Primary Aldosteronism Imaging Findings
Primary aldosteronism is a condition in which one or both adrenal glands produce too much aldosterone, a hormone that helps regulate sodium, potassium, fluid balance, and blood pressure. It is an important and frequently underdiagnosed cause of high blood pressure and may also cause low potassium. On imaging, primary aldosteronism may be associated with a small adrenal nodule, bilateral adrenal thickening or nodularity, unilateral adrenal enlargement, or adrenal glands that appear normal. Imaging alone usually cannot determine which adrenal gland is producing excess aldosterone. Biochemical testing and, in selected patients considering surgery, adrenal vein sampling are central to identifying the source and selecting treatment.
What is it?
The adrenal glands are two small triangular organs located above the kidneys. They produce several important hormones.
Aldosterone is produced by the zona glomerulosa, the outermost layer of the adrenal cortex. It acts mainly on the kidneys to increase sodium retention and potassium excretion, helping regulate blood volume and blood pressure.
Under normal circumstances, aldosterone production is regulated primarily by the renin-angiotensin system and by potassium levels. Aldosterone levels change in response to factors such as blood pressure, circulating blood volume, dietary sodium, and potassium.
Primary aldosteronism occurs when aldosterone production becomes relatively autonomous and renin is suppressed. Excess aldosterone promotes sodium retention, increases potassium loss, and contributes to high blood pressure. The body may partially compensate for sodium and water retention, so obvious swelling is not usually a prominent feature.
Primary aldosteronism is an important treatable cause of hypertension. Appropriate treatment can improve blood pressure and potassium levels and reduce the elevated cardiovascular and kidney risks associated with continued aldosterone excess.
Several subtypes are recognized.
An aldosterone-producing adenoma is a benign adrenal cortical nodule that produces aldosterone. These nodules are often small and may be less than two centimeters.
Bilateral primary aldosteronism involves aldosterone overproduction from both adrenal glands. The adrenal glands may appear enlarged or nodular, but they can also appear normal on imaging.
Unilateral adrenal hyperplasia causes aldosterone excess from one adrenal gland without a clearly defined adenoma.
Less common causes include familial forms of primary aldosteronism and rare aldosterone-producing adrenal cortical carcinomas.
Familial primary aldosteronism includes several genetically distinct conditions. Some present at a young age or occur in families with early hypertension, primary aldosteronism, or stroke.
The imaging appearance varies according to the underlying adrenal anatomy. CT may show a small, well-defined adrenal nodule with characteristics similar to a benign adrenal adenoma. It may instead show unilateral or bilateral nodularity, diffuse thickening, a larger atypical mass, or no visible abnormality.
A normal adrenal CT does not exclude primary aldosteronism because aldosterone-producing abnormalities may be too small to see. Likewise, a visible adrenal nodule may be a nonfunctioning incidental adenoma rather than the source of aldosterone excess.
Incidental adrenal nodules become more common with age. For this reason, selecting a gland for surgery solely from CT or MRI findings can result in removal of the wrong adrenal gland or ineffective treatment.
Primary aldosteronism should be considered in people with resistant or severe hypertension, hypertension with spontaneous or diuretic-associated hypokalemia, hypertension and an adrenal mass, or hypertension beginning at an unusually young age.
Screening may also be appropriate in people with a family history of primary aldosteronism or early-onset hypertension or stroke, as well as in certain patients with obstructive sleep apnea or disproportionate cardiovascular disease.
Many patients have no distinctive symptoms. Low potassium may cause weakness, cramps, palpitations, constipation, frequent urination, or excessive thirst, but hypokalemia occurs in only a minority of affected patients.
Primary aldosteronism carries health risks beyond the blood-pressure reading alone. Compared with people who have similar blood pressure without primary aldosteronism, affected patients have higher rates of atrial fibrillation, stroke, coronary disease, heart failure, and kidney damage.
Diagnosis begins with biochemical testing. Aldosterone and renin are measured and interpreted together, commonly through an aldosterone-to-renin ratio.
Because laboratory methods and diagnostic thresholds vary, results must be interpreted according to the specific assays, units, testing conditions, and clinical circumstances.
Potassium should be measured and corrected when low because hypokalemia can suppress aldosterone and potentially produce a misleading result.
Dietary sodium, body position, time of collection, kidney function, age, and numerous medications can affect aldosterone and renin. Mineralocorticoid receptor antagonists, diuretics, beta blockers, ACE inhibitors, angiotensin receptor blockers, and other medications may alter the result.
Some interfering medications may be temporarily changed when this can be done safely. In other patients, testing proceeds while medications are continued, with cautious interpretation and repeat testing when needed. Blood-pressure treatment should not be withdrawn when doing so would create an unacceptable risk.
Confirmatory suppression testing may be used after an abnormal screening result, although it is not required in every patient. The need for and choice of confirmatory testing depend on the strength of the biochemical findings, medications, potassium level, kidney and heart function, and the patient’s overall clinical circumstances.
Available tests include saline infusion, oral sodium loading with urinary aldosterone measurement, captopril challenge, and fludrocortisone suppression. Sodium-loading procedures may be unsuitable for some patients with uncontrolled hypertension, heart failure, advanced kidney disease, or significant fluid-overload risk.
After primary aldosteronism is biochemically established, adrenal CT is generally used to evaluate adrenal anatomy, identify large or suspicious lesions, and support procedural or surgical planning.
MRI may be used when CT is unsuitable or when additional tissue characterization is necessary. Neither CT nor MRI can reliably determine whether excess aldosterone production is unilateral or bilateral.
Adrenal vein sampling is a specialized procedure in which blood is collected from both adrenal veins and compared with peripheral blood. Aldosterone and cortisol measurements are used to assess successful sampling and determine whether aldosterone production is lateralized to one gland.
Adrenal vein sampling is generally recommended for appropriate surgical candidates when establishing unilateral disease would lead to adrenalectomy. The procedure is technically demanding and is best performed and interpreted by an experienced multidisciplinary team.
In carefully selected very young patients with spontaneous hypokalemia, marked biochemical primary aldosteronism, a solitary unilateral adenoma, and a normal opposite adrenal gland, surgery may occasionally be considered without adrenal vein sampling. Because imaging can still misidentify the source, this exception is used cautiously and decisions are individualized.
Important to Know
Treatment is based primarily on whether aldosterone excess is unilateral or bilateral, whether the patient is an appropriate surgical candidate, and the patient’s treatment preferences.
The goals are to control blood pressure, normalize potassium, reduce inappropriate mineralocorticoid-receptor activation, protect the cardiovascular system and kidneys, and cure unilateral disease when possible.
Care is usually coordinated by primary care clinicians and endocrinologists. Hypertension specialists, nephrologists, cardiologists, endocrine surgeons, and interventional radiologists may also be involved.
For confirmed unilateral primary aldosteronism, laparoscopic unilateral adrenalectomy is generally the preferred treatment for suitable surgical candidates.
Surgery often normalizes aldosterone and potassium. Blood pressure may be cured completely or may improve while still requiring medication. The likelihood of complete blood-pressure cure depends on factors such as age, duration of hypertension, number of medications, vascular health, kidney function, and other causes of hypertension.
Before surgery, a mineralocorticoid receptor antagonist and potassium supplementation may be used to improve blood pressure and correct hypokalemia.
After surgery, potassium supplements and mineralocorticoid receptor antagonists are usually stopped or reassessed under medical supervision. Blood pressure, potassium, kidney function, aldosterone, and renin are monitored.
Adrenal insufficiency is not expected after uncomplicated unilateral adrenalectomy for isolated aldosterone excess. However, some adrenal nodules produce both aldosterone and cortisol. Cortisol evaluation may therefore be appropriate before surgery, and temporary glucocorticoid treatment may be needed if postoperative adrenal insufficiency develops.
Patients with bilateral primary aldosteronism are generally treated medically. Mineralocorticoid receptor antagonists block aldosterone’s effects and are the mainstay of treatment.
Spironolactone is commonly used and is effective, but it can cause breast tenderness or enlargement, menstrual changes, reduced libido, or other sex-hormone-related adverse effects.
Eplerenone is more selective and generally causes fewer sex-hormone-related effects, although it may require more frequent dosing and can be more expensive.
Medication doses are adjusted according to blood pressure, potassium, kidney function, tolerance, and the biochemical response. Both spironolactone and eplerenone can cause high potassium, particularly in patients with kidney impairment, so laboratory monitoring is essential.
Selected patients with bilateral disease and strongly asymmetric adrenal vein sampling results may sometimes be considered for unilateral surgery when medical treatment is ineffective or poorly tolerated. Surgery in this setting may improve disease control but is less likely to provide a complete biochemical cure than surgery for clearly unilateral disease.
Familial hyperaldosteronism type 1, also called glucocorticoid-remediable aldosteronism, may be treated with carefully selected low-dose glucocorticoid therapy to suppress abnormal ACTH-dependent aldosterone production. Treatment requires specialist supervision to avoid excessive glucocorticoid exposure.
Other familial forms are managed according to their genetic cause, biochemical subtype, and whether disease is unilateral or bilateral. Genetic counseling and testing may be appropriate in young patients and families with early hypertension, primary aldosteronism, or early stroke.
Aldosterone-producing adrenal cortical carcinoma is extremely rare. A large or radiologically suspicious adrenal mass requires specialized evaluation and should not be assumed to be a benign aldosterone-producing adenoma.
Lifestyle measures support medical or surgical treatment but do not replace condition-specific therapy. Reducing excessive dietary sodium can lessen aldosterone’s effects and may improve blood-pressure control.
Regular physical activity, achieving a healthy weight, avoiding tobacco, and managing diabetes and cholesterol can further reduce cardiovascular risk.
Alcohol guidance should be individualized. Patients who do not drink alcohol do not need to begin, and those who do should discuss safe limits with their healthcare professional.
Biopsy has no routine role in determining whether primary aldosteronism is unilateral or bilateral. It cannot establish whether an adrenal nodule is producing aldosterone.
When an invasive procedure is being considered for an indeterminate adrenal mass, pheochromocytoma must be considered and excluded when clinically appropriate because biopsy or surgical manipulation can trigger a dangerous catecholamine surge.
Patients who undergo unilateral adrenalectomy generally retain normal overall adrenal function through the remaining gland. Temporary glucocorticoid treatment may be necessary in selected patients with coexisting cortisol excess or evidence of postoperative adrenal insufficiency.
Long-term follow-up remains important after either surgical or medical treatment. Monitoring may include blood pressure, medication requirements, potassium, kidney function, aldosterone, renin, and cardiovascular health.
Patient education should explain why biochemical testing and adrenal vein sampling may be necessary even when imaging shows an apparently clear adrenal nodule. Imaging identifies anatomy, while biochemical testing and adrenal vein sampling determine hormonal function.
Red-flag symptoms include very high blood pressure with severe headache, chest pain, shortness of breath, confusion, palpitations, or visual changes; sudden weakness, facial drooping, difficulty speaking, or other possible signs of stroke; severe muscle weakness or paralysis; irregular heartbeat with dizziness or fainting; or rapid clinical deterioration.
These symptoms require immediate medical evaluation because they may indicate a hypertensive emergency, severe potassium disturbance, stroke, cardiac arrhythmia, or another serious complication.