This guideline is directed at clinicians diagnosing high-risk patients with hypertension and has been prompted by the appreciation that hypokalaemia is not such a crucial trigger in screening for primary aldosteronism as claimed until recently. The article includes a number of points for laboratories to consider seriously. A table in the guidelines includes 20 cut-off values in use for the aldosterone/renin ratio (ARR), which is the recommended screening test. The aldosterone concentration to renin activity (PRA) or concentration (PRC or DRC) ratios vary from 1.6 to 1000 depending on the units (ng, pmol, mU), volume of sample (mL/dL/L) and time of enzyme activity (min or h, s were not quoted but are found in the literature). There will be further variations in use through differences in methodology, assay standardization and reaction conditions. The guideline highlights the most commonly adopted cut-off values of 30 (aldosterone ng/dL: PRA ng/mL/h) and 750 (aldosterone pmol/L: PRA ng/mL/h). The immunometric (automated) methods for PRC are in evolution but are presumably formulated differently because in a discontinued automated assay for PRC the 1 ng/mL/h PRA converts to 8.2 mU/L PRC, whereas in the new Diasorin method this converts to 12 mU/L. The need for improvement in aldosterone assays has been discussed elsewhere (Stowasser and Gordon, Clin Chem 2006;52:1640–2). Measurements of the suppressed PRA or PRC/DRC also need careful assessment for value, imprecision and accuracy in this area. Incubation times for renin activity can be extended to increase the amount of angiotensin 1 generated for measurement but the approach for low renin concentration needs to be addressed. Many patients likely in need of ARR testing will be on cocktails of drugs, several of which, as the guidelines state, affect renin and or aldosterone and can complicate interpretation of ARR. The guideline proposes four confirmatory tests – oral salt loading, saline infusion, fludrocortisone suppression or captopril challenge. After oral salt loading, the guideline only recommends measurement of urine aldosterone. This is available in few laboratories in the UK, so a blood test will be substituted in any laboratory-approved protocol. The guidelines recommend turning to tandem mass spectrometry for urine aldosterone after the oral sodium load despite only three laboratories having published serum (not urine) methods by mass spectrometry. The urine assay is based on measurement of aldosterone after a pH 1 hydrolysis. Following these tests, computed tomography scanning and adrenal venous sampling are recommended. Venous sampling needs an experienced radiologist because of the anatomical differences between left and right adrenal vasculature. Accurate analysis of aldosterone (and cortisol) at high concentrations found in normal and diseased adrenal venous effluents again requires careful validation. Few centres will have sufficient experience with surgically proven cases to establish reliable reference ranges. Without this, laboratories should refrain from offering the service based on literature-quoted values.