# Primary Hyperaldosteronism > Primary hyperaldosteronism for NEET-PG Medicine, covering Conn syndrome, aldosterone-renin ratio, saline suppression testing and adrenal vein sampling. - Canonical URL: https://prepelephant.com/topics/neet-pg/medicine/primary-hyperaldosteronism - Exam / course: NEET-PG · Subject: Medicine - Publisher: PrepElephant (https://prepelephant.com) — Prepared and reviewed by the PrepElephant Academic Review Team - First published: 2026-10-08 - Last updated: 2026-10-08 - Reference basis: Williams Textbook of Endocrinology; Endocrine Society Guideline on Primary Aldosteronism; Harrison's Principles of Internal Medicine - How to cite: "Primary Hyperaldosteronism", PrepElephant, https://prepelephant.com/topics/neet-pg/medicine/primary-hyperaldosteronism ## Direct answer Primary hyperaldosteronism is autonomous aldosterone production by the adrenal glands, causing hypertension, suppressed renin and often hypokalaemia, and it is a leading cause of secondary hypertension. Screening uses the aldosterone-to-renin ratio, and a positive result is confirmed with a suppression test such as saline infusion. Adrenal vein sampling separates a unilateral adenoma, which may be removed, from bilateral hyperplasia, which is treated medically. ## What you must remember - **Clinical clue:** hypertension with suppressed renin; hypokalaemia is common but not essential. - **Screening:** aldosterone-to-renin ratio drawn in the morning after potassium correction; cut-offs vary, but a ratio above about 20 to 30 with aldosterone above about 10 to 15 ng/dL and suppressed renin is usually taken as positive. - **Confirmation:** saline infusion, oral salt loading or captopril challenge; aldosterone that stays high confirms autonomous secretion. - **Subtyping:** CT of the adrenals, then adrenal vein sampling in selected patients, using cortisol-normalised aldosterone. - **Adenoma:** a unilateral aldosterone-producing adenoma is treated by laparoscopic adrenalectomy. - **Hyperplasia:** bilateral disease is treated with a mineralocorticoid receptor antagonist such as spironolactone or eplerenone. - **Interfering drugs:** ACE inhibitors, ARBs and diuretics raise renin and can produce false negatives. ## A woman with resistant hypertension and low potassium A 40-year-old woman has blood pressure of 168/102 mmHg on three drugs and a potassium of 2.9 mmol/L. Renin is suppressed, so an aldosterone-to-renin ratio is calculated after stopping interfering drugs for several weeks and correcting her potassium. 1. **Screen the ratio:** aldosterone is 22 ng/dL with suppressed renin, which is a positive screen. 2. **Confirm secretion:** a saline infusion test shows aldosterone that stays high, confirming autonomous secretion. 3. **Image the adrenals:** CT shows a 1.4 cm left adrenal nodule. 4. **Subtype the gland:** because the adenoma could be a bystander, adrenal vein sampling is performed to see which gland is overproducing. Lateralisation to the left side supports unilateral disease, and laparoscopic left adrenalectomy is planned. 5. **Prepare for surgery:** before surgery, the mineralocorticoid antagonist is used to correct potassium and blood pressure. 6. **Watch after operation:** the risk of postoperative hypoaldosteronism and hyperkalaemia is watched for, and blood pressure medicines are reduced gradually because pressure often falls sharply once the adenoma is removed. Had the sampling shown bilateral overproduction, a mineralocorticoid receptor antagonist would have been the appropriate long-term treatment. ## Where the exam tries to catch you Four traps recur in examiners' questions. - **Trap:** assuming a normal potassium excludes the diagnosis. — **Correct:** many patients are normokalaemic, so a normal potassium does not exclude primary hyperaldosteronism. - **Trap:** attributing hypertension to an incidental adrenal nodule. — **Correct:** confirm aldosterone excess first, since an incidental nodule on CT does not prove the diagnosis. - **Trap:** trusting the aldosterone-to-renin ratio on interfering drugs. — **Correct:** ACE inhibitors, ARBs and diuretics raise renin and can cause false negatives, while beta-blockers suppress renin and can cause false positives. - **Trap:** choosing spironolactone without asking about gynaecomastia. — **Correct:** spironolactone causes gynaecomastia, and eplerenone is chosen when that is a problem. ## Frequently asked questions ### What is the screening test for primary hyperaldosteronism? The aldosterone-to-renin ratio is the screening test for primary hyperaldosteronism. It is drawn in the morning after potassium is corrected, ideally with interfering drugs withdrawn where safe. A raised ratio with aldosterone above a common threshold is considered positive and needs confirmation. ### Which drugs can cause false negative aldosterone-renin ratio results? ACE inhibitors, ARBs and diuretics raise renin and can lower the ratio, producing false negatives. Beta-blockers and some other agents can cause false positives by suppressing renin. Interfering drugs are withdrawn for several weeks where this is safe. ### Why is adrenal vein sampling needed before surgery in primary hyperaldosteronism? Adrenal vein sampling is needed to determine whether overproduction comes from one gland or both. A unilateral adenoma can be cured by adrenalectomy, whereas bilateral hyperplasia requires medical treatment. CT alone cannot separate these conditions reliably, especially in older patients. ### What is the treatment for bilateral adrenal hyperplasia causing primary hyperaldosteronism? Bilateral adrenal hyperplasia causing primary hyperaldosteronism is treated with a mineralocorticoid receptor antagonist such as spironolactone or eplerenone. Blood pressure and potassium are controlled with this medical approach. Surgery is not indicated for bilateral disease. ### Which confirmatory test follows a positive aldosterone-renin ratio? A saline infusion test, oral salt loading or a captopril challenge can confirm primary hyperaldosteronism after a positive aldosterone-renin ratio. In each test, aldosterone that fails to suppress indicates autonomous production. The choice depends on the patient's safety and local expertise.