Surgical Hypertension

1

What are the surgically correctable causes of hypertension?

Renovascular hypertension, pheochromocytoma, Cushing’s syndrome, primary hyperaldosteronism (Conn’s syndrome), coarctation of the aorta, and unilateral renal parenchymal disease. Surgical hypertension accounts for 5%–10% of all hypertensive patients.

2

Which form of surgical hypertension is most common?

Renovascular hypertension is the most common cause of surgical hypertension (approximately 3% of patients with hypertension), followed by primary hyperaldosteronism (1.5%), Cushing’s syndrome (0.5%), pheochromocytoma (0.1%–0.3%), and coarctation of the aorta (0.1%). However, in patients with resistant hypertension, defined as uncontrolled blood pressure despite the use of three or more antihypertensive agents, secondary forms of hypertension are much more prevalent. Renal artery stenosis may be present in up to 24% of patients with resistant hypertension. Also, primary aldosteronism is present 7%–20% of patients with resistant hypertension, particularly those with concurrent type 2 diabetes mellitus.

3

What are the most common causes of renovascular hypertension?

The two major causes of renovascular hypertension are atherosclerosis and fibromuscular dysplasia. Atherosclerosis causes about 90% of cases and affects men twice as often as women. It usually involves the ostium and proximal third of the main renal artery, although, in advanced cases, segmental and diffuse intrarenal atherosclerosis may also be observed. The second most common cause is fibromuscular dysplasia (10%). Fibromuscular dysplasia may affect the intima, media, or adventitia, although 90% of cases involve the media. It tends to affect women between 15 and 50 years of age, frequently involves the distal two-thirds of the renal artery, and is characterized by a beaded, aneurysmal appearance on angiography.

4

What clinical criteria support the pursuit of investigative studies for suspected renovascular hypertension?

Although no clinical characteristics are pathognomonic of renovascular hypertension, the following findings strongly suggest the presence of an underlying renal artery stenotic lesion:

• Hypertension in very young individuals or in women younger than 50 years of age (suggestive of fibromuscular dysplasia)

• Rapid onset of severe hypertension after age 50 years (suggestive of atherosclerotic renal artery stenosis)

• Hypertension refractory to three-drug regimens

• Accelerated or malignant hypertension

• Deterioration of renal function after the initiation of antihypertensive agents, especially angiotensin-converting enzyme (ACE) inhibitors

• Unilateral small kidney

• Systolic or diastolic upper abdominal or flank bruits

5

What is the renin-angiotensin-aldosterone system (RAAS)?

Renin is released from the juxtaglomerular apparatus of the kidney in response to changes in renal cortical afferent arteriolar perfusion pressure and sodium concentration. Renin acts locally and in the systemic circulation to cleave angiotensinogen, a nonvasoactive α ₂ globulin that is produced in the liver, to form angiotensin I. Angiotensin I undergoes enzymatic cleavage by ACE in the pulmonary circulation to produce angiotensin II, a potent vasopressor responsible for the vasoconstrictive element of renovascular hypertension. Angiotensin II increases adrenal gland production of aldosterone with subsequent retention of sodium, which acts to increase blood volume.

6

How do ACE inhibitors work?

Direct inhibition of ACE decreases concentrations of angiotensin II, which leads to decreased vasopressor activity and decreased aldosterone secretion. Removal of angiotensin II mediated negative feedback on renin secretion leads to increased plasma renin activity. A similar class of drugs, angiotensin receptor blockers (ARBs), antagonizes the action of angiotensin II at the angiotensin AT1-receptor. Because there are enzymatic pathways capable of converting angiotensin I to angiotensin II independent of ACE, there is a theoretical advantage to direct inhibition of angiotensin II using ARBs.