Secondary hypertension

Morris J. Brown and Fraz Mir

in Oxford Textbook of Medicine

Fifth edition

Published on behalf of Oxford University Press

Published in print May 2010 | ISBN: 9780199204854
Published online May 2011 | e-ISBN: 9780199570973 | DOI:

Series: Oxford Textbooks

Secondary hypertension

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The term ‘secondary hypertension’ is used to describe patients whose blood pressure is elevated by a single, identifiable cause, with an important subdivision being into reversible and irreversible causes: clinically, it is important to exclude the former, but not necessarily to find the latter.

In the first two decades of life, the prevalence of secondary hypertension is greater than that of essential hypertension; thereafter, a patient is much more likely to have essential hypertension, but investigations for secondary hypertension should still be assiduous in the twenties and thirties because the alternative entails so many years of tablet-taking.

All patients with hypertension should have a minimum set of investigations (see Chapter 16.7.2). Common indications for further investigations are (1) any evidence of an underlying cause on history or examination; (2) proteinuria, haematuria, or elevated serum creatinine (eGFR<30; CKD 4/5); (3) hypokalaemia, even if caused by diuretics; (4) accelerated (malignant) hypertension; (5) documented recent onset or recent worsening of hypertension; (6) resistant hypertension (not controlled with three antihypertensive drugs); (7) young age—any hypertension at less than 20 years; any hypertension needing treatment at less than 35 years.

The minimum screen in younger patients should include plasma bicarbonate, plasma renin, and a 24-h urine test to exclude phaeochromocytoma; 24-h electrolyte excretion should be measured either in all patients, or in those with abnormal renin levels.

Renovascular hypertension

This is most commonly due to intrinsic disease of the intima (acquired, atherosclerosis, etc.) or media (congenital, fibromuscular dysplasia (FMD), etc.). FMD accounts for only 10–20% of all cases, but is the commonest cause under the age of 40.

Most cases of renovascular hypertension are probably not diagnosed because of the absence of sensitive clinical or biochemical markers. The main clinical clue is the finding in 50% of cases of a bruit anteriorly or posteriorly over a renal area, but it is important to remember that such a bruit is never diagnostic. The diagnosis is made radiologically, most commonly by CT or MR angiography.

In FMD, angioplasty is usually curative, with about three-quarters of patients able to discontinue antihypertensive treatment. In atheromatous disease, angioplasty is much less likely to be successful: complete cure of hypertension is rare, and often the purpose of intervention is to protect declining renal function.

Coarctation of the aorta

Coarctation causes less than 1% of all cases of hypertension. The classical clinical finding is radio–femoral pulse delay. Diagnosis is confirmed by two-dimensional echocardiography, or by CT or MR angiography. Treatment is by surgery, balloon dilatation, or stenting.

Primary hyperaldosteronism (Conn’s syndrome)

Primary hyperaldosteronism causes increased sodium retention through the epithelial sodium channel (ENaC) in the distal tubule and cortical collecting duct, which leads to hypertension. It can be caused by (1) Conn’s adenoma—a small (0.5–3.5 cm) benign tumour of the adrenal gland; (2) bilateral adrenal hyperplasia—where there are macro- or micronodules in the adrenal cortex; (3) the very rare condition of glucocorticoid-remediable aldosteronism (see Chapter 16.7.4).

Diagnosis—the classic clinical picture is hypertension with plasma electrolytes showing low K+, elevated bicarbonate, and Na+ typically at the upper end of the normal range, together with suppressed plasma renin and elevated aldosterone—but these findings are not invariable and diagnosis can be difficult. The adrenals are usually easily imaged by either CT or MRI, but functional lateralization can be difficult, although essential for predicting that removal of one adrenal will have a substantial benefit, as well as indicating which adrenal to remove. The most reliable technique is adrenal vein sampling: all samples need to be assayed for aldosterone and cortisol, with the ratio compared between the two sides.

Management—medical treatment is preferred for bilateral adrenal hyperplasia, before surgery for adenoma, in older patients with adenoma who are well controlled, or where there is any doubt about diagnosis or lateralization. High doses of spironolactone or amiloride are most commonly used. Elective surgery is indicated for younger patients with macroadenoma, and older patients intolerant of—or uncontrolled by—medical treatment.


Phaeochromocytomas are rare tumours of chromaffin tissue that account for 0.1 to 1% of cases of hypertension: 90% are benign and 90% are located in the adrenal gland. Most are sporadic, but some are associated with genetic syndromes, including von Hippel–Lindau and multiple endocrine neoplasia type 2.

Hypertension, usually in association with one or more symptoms of headache, sweating, and palpitations, is the most common presentation. Other rarer presentations include unexplained heart failure or paroxysmal arrhythmia. Four per cent of adrenal incidentalomas are phaeochromocytomas.

Diagnosis—this is usually not difficult once the possibility of phaeochromocytoma has been entertained; more difficult is excluding the diagnosis in patients who have clinical and/or biochemical features of physiological catecholamine excess. Investigation must first determine whether the patient has a phaeochromocytoma, and then where the tumour is. The best screening test is to measure plasma or 24 h urine normetanephrine (normetadrenaline) and metanephrine (metadrenaline): their assay in a reliable laboratory is more sensitive and specific than measurement of catecholamines or vanillylmandelic acid (VMA). Detection of elevated metadrenaline is a useful clue to the usual adrenal location of the phaeochromocytoma. A pharmacological suppression test can be performed where doubt about the diagnosis remains: physiological elevations of noradrenaline release are temporarily suppressed by administration of the ganglion-blocking drug pentolinium, or the centrally acting α2-agonist clonidine, but these drugs do not suppress autonomous secretion by tumour. CT or MRI scanning usually provides excellent imaging of the adrenal. Radioisotope scanning with the iodinated analogue of noradrenaline, m-iodobenzylguanidine (mIBG), can be helpful in localizing extra-adrenal tumours. Selective venous sampling is occasionally required.

Management—the task for the physician is to make surgery—the definitive treatment that cures hypertension in most patients—safe. This should be done by α-blockade with phenoxybenzamine, with a low dose of a β1-selective blocker used to prevent tachycardia.

Chapter.  10561 words.  Illustrated.

Subjects: Cardiovascular Medicine

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