Richard D. Gordon, an Australian pioneer of endocrinology and hypertension research, recently passed away after a brief illness, aged 89. Born in Brisbane, Gordon’s training as an endocrinologist included research fellowships in Melbourne, Nashville (Vanderbilt University) under Grant Liddle and the University of Adelaide. In addition to clinical work, these fellowships heavily involved laboratory bench work, setting up, validating and trouble-shooting new assays, which added an invaluable dimension to his critical judgement and expertise as a clinical scientist. Gordon returned to Brisbane in 1970 and established Endocrine Units at Greenslopes and Princess Alexandra Hospitals and a Hypertension Unit (later Endocrine Hypertension Research Centre) at Greenslopes Hospital. During over 50 years of clinical investigation, Gordon’s scientific contributions included: (1) description of the circadian rhythm for renin; (2) defining the role of the sympathetic nervous system in the regulation of renin and aldosterone in man; (3) demonstrating salt-sensitivity and the variable phenotype of a new syndrome of hypertension and hyperkalemia that bears his name; (4) drawing attention to and defining in detail a variety of aldosterone-producing adenoma responsive to angiotensin; (5) describing a new variety of familial primary aldosteronism (PA) (familial hyperaldosteronism type II); and (6) showing that PA is much more common than previously thought, and the commonest potentially curable cause of hypertension.
Among patients with PA, unilateral adrenalectomy (ADX) for those with unilateral forms affords superior outcomes in terms of cardiovascular morbidity and quality of life compared with specific medical treatment with mineralocorticoid receptor antagonists (MRAs). Adrenal venous sampling (AVS) is superior to computed tomography (CT) for differentiating unilateral from bilateral PA. AV cannulation can be difficult, but success rates can be markedly improved by using a dedicated operator, ACTH stimulation, contrast CT and POC cortisol testing. If AVS is contraindicated or declined, CT can be combined with other ancillary information (e.g. age, severity of PA, hypokalemia) to decide re ADX vs medical treatment. 18F aldosterone synthase ligand PET-CT and steroid profiling are in development and hold promise as alternatives to, or in combination with, AVS. Until then, subtype differentiation should include CT to seek obvious mass lesions (including those large enough to warrant removal because of their malignant potential) and to localize adrenal veins AND AVS as the criterion standard for differentiating unilateral forms from bilateral forms. Australian and New Zealand guidelines for AVS are currently in development.