
  6. Department of Endocrinology, Monash Health, Clayton, Victoria, Australia, Melbourne, Victoria, Australia
  7. School of Clinical Sciences , Monash University , Melbourne, Victoria, Australia

Objectives: Primary aldosteronism (PA) is an under-diagnosed cause of hypertension characterised by autonomous aldosterone production with renin suppression and an elevated aldosterone:renin ratio (ARR). PA may be confirmed by an oral salt-loading test where 24-hour urinary aldosterone excretion (UAE) remains elevated (>33.3nmol/d) after 3 days of high salt intake with urinary sodium (UrNa) >200mmol/d.  Given the high sodium intake in our community, we hypothesise that PA may be diagnosed, or at least suggested, by an elevated aldosterone level in a routine 24-hour urine sample.

Methods: A retrospective analysis of 24-hour UrNa and UAE measurements from 151 patients (20 with confirmed PA, 131 without known PA) with corresponding plasma aldosterone and renin levels was performed. The clinical and biochemical data were obtained from Monash Health medical records. Statistical significance was set at p<0.05.

Results: Twenty-four-hour UrNa and UAE met salt-loading criteria for PA in 5 of 20 PA patients (25%) and 28 of 131 patients without known PA (21%). Of the 131 without known PA, 85 had UrNa < 200 mmol/L of whom 14 had renin < 4.4mU/L.  A suppressed plasma renin in the absence of high sodium intake is not physiological and should prompt further testing for PA. Urinary sodium may also be important for the interpretation of a normal plasma renin.  In the setting of low urinary sodium, renin may be falsely normal (or un-suppressed), leading to a normal ARR and therefore mask the underlying hyperaldosteronism.  This was observed in 3 patients with confirmed PA who had ARRs in the normal range.

Conclusion: PA is common but infrequently diagnosed. It is important to maximise the utility of common tests in facilitating its diagnosis. Our study demonstrates that 24-hour urinary sodium and aldosterone measurements can affect the interpretation of plasma aldosterone and renin and aid PA detection.