Causes of Secondary Hypertension — Evaluation and Treatment

Secondary hypertension is high blood pressure due to an identifiable and often correctable underlying cause.

It is uncommon in older adults overall, but should be actively considered in treatment-resistant hypertension and in those with diastolic pressures >115 mmHg.

Atherosclerotic renovascular hypertension and primary hyperaldosteronism occur more frequently in older persons than in the young.

Pheochromocytoma is uncommon in older adults and particularly unusual after age 75.

Renovascular disease — abdominal bruit, a rise in serum creatinine of >30% after starting an ACE inhibitor or ARB, and asymmetrical kidney size differing by >1.5 cm on ultrasound.

Renoparenchymal disease — often asymptomatic; raised urea and creatinine, small kidneys, and abnormal urinalysis.

Conn’s syndrome (primary hyperaldosteronism) — elevated serum aldosterone with resistant hypokalaemia.

Cushing’s syndrome — elevated serum cortisol, cushingoid facies, persistent hypokalaemia.

Pheochromocytoma — elevated urinary metanephrines, episodic sympathetic overactivity (headache, palpitation, sweating).

Hypothyroidism — constipation, bradycardia, high TSH with low thyroxine. Hyperthyroidism — diarrhoea, tachycardia, low TSH with high thyroxine.

Hyperparathyroidism — high serum calcium and PTH, constipation. Increasingly diagnosed with automated calcium testing, particularly in postmenopausal women; treating it may ameliorate the blood pressure.

Drugs — NSAIDs and corticosteroids are the commonest culprits; also sodium-containing antacids, antidepressants, nicotine, and oral contraceptives.

Obstructive sleep apnoea — daytime sleepiness and nocturnal snoring.

Excess alcohol — established by careful history taking.

Oestrogen therapy in the postmenopausal woman may cause hypertension; this can be tested by withdrawing oestrogen for several months and observing the blood pressure response.

Pseudohypertension — falsely elevated readings due to non-collapsible sclerotic arteries. Suspect it in apparently resistant hypertension with no end-organ damage. Detected by the Osler manoeuvre (radial artery remains palpable when the cuff is inflated above systolic pressure), which suggests a 10–15 mmHg error; confirmed by intra-arterial monitoring.

White-coat hypertension — high office but normal home BP. Masked hypertension — normal office but high home BP. Both need ambulatory or home BP monitoring.

Non-adherence and inadequate diuretic dosing are the commonest reasons for apparent resistance and must be excluded before labelling a patient resistant.

Resistant hypertension is BP uncontrolled despite three or more antihypertensive agents including a diuretic.

Initial laboratory evaluation: urinalysis, complete blood count, serum electrolytes and calcium, estimated GFR, fasting glucose, lipids, and a 12-lead ECG.

Second-line testing is directed by clinical suspicion — aldosterone-renin ratio, urinary metanephrines, TSH, renal Doppler/CT angiography, overnight dexamethasone suppression test, polysomnography.

Treat the cause where possible — adrenalectomy for aldosterone-producing adenoma or pheochromocytoma, parathyroidectomy for hyperparathyroidism, thyroid hormone replacement, CPAP for sleep apnoea, and withdrawal of the offending drug.

Spironolactone or eplerenone is the drug of choice in primary aldosteronism and in resistant hypertension generally. Eplerenone avoids gynaecomastia but both require careful potassium and renal function monitoring in older patients.

Renal artery revascularisation is reserved for flash pulmonary oedema, rapidly deteriorating renal function, or truly refractory hypertension — medical therapy is otherwise preferred.

Targets should be individualised by functional status rather than chronological age — approximately <130/80 mmHg in the independent older person, <140/90 in the partially dependent, and <150/90 in the dependent or frail.