Primary aldosteronism (PA) is the commonest specifically treatable and sometimes curable cause of hypertension, and delay in diagnosis is associated with cardiovascular morbidity not explained by hypertension alone. Controversy is high regarding screening, diagnostic and sub-typing tests, and especially their “cut-off” points. This is not surprising, given biological variability of renin, aldosterone, ACTH and cortisol, based on circadian rhythms, posture and stress responses. Unfortunately, emphasis in clinical testing has shifted from precision and reliability to utility and reduced technician time, devaluing diagnostic criteria. Thus plasma concentration of active renin is currently widely preferred to plasma renin activity, but does not take into account the role of endogenous substrate in determining angiotensin II levels, leading to the need for separate normal ranges for the aldosteronerenin ratio (ARR) for men and pre-menopausal women and to changes in the ARR during phases of the menstrual cycle.1Because most medications affect renin levels, a strong argument exists for screening for PA before commencing medications. Plasma aldosterone measurement by immunoassay (IA) has limited specificity and high-throughput mass spectrometry should gradually replace IA, and eventually angiotensin by IA also. While exciting new information on genetic bases brings the future possibility of definitive (-) blood tests for susceptibility to PA, until then we should critically re-examine diagnostic criteria dependent on measurements with limited precision or discriminatory power.