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Secondary hypertension

TL;DR — The category "secondary hypertension" is being redrawn by primary aldosteronism. Systematic oral sodium suppression testing across the whole blood-pressure range found biochemically overt primary aldosteronism in 11.3% of normotensive people (95% CI 5.9–16.8), 15.7% of stage 1, 21.6% of stage 2 and 22.0% of resistant hypertension, with a continuum of renin-independent aldosterone production underneath, and the aldosterone-renin ratio performing poorly on sensitivity and negative predictive value (Brown 2020, PMID 32449886). Primary aldosteronism is not a benign biochemical label: compared with essential hypertension at similar pressures it carries roughly 2.6-fold odds of stroke, 3.5-fold of atrial fibrillation and 2.1-fold of heart failure (Monticone 2018, PMID 29129575), and the excess persists on mineralocorticoid receptor antagonists unless renin is allowed to rise (Hundemer 2018, PMID 29129576). In 2025 the Endocrine Society moved to suggesting that all people with hypertension be screened (Adler 2025, PMID 40658480). Meanwhile the two classic revascularisation targets have both failed randomised tests — renal-artery stenting added nothing to medical therapy in CORAL (Cooper 2014, PMID 24245566) or ASTRAL (ASTRAL Investigators 2009, PMID 19907042) — and CPAP lowers blood pressure only in people whose pressure is uncontrolled to begin with (Pengo 2025, PMID 39401854).

Prevalence by cause

Cause Prevalence estimate Population Source
Primary aldosteronism (biochemically overt) 11.3% / 15.7% / 21.6% / 22.0% Normotension / stage 1 / stage 2 / resistant (Brown 2020, PMID 32449886)
Primary aldosteronism (Endocrine Society criteria) 5.9% overall; 3.9% stage 1 → 11.8% stage 3 1,672 unselected primary-care hypertensives, Italy (Monticone 2017, PMID 28385310)
Obstructive sleep apnoea Very common in resistant hypertension; effect on BP conditional on baseline control Meta-analytic (Pengo 2025, PMID 39401854; Labarca 2021, PMID 33607443)
Atherosclerotic renal artery stenosis Common in older people with vascular disease; revascularisation not beneficial RCT populations (Cooper 2014, PMID 24245566)
Fibromuscular dysplasia Multi-bed involvement common once identified ARCADIA registry (Plouin 2017, PMID 28716989)
Phaeochromocytoma/paraganglioma Rare; ~30–40% germline-driven in contemporary series Referral (Pacak 2015, PMID 25716634; Eisenhofer 2012, PMID 22258313)
Coarctation of the aorta Hypertension persists or recurs in a large minority after repair Post-repair cohorts (Panzer 2022, PMID 35282025; Salciccioli 2023, PMID 37476999)
Drug- and substance-induced Under-recognised; NSAIDs, oral contraceptives, sympathomimetics, VEGF inhibitors, calcineurin inhibitors, licorice, alcohol Reviews (Grossman 2012, PMID 22195528; Foy 2019, PMID 31655781; Lovell 2017, PMID 28451850)

Primary aldosteronism

The prevalence argument

Brown and colleagues did not screen with the aldosterone-renin ratio and then confirm; they performed confirmatory oral sodium suppression testing on everyone, regardless of screening biochemistry. That design is why the numbers are so much higher than conventional estimates, and why the aldosterone-renin ratio's poor sensitivity was visible at all (Brown 2020, PMID 32449886). The authors' own caveat is that prevalence estimates depend on arbitrary diagnostic thresholds applied to a continuum. Conventional-criteria studies in unselected primary care give 5.9%, still far above the 1% figure long taught, and rising with hypertension stage (Monticone 2017, PMID 28385310; Buffolo 2018, PMID 29629943).

The continuum extends below the diagnostic threshold. In 1,284 population-based participants aged 40–69, a higher aldosterone-to-renin ratio — subclinical primary aldosteronism — was associated with greater arterial stiffness (central pressure, pulse wave velocity), adverse cardiac remodelling on MRI (left atrial volume, left ventricular mass and remodelling indices), higher odds of left ventricular hypertrophy (OR 1.32, 95% CI 1.002–1.73) and incident hypertension (OR 1.29, 1.03–1.62), all independent of brachial pressure and present in the normotensive subgroup alone (Hundemer 2024, PMID 38031887).

The harm argument

Meta-analysis of 31 studies (3,838 with primary aldosteronism, 9,284 with essential hypertension), median 8.8 years from hypertension diagnosis, found higher odds of stroke (2.58, 95% CI 1.93–3.45), coronary artery disease (1.77, 1.10–2.83), atrial fibrillation (3.52, 2.06–5.99), heart failure (2.05, 1.11–3.78), diabetes (1.33, 1.01–1.74), metabolic syndrome (1.53, 1.22–1.91) and left ventricular hypertrophy (2.29, 1.65–3.17), with no difference between adenoma and bilateral hyperplasia (Monticone 2018, PMID 29129575). Long-term mortality comparisons point the same way (Meng 2020, PMID 32210920), and atrial fibrillation is a signature complication (Pan 2020, PMID 32289838; Rossi 2021, PMID 32192789).

Crucially, treatment as usually delivered does not abolish the excess. In 602 medically treated patients on mineralocorticoid receptor antagonists versus 41,853 matched essential-hypertensive controls at comparable blood pressure, cardiovascular event rates were 56.3 versus 26.6 per 1,000 person-years (adjusted HR 1.91, 95% CI 1.63–2.25; 14.1 excess events per 100 people at 10 years), with excess mortality (HR 1.34, 1.06–1.71), diabetes (1.26, 1.01–1.57) and atrial fibrillation (1.93, 1.54–2.42). The excess was confined to patients whose renin remained suppressed (<1 μg/L/h) on treatment (HR 2.83, 2.11–3.80); those titrated to unsuppressed renin had no significant excess (Hundemer 2018, PMID 29129576). This is the origin of the "titrate to raise renin" recommendation now in guidance (Adler 2025, PMID 40658480).

Subtyping and surgery

Adrenal vein sampling has been the reference standard for lateralisation, but the SPARTACUS randomised diagnostic trial found no difference between CT-based and AVS-based management at one year in drug intensity (median 3.0 vs 3.0 defined daily doses), target attainment (42% vs 45%), quality of life or biochemical cure after adrenalectomy (80% vs 89%), with AVS costing €2,285 more per patient and a <0.2 probability of being cost-effective at €30,000/QALY (Dekkers 2016, PMID 27325147). This directly challenged the universal-AVS recommendation; the 2025 Endocrine Society guideline responds with a probability-stratified pathway rather than either extreme (Adler 2025, PMID 40658480).

Surgical outcomes are heterogeneous and now standardised. The PASO international consensus defined complete/partial/absent clinical and biochemical success; in 705 patients from 12 centres in nine countries, complete clinical success was 37% (range across centres 17–62), clinical benefit 84%, and complete biochemical success 94% (range 83–100). Female sex (OR 2.25, 95% CI 1.40–3.62), younger age (OR 0.95 per year, 0.93–0.98) and lower preoperative drug burden predicted complete clinical success (Williams 2017, PMID 28576687; Vorselaars 2019, PMID 31053245; Miller 2018, PMID 29134312). Prediction models for postoperative hypertension resolution exist but are not widely validated (Araujo-Castro 2022, PMID 36018220), and persistent renin suppression after adrenalectomy may itself mark residual risk (Stüfchen 2026, PMID 41175007).

Where diagnosis is still unsettled

Whether confirmatory aldosterone suppression testing should be retained at all is under active argument (Kline 2026, PMID 40887827). Age materially affects the aldosterone-renin ratio (Peng 2025, PMID 40065694), cut-points have been re-derived against cardiovascular risk rather than against a diagnostic gold standard (He 2024, PMID 38270079), and the practical problem of screening people already taking renin-angiotensin inhibitors persists (Wang 2026, PMID 41491647). General reviews frame the field's direction (Funder 2022, PMID 33775861; Ekman 2024, PMID 38255973; Yang 2017, PMID 28556585). Aldosterone synthase inhibition is now being tested in primary aldosteronism itself (Turcu 2025, PMID 40658651).

Renovascular hypertension

Two large randomised trials removed revascularisation from routine practice.

Trial n Design Result
ASTRAL (PMID 19907042) 806 Revascularisation + medical vs medical No significant difference in renal-function slope (P=0.06 favouring revascularisation), blood pressure, renal events (HR 0.97, 95% CI 0.67–1.40), cardiovascular events (0.94, 0.75–1.19) or death (0.90, 0.69–1.18); 23 serious procedural complications including 2 deaths and 3 amputations
CORAL (PMID 24245566) 947 Stenting + medical vs medical Composite endpoint 35.1% vs 35.8% (HR 0.94, 95% CI 0.76–1.17); consistent modest systolic difference of −2.3 mm Hg (−4.4 to −0.2) favouring stenting

Post-CORAL practice therefore reserves intervention for narrow indications — flash pulmonary oedema, rapidly deteriorating renal function, refractory hypertension on maximal therapy — and the literature since has focused on identifying who those patients are (Herrmann 2015, PMID 24723543; Tuttle 2016, PMID 27225988; Grillo 2026, PMID 41167516; Green 2026, PMID 41623301). Quality-of-life outcomes in CORAL were also neutral (Arnold 2025, PMID 39402005).

Fibromuscular dysplasia is a distinct entity with a distinct approach: an international consensus covers diagnosis and management (Gornik 2019, PMID 30648921), and the ARCADIA registry showed that multiple arterial beds are involved in most patients once one lesion is found, so imaging should not stop at the renal arteries (Plouin 2017, PMID 28716989). Dissection is a linked phenotype (Huart 2023, PMID 37379454; Kadian-Dodov 2018, PMID 30064124).

Obstructive sleep apnoea

The blood-pressure effect of CPAP is real but conditional. In an individual-patient meta-analysis of 36 parallel trials and 9,434 patients, CPAP reduced blood pressure only in those with uncontrolled office systolic pressure at baseline (−2.6 vs 0 mm Hg, p<0.0001); there was no reduction in patients whose pressure was already controlled, and no difference by severity of nocturnal hypoxia (Pengo 2025, PMID 39401854). Effects are larger in resistant hypertension (Labarca 2021, PMID 33607443; Sun 2024, PMID 38460066; Shang 2022, PMID 35701490), and mandibular advancement devices achieve comparable pressure reduction in network meta-analysis (Bratton 2015, PMID 26624827). CPAP has not shown cardiovascular event reduction except in adherence-based analyses, which are confounded by the healthy-adherer effect (Sánchez-de-la-Torre 2023, PMID 37787793). Mechanistic reviews cover the sympathetic and aldosterone links (Shiina 2024, PMID 39210083).

Other causes

  • Phaeochromocytoma and paraganglioma. Biochemical diagnosis rests on plasma or urinary metanephrines; a large minority carry germline mutations, so genetic testing is part of the diagnostic pathway rather than an afterthought (Pacak 2015, PMID 25716634; Eisenhofer 2012, PMID 22258313; Cano Megías 2016, PMID 27161309; Tanabe 2020, PMID 32778780). Presentations extend to paediatrics and to congenital cyanotic heart disease (Jain 2020, PMID 30603807; Jones 2023, PMID 37847359).
  • Coarctation of the aorta. Hypertension frequently persists or recurs after successful repair, including exercise-induced hypertension with normal resting pressure, and long-term surveillance is required (Panzer 2022, PMID 35282025; Salciccioli 2023, PMID 37476999; Ylinen 2022, PMID 35944231; Correia 2013, PMID 24239395; Toro-Salazar 2002, PMID 11867038; Ye 2025, PMID 40260103).
  • Chronic kidney disease. Both cause and consequence; covered in special populations (Burnier 2023, PMID 37053276; Ku 2019, PMID 30898362; Hamrahian 2017, PMID 27873228).
  • Drug- and substance-induced. NSAIDs, combined oral contraceptives, sympathomimetic decongestants, VEGF-pathway inhibitors, calcineurin inhibitors, erythropoiesis-stimulating agents, glucocorticoids, licorice and alcohol all raise pressure by identifiable mechanisms and are systematically under-elicited in history-taking (Grossman 2012, PMID 22195528; Foy 2019, PMID 31655781; Lovell 2017, PMID 28451850; Jurca 2016, PMID 27671491). See red flags and safety concerns.

Who to screen, and for what

Traditional triggers — resistant hypertension, hypokalaemia, early onset, severe or accelerated hypertension, adrenal incidentaloma, target-organ damage out of proportion to pressure — remain valid but, on the prevalence data above, are now known to be insensitive for primary aldosteronism specifically (Brown 2020, PMID 32449886; Monticone 2017, PMID 28385310). The 2025 Endocrine Society position of screening everyone with hypertension is the most consequential open policy question in this area (Adler 2025, PMID 40658480), and it is not yet reflected in the general hypertension guidelines — see guidelines.

Open questions

  • Universal aldosterone-renin screening in hypertension would generate a very large number of intermediate results in a population where the underlying trait is continuous. What is the false-positive burden, and has any health system modelled it? (Adler 2025, PMID 40658480; Brown 2020, PMID 32449886)
  • If the excess cardiovascular risk of medically treated primary aldosteronism is confined to those with persistently suppressed renin (Hundemer 2018, PMID 29129576), should renin be a treatment target in ordinary low-renin hypertension too? Renin-guided therapy has been randomised in a small primary-care resistant-hypertension pilot: blood-pressure change did not differ from aldosterone-antagonist care, but control was 62.5% versus 25% and fewer drugs were added (Egan 2016, PMID 27076600). The remaining gap is outcomes: RETAME-PA is randomising renin-guided mineralocorticoid-receptor-antagonist titration in primary aldosteronism with biochemical efficacy, not cardiovascular events, as its primary endpoint (Merabtine 2025, PMID 41419284; NCT06108427).
  • Does subclinical primary aldosteronism — an aldosterone-renin ratio below diagnostic threshold — warrant mineralocorticoid receptor antagonism, given its independent association with remodelling and incident hypertension? (Hundemer 2024, PMID 38031887)
  • SPARTACUS found CT non-inferior to adrenal vein sampling at one year in a modest sample (Dekkers 2016, PMID 27325147). Does that hold for long-term biochemical outcome in larger, more heterogeneous populations?
  • Is there any subgroup in whom renal-artery revascularisation improves hard outcomes, given two neutral trials and no positive one? (Cooper 2014, PMID 24245566; ASTRAL 2009, PMID 19907042)
  • Why does CPAP lower pressure only when pressure is uncontrolled, and does that pattern indicate a ceiling effect or a distinct responsive phenotype? (Pengo 2025, PMID 39401854)

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