Primary Aldosteronism: When a Hormone Disorder Drives High Blood Pressure

High blood pressure is not always “essential” hypertension. In primary aldosteronism (PA), one or both adrenal glands produce aldosterone partly independently of the body’s normal renin control system. The result can be sodium retention, suppressed renin, persistent or resistant hypertension, and—sometimes, but not always—low potassium.

Direct answer: Primary aldosteronism screening is built around the relationship between aldosterone and renin, not potassium alone. A pattern of suppressed renin with aldosterone that is inappropriately active for that renin level—usually assessed with an aldosterone-to-renin ratio (ARR)—raises concern. Potassium, kidney function, medications, sodium intake, posture, collection time, assay method, units, and blood-pressure history all affect interpretation.

Medical note: Laboratory testing can identify a biochemical pattern that warrants evaluation, but it does not by itself determine whether PA is unilateral or bilateral, whether an adrenal nodule is the source, or whether surgery is appropriate. Medication changes, suppression testing, adrenal imaging, adrenal venous sampling, and treatment decisions should be clinician directed.

Part of the Ulta Lab Tests Knowledge Center

This condition-specific guide complements the Hypertension Lab Tests: What Blood and Urine Testing Can Reveal After a High Reading hub.

For broader context, see Heart Health Blood Tests, Kidney Function Tests, Endocrine Disorders: Causes, Symptoms, Lab Tests, and Management, and the Blood Biomarker Ratios Guide.

For testing fundamentals and result interpretation, use The Complete Guide to Lab Tests and Blood Work, How to Read and Understand Your Lab Results, and Direct-Access Lab Testing: How It Works and What to Expect.

Key Takeaways

• Normal potassium does not rule out primary aldosteronism. Many affected people are not hypokalemic.
• The most useful screening pattern is aldosterone + renin + ARR, with potassium measured at the same time.
• An aldosterone result that appears “normal” can still be inappropriate when renin is strongly suppressed.
• ARR cutoffs depend on the renin method, aldosterone assay, units, laboratory, and clinical context; an internet cutoff should not be applied blindly.
• Low potassium can suppress aldosterone and create a falsely reassuring result.
• Blood-pressure medicines can push renin and aldosterone in different directions. Do not stop antihypertensive medication on your own to prepare for testing.
• A suspicious negative screen may need to be repeated after a correctable confounder is addressed.
• A positive screening pattern does not reveal which adrenal gland is responsible.
• Suppression testing, imaging, and adrenal venous sampling answer different questions and should be clinician directed.
• After treatment, blood pressure, potassium, kidney function, and renin can become important monitoring markers.

Primary Aldosteronism at a Glance

Question	What matters most	Why it changes the next step
Is aldosterone escaping normal renin control?	Suppressed renin + aldosterone inappropriate for that renin level + elevated ARR	This is the central screening pattern for PA.
Does potassium exclude PA?	No. Potassium may be normal.	Waiting for hypokalemia can miss cases; low potassium can also lower aldosterone and distort screening.
Can one ARR diagnose PA?	Not always. Assay, units, medicines, kidney function, sodium intake, posture, timing, and potassium matter.	Borderline or discordant results may require repeat testing or clinician-directed confirmation.
Does CT show which gland is responsible?	CT shows anatomy, not necessarily hormone production.	Adrenal venous sampling is often used to establish functional laterality before surgery.
What is monitored after treatment?	Potassium, creatinine/eGFR, renin, and blood pressure	These markers help assess physiologic response and treatment safety.

What Is Primary Aldosteronism?

Aldosterone is a mineralocorticoid hormone made by the adrenal cortex. It helps regulate sodium, potassium, circulating volume, and blood pressure. Under ordinary physiology, the kidneys participate in a renin–angiotensin–aldosterone system that increases aldosterone when the body needs to conserve sodium and maintain circulation.

In primary aldosteronism, aldosterone production becomes partly independent of that normal renin signal. Renin becomes suppressed while aldosterone remains inappropriately active. The kidney retains more sodium and may lose more potassium and hydrogen ions, contributing to hypertension, hypokalemia, or metabolic alkalosis in some patients.

The word primary is important. In secondary hyperaldosteronism, renin is usually activated first—for example, when the kidney senses reduced effective circulation—and aldosterone rises in response. PA is instead characterized by aldosterone production that is inappropriate for a suppressed-renin state.

Why Primary Aldosteronism Matters Beyond the Blood Pressure Number

PA is clinically important because it is a potentially targetable cause of hypertension. Compared with people who have otherwise similar primary hypertension, untreated PA is associated with greater cardiovascular and kidney risk. Once the biochemical disorder is recognized, treatment can be directed at the underlying mechanism rather than only at the blood-pressure reading.²

The broader cardiovascular and kidney picture still matters. The hypertension lab testing hub explains how urine albumin-to-creatinine ratio, creatinine/eGFR, glucose testing, lipid testing, and other markers help define organ effects and cardiometabolic risk without duplicating the disease-specific PA workup here.

Who Should Be Screened for Primary Aldosteronism?

The 2025 Endocrine Society guideline represents a major shift: it conditionally suggests screening all individuals with hypertension for PA when the health system has the resources, expertise, and follow-up capacity to do so.¹ This is a conditional suggestion rather than an instruction that every person must be screened in every setting.

Even where broad screening is not feasible, the case for testing is especially compelling when the clinical pattern includes:

• Resistant hypertension or pressure that is becoming progressively harder to control
• Stage 2 hypertension
• Spontaneous or diuretic-associated hypokalemia
• Hypertension with obstructive sleep apnea
• An adrenal incidentaloma together with hypertension
• Hypertension beginning at a relatively young age
• A strong family history of early hypertension, known PA, or premature stroke
• Atrial fibrillation without a clear structural or thyroid explanation
• Hypertension requiring several medications

These features increase the pretest probability, but their absence does not rule PA out.

The Key Screening Pattern: Aldosterone + Renin + ARR

An isolated aldosterone value is difficult to interpret. A result can fall inside a laboratory reference interval yet still be inappropriate when renin is nearly completely suppressed. Conversely, aldosterone may be elevated in circumstances where renin is also appropriately elevated.

The screening question is therefore relational:

Is aldosterone inappropriately active despite suppressed renin?

The most direct Ulta option is the Aldosterone and Plasma Renin Activity Ratio Test. Individual Aldosterone and Plasma Renin Activity tests may also be used when clinically appropriate, but interpretation should preserve the relationship between the two measurements.

Do not use the ratio alone. A very high ARR can result from renin approaching zero even when aldosterone is not convincingly elevated. Clinicians review the ARR together with the absolute aldosterone and renin values, the assay, the units, potassium, medications, kidney function, and the clinical probability of PA.

How to Understand ARR Thresholds Without Treating Them as Universal Cutoffs

The 2025 guideline provides practical guidance for commonly used assays. In its framework, a positive screen generally requires suppressed renin, aldosterone that is sufficiently high for the assay and physiologic context, and an elevated aldosterone-to-renin relationship.¹

Examples include:

• Plasma renin activity at or below approximately 1 ng/mL/hour, or direct renin concentration at or below approximately 8.2 mU/L
• Aldosterone at least approximately 10 ng/dL by immunoassay, or approximately 7.5 ng/dL by LC-MS/MS
• An aldosterone-to-PRA ratio generally above 20 when aldosterone is expressed in ng/dL and PRA in ng/mL/hour

These are guidance thresholds, not universal biological dividing lines. Laboratories may use different assays, units, reference information, and validated cutoffs. Interpretation should use the method and reference information on the actual laboratory report.¹

Why PRA vs. Direct Renin and Immunoassay vs. LC-MS/MS Matter

Plasma renin activity and direct renin concentration are different measurements and are not numerically interchangeable. Aldosterone measured by immunoassay and aldosterone measured by liquid chromatography–tandem mass spectrometry can also produce systematically different values. In the 2025 guideline framework, the ARR threshold associated with LC-MS/MS aldosterone is approximately 25% lower than the immunoassay threshold.²

Practical rule: Never copy an ARR cutoff from an online chart without first knowing how aldosterone and renin were measured and which units appear on the report.

Why Normal Potassium Does Not Rule Out Primary Aldosteronism

The older stereotype of PA was “high blood pressure plus low potassium.” That misses many patients. Most people with PA do not need to be hypokalemic for the condition to be present.

Potassium still matters for two reasons:

1. Low potassium can be a consequence of aldosterone excess.
2. Hypokalemia can itself suppress aldosterone secretion enough to make an initial screen look less abnormal than it should.

When suspicion remains high and potassium is low, correction into the laboratory reference range and repeat aldosterone-renin testing may be appropriate under clinician guidance.¹

Direct answer: Normal potassium does not exclude PA. Low potassium can paradoxically make aldosterone look falsely low, so potassium is both a clinical clue and an interpretation variable.

Primary Aldosteronism Lab Tests: What to Order and What Each Adds

The highest-value starting set is intentionally focused. Broader diabetes, lipid, thyroid, anemia, or autoimmune testing belongs in a general hypertension or symptom-directed evaluation rather than being presented as if it confirms PA.

Test and quick facts	What it shows and how it is used	Preparation, influences, and limitations
CORE Aldosterone and Plasma Renin Activity Ratio Test Blood	Measures aldosterone and plasma renin activity and calculates the ARR. Helps identify a suppressed-renin/inappropriate-aldosterone screening pattern.	Strongly affected by medication classes, potassium, sodium intake, posture, collection time, kidney function, and assay method. A positive screen does not establish unilateral disease.
CORE Aldosterone Test Blood	Measures circulating aldosterone. The value is most meaningful when interpreted with renin rather than alone.	Assay method and collection conditions matter. Hypokalemia can lower aldosterone and cause a misleading result.
CORE Plasma Renin Activity Test Blood	Shows renin activity. Marked renin suppression is central to the PA pattern and can later become a treatment-response marker.	Diuretics, MRAs, ACE inhibitors, ARBs, beta blockers, central alpha-2 agonists, sodium intake, kidney disease, and posture can shift renin substantially.
CORE Potassium Test Blood	Identifies hypokalemia or hyperkalemia, supports aldosterone interpretation, and helps assess treatment safety.	Normal potassium does not exclude PA. Low potassium may suppress aldosterone. Supplements and medication changes should be clinician directed.
SUPPORTING Comprehensive Metabolic Panel or Basic Metabolic Panel Blood	Adds sodium, potassium, carbon dioxide/bicarbonate, creatinine, glucose, and other kidney and electrolyte context.	Does not diagnose PA. Serum sodium is not a measurement of dietary sodium intake.
SUPPORTING Creatinine with eGFR Blood	Estimates kidney filtration. Kidney function affects screening interpretation and becomes central to treatment safety.	CKD can alter renin and aldosterone physiology. Creatinine is also influenced by muscle mass, acute illness, hydration, and some medicines.
SUPPORTING Sodium Test Blood	Adds electrolyte context and may be included in a metabolic panel.	Serum sodium does not show how much salt a person eats. Intentional sodium restriction before PA screening can alter renin-aldosterone physiology.
SUPPORTING Magnesium Test Blood	May be useful when cramps, arrhythmia, diuretic use, or multiple electrolyte abnormalities are present.	Not a PA screening test and should not be interpreted as evidence for or against PA.
SUPPORTING CARDIORENAL Urine Albumin-to-Creatinine Ratio Urine	Assesses albumin leakage and kidney/cardiovascular risk in a person with hypertension.	Does not diagnose PA. Temporary illness, exercise, infection, urinary bleeding, or menstrual bleeding can raise UACR.

How to Prepare for Aldosterone and Renin Testing

Collection conditions matter because the renin-aldosterone system responds quickly to volume, sodium, potassium, posture, and medication effects. Current guidance favors morning screening with the person seated, potassium measured at the same time, and no deliberate dietary sodium restriction during the preceding few days.¹

• Follow the specific collection instructions. Timing and posture should match the laboratory protocol.
• Do not intentionally restrict sodium solely to “improve” the test. Sodium restriction can stimulate renin and change the screening pattern.
• Know the potassium result. If potassium is low, the screen may underestimate aldosterone.
• Record all blood-pressure medicines and doses. Include recent changes.
• Do not salt-load, potassium-load, or stop medications independently. Diagnostic accuracy must be balanced against blood-pressure, electrolyte, and kidney safety.

Medications Can Change the Aldosterone-to-Renin Ratio

Modern PA evaluation recognizes that medication withdrawal is not always safe or practical. The Endocrine Society provides no-withdrawal, minimal-withdrawal, and fuller-withdrawal strategies that clinicians can choose based on safety and the probability of disease.¹

Medication pattern	Possible effect on screening	What the patient should do
Mineralocorticoid receptor antagonists, amiloride, triamterene, and other diuretics	Can raise renin and make a PA pattern less obvious, creating a possible false-negative-looking result.	Do not stop independently. Record the drug and dose and review the result with the clinician who manages blood pressure.
ACE inhibitors and ARBs	Can raise renin and/or lower aldosterone, potentially reducing the ARR.	Do not change therapy solely for a direct-access test without clinician guidance.
Beta blockers and centrally acting alpha-2 agonists	Can suppress renin and make the ARR appear higher, creating a possible false-positive-looking pattern.	Interpret aldosterone, renin, and ARR in the context of medication exposure.

The practical takeaway is not “stop the interfering drug.” It is:

Know the medication pattern before interpreting the laboratory pattern.

How to Understand a Positive, Negative, or Borderline PA Screen

Positive-Looking Pattern

Suppressed renin together with aldosterone that is inappropriately high and an elevated ARR supports renin-independent aldosterone secretion. The strength of that conclusion depends on the assay, units, potassium, medications, kidney function, and clinical probability.

Negative-Looking Pattern

A negative screen is more reassuring when potassium is normal, preparation was appropriate, the medication pattern does not strongly favor a false negative, and pretest probability is low. It is less reassuring when resistant hypertension, hypokalemia, or a strongly interfering medication is present.

Borderline or Discordant Pattern

Examples include suppressed renin with aldosterone near the laboratory decision range, an elevated ARR driven almost entirely by extremely low renin, or a negative ratio while taking a medicine known to raise renin. These situations often call for clinical review rather than a simple yes/no interpretation from one calculation.

When Repeat Testing May Be Appropriate

A single negative ARR does not always end the evaluation. Repeat aldosterone-renin testing may be reasonable when:

• Hypokalemia was present during the first test
• A medication pattern could have produced a false negative
• Resistant hypertension or another strong clinical feature creates substantial pretest probability
• Renin is suppressed but aldosterone falls into a borderline range
• Collection conditions were not standardized
• Clinical suspicion remains high despite the first result

A useful sequence is:

Identify the possible confounder → correct or account for it safely → repeat under better-defined conditions → compare the full aldosterone-renin pattern.

What Happens After a Positive Primary Aldosteronism Screen?

Screening is only the first layer. The next question is whether the evidence is strong enough to proceed directly to subtype and treatment planning or whether a clinician-directed aldosterone-suppression test would clarify the diagnosis.

Suppression Testing Is Clinician Directed

Examples include saline suppression, oral sodium suppression, and the captopril challenge. These procedures have defined protocols and safety restrictions. Salt-loading or saline-suppression experiments should not be attempted independently, particularly in people with uncontrolled hypertension, heart failure, substantial kidney disease, or risk of fluid overload.²

Under the 2025 guideline, suppression testing is not automatically required after every positive ARR. It is most useful when the probability of lateralizing PA remains intermediate and the patient is considering surgery. It may be bypassed when the biochemical evidence is very strong or when the person will pursue PA-specific medical treatment rather than surgery.¹

One example of overt biochemical evidence described by the guideline is resistant hypertension or hypertension with hypokalemia together with:

• PRA below 0.2 ng/mL/hour, or direct renin below 2 mU/L
• Aldosterone above 20 ng/dL by immunoassay, or above 15 ng/dL by LC-MS/MS

These values are not stand-alone self-diagnostic cutoffs. They are part of a clinician-directed decision about whether suppression testing adds useful information.¹

Unilateral vs. Bilateral PA: Why CT and Adrenal Venous Sampling Answer Different Questions

After PA is established, treatment depends heavily on whether aldosterone excess comes predominantly from one adrenal gland or from both.

• Unilateral/lateralizing PA: A surgically suitable patient may be considered for unilateral adrenalectomy.
• Bilateral PA or nonsurgical management: Treatment is generally medical with a mineralocorticoid receptor antagonist.

Adrenal CT identifies anatomy, but a visible nodule is not automatically the aldosterone-producing source. Nonfunctioning adrenal nodules become more common with age. For patients considering surgery, adrenal venous sampling is generally used with CT to establish functional laterality.¹

A limited exception may apply to a younger patient—roughly under age 35—with marked PA, hypokalemia, and a clear unilateral adrenal adenoma larger than 1 cm, after specialist review. This is not a rule for self-selection; it is an expert-level decision.¹

When an Adrenal Adenoma Is Present, Cortisol May Need to Be Evaluated Too

Some adrenal adenomas can participate in more than one hormonal abnormality. The 2025 guideline suggests a 1-mg overnight dexamethasone suppression test when PA coexists with an adrenal adenoma.¹

In the guideline protocol, dexamethasone is taken late at night and serum cortisol is measured the next morning. A post-dexamethasone cortisol above 1.8 µg/dL suggests autonomous cortisol secretion and warrants further endocrine evaluation.¹

A stand-alone Cortisol Total Test is not equivalent to a clinician-directed dexamethasone suppression protocol. Medication timing, cortisol timing, and interpretation are part of the protocol.

Monitoring After Surgery or Mineralocorticoid Receptor Antagonist Therapy

After Unilateral Adrenalectomy

Follow-up commonly centers on potassium, creatinine/eGFR, blood pressure, medication requirements, and—when clinically appropriate—aldosterone and renin. The goal is correction of the renin-independent aldosterone state and its physiological consequences, not simply removal of a nodule.

During MRA Therapy

For bilateral PA, uncertain laterality, or nonsurgical care, a mineralocorticoid receptor antagonist such as spironolactone or a more selective alternative may be used under medical supervision. Monitoring includes potassium, kidney function, renin, and blood pressure.¹

Why Renin Can Become a Treatment Marker

Untreated PA usually suppresses renin. With adequate mineralocorticoid receptor blockade, renin often rises. In patients whose hypertension remains uncontrolled and whose renin remains suppressed, current guidance suggests clinician-directed intensification of PA-specific therapy to produce a rise in renin when potassium, kidney function, and blood pressure allow. The guideline does not specify one universal numerical renin target.¹

A useful treatment-response pattern is:

Blood pressure improving + potassium safe + renin no longer fully suppressed + kidney function stable.

Common Primary Aldosteronism Lab Patterns

• Hypertension + low potassium + suppressed renin + elevated aldosterone/ARR: Strongly supports renin-independent aldosterone production. Potassium still needs correction because hypokalemia can distort repeat testing.
• Resistant hypertension + normal potassium + suppressed renin + elevated ARR: Normal potassium does not rule PA out.
• Suppressed renin + modest aldosterone while taking a beta blocker: Possible false-positive-looking ARR because renin may be medication-suppressed.
• Resistant hypertension + negative ARR while taking an MRA: Possible false-negative-looking result because renin may rise on therapy.
• Low renin + borderline aldosterone + CKD: Interpretation can be more difficult because kidney disease alters renin and aldosterone physiology.
• Confirmed PA + unilateral adrenal nodule on CT: Anatomy alone usually does not prove the nodule is the functional source; AVS may be needed before surgery.
• MRA therapy + rising potassium + falling eGFR: Treatment safety takes priority and requires prompt clinician review.

Testing Cautions and Common Mistakes

• Do not use potassium as the screening test. Most PA is not identified by waiting for hypokalemia.
• Do not interpret aldosterone without renin. The relationship is the point.
• Do not interpret ARR without knowing the assay and units. PRA and direct renin are not interchangeable.
• Do not deliberately restrict sodium before routine screening unless instructed.
• Do not stop blood-pressure medication on your own.
• Do not assume one negative ARR permanently excludes PA. Confounding conditions can matter.
• Do not assume one positive ARR proves unilateral disease.
• Do not assume an adrenal nodule is the source.
• Do not perform salt-loading or saline-suppression protocols independently.
• Do not increase an MRA dose on your own because renin remains low. Potassium, kidney function, and blood pressure must be monitored together.

When Prompt Medical Evaluation Is Needed

Direct-access testing is not an emergency pathway. Prompt or urgent medical evaluation is appropriate for:

• Very high blood pressure with chest pain, severe shortness of breath, new neurologic symptoms, confusion, or visual change
• Severe hypokalemia
• Palpitations, fainting, or a significant arrhythmia together with an electrolyte abnormality
• Marked muscle weakness with low potassium
• Rapid worsening of kidney function
• Significant hyperkalemia after starting or increasing an MRA
• Resistant hypertension accompanied by rapidly progressive organ injury
• An adrenal mass with substantial hormonal abnormalities

A blood-pressure reading above 180/120 mm Hg together with new chest pain, shortness of breath, weakness, numbness, vision change, difficulty speaking, or another concerning symptom requires emergency assessment.⁴

How Ulta Lab Tests Can Help

Ulta Lab Tests offers direct access, where available, to focused testing that can make the PA biochemical pattern visible. The Aldosterone and Plasma Renin Activity Ratio Test is the most directly aligned single order.

Individual Aldosterone, Plasma Renin Activity, Potassium, Comprehensive Metabolic Panel, Creatinine with eGFR, and Urine Albumin-to-Creatinine Ratio tests can add specific context when clinically appropriate.

Direct access does not turn screening into a complete diagnosis. A qualified healthcare professional—often a primary-care clinician, hypertension specialist, endocrinologist, nephrologist, or adrenal specialist—should interpret a positive, negative, or discordant pattern in the context of medications, kidney function, collection conditions, and treatment goals.

Explore high blood pressure testing options at Ulta Lab Tests or review hormone testing options.

Recommended Lab Tests Discussed in This Article

The appropriate test selection depends on the individual’s blood-pressure pattern, medications, potassium level, kidney function, symptoms, previous results, and healthcare-provider guidance.

Core Primary Aldosteronism Screening

Aldosterone and renin are interpreted together, usually through the aldosterone-to-renin ratio. Potassium is measured at the same time because low potassium can make aldosterone appear falsely low.

• Aldosterone and Plasma Renin Activity Ratio Test
• Aldosterone Test
• Plasma Renin Activity Test
• Potassium Test

Kidney Function and Electrolyte Context

CMP or BMP, creatinine with eGFR, sodium, potassium, and magnesium provide kidney, electrolyte, and treatment-safety context. These tests do not diagnose primary aldosteronism by themselves.

• Comprehensive Metabolic Panel
• Basic Metabolic Panel
• Creatinine with eGFR
• Sodium Test
• Magnesium Test

Kidney Damage and Cardiorenal Risk

UACR evaluates albumin leakage and cardiorenal risk in people with hypertension. It provides useful health context but does not diagnose primary aldosteronism.

• Albumin, Random Urine with Creatinine — UACR

Adrenal and Cortisol Evaluation

When primary aldosteronism coexists with an adrenal adenoma, a clinician may recommend a formal 1-mg overnight dexamethasone suppression test. A stand-alone cortisol measurement is not equivalent to that protocol.

• Cortisol Total Test

Related Health Resources

• High Blood Pressure Tests
• Hormone Tests
• Endocrine Tests
• Kidney Tests
• Heart & Cardiovascular Tests
• Kidney Health Tests

Questions to Ask Your Healthcare Provider

• Does my hypertension pattern make primary aldosteronism screening appropriate?
• Which of my medications could change renin, aldosterone, or the ARR?
• Should I remain on my current medicines for the first screen, or is a supervised adjustment necessary?
• Is my potassium low enough to make aldosterone falsely reassuring?
• Which assay and units were used for aldosterone and renin?
• If my first screen is negative, is the clinical probability high enough to repeat it?
• If the screen is positive, do I need suppression testing before deciding on treatment?
• If an adrenal nodule is present, would AVS be needed before surgery?
• Should cortisol autonomy be evaluated as well?
• If I am treated medically, which potassium, kidney, renin, and blood-pressure markers will be monitored?

Frequently Asked Questions

Can I have primary aldosteronism with normal potassium?

Yes. Normal potassium does not rule PA out. Potassium is important for interpretation and safety, but the core screening relationship is aldosterone relative to renin.

What is the best blood test for primary aldosteronism?

Screening generally uses aldosterone and renin together with an ARR. The Aldosterone and Plasma Renin Activity Ratio Test is designed around that relationship. The result still requires interpretation of the absolute hormone values, potassium, medications, kidney function, and collection conditions.

Does a high aldosterone result mean I have PA?

No. Aldosterone can rise for reasons in which renin is also appropriately active. PA is specifically a pattern of aldosterone production that is inappropriate for a suppressed-renin state.

Does a high ARR prove primary aldosteronism?

No. The ratio can be distorted by very low renin, medication effects, assay methodology, kidney disease, potassium, sodium intake, posture, and timing. A positive-looking screen may need repeat or confirmatory evaluation depending on the clinical context.

Should I stop my blood-pressure medicine before an ARR test?

Not on your own. Some medicines can cause false-positive- or false-negative-looking patterns, but stopping them can be unsafe. Modern guidelines allow different medication strategies based on safety and the likelihood of PA.

Why might an ARR be repeated?

Repeat testing can help when low potassium, interfering medication, nonstandard collection conditions, borderline results, or high clinical probability makes the first screen less reliable.

Can CT alone tell whether surgery will cure PA?

Usually not. CT shows adrenal anatomy. In many surgical candidates, AVS is used to determine whether aldosterone production is functionally lateralized to one gland.

What should be monitored after PA treatment?

Monitoring commonly includes blood pressure, potassium, kidney function, and renin. Aldosterone may also be reassessed when clinically appropriate.

Summary

Primary aldosteronism is a renin-independent adrenal aldosterone disorder that can drive hypertension even when potassium is normal. Screening is based on aldosterone and renin together, usually expressed as an aldosterone-to-renin ratio. Interpretation requires the absolute aldosterone and renin results, potassium, kidney function, medication exposure, sodium intake, posture, timing, units, and assay method. Low potassium can falsely lower aldosterone.

A positive ARR does not establish which adrenal gland is responsible; subtype testing and treatment planning are clinician directed. During treatment, blood pressure, potassium, kidney function, and renin are important monitoring markers.

Conclusion

Primary aldosteronism is a hormone-driven cause of high blood pressure that is best recognized by reading aldosterone and renin together.

The highest-value screening question is whether renin is suppressed while aldosterone remains inappropriately active. Potassium and kidney function provide essential context, while medication effects and assay methods can change the apparent ARR.

A practical pathway is:

Hypertension → aldosterone + renin + ARR + potassium/kidney function → identify the suppressed-renin pattern → repeat when confounded → decide whether clinician-directed confirmation is needed → determine unilateral vs. bilateral disease when treatment planning requires it → monitor blood pressure, potassium, kidney function, and renin after treatment.

For the broader workup around a high reading—including UACR, glucose, lipids, thyroid, kidney testing, and medication safety—continue with the Hypertension Lab Tests hub.

References

1. Endocrine Society. Primary Aldosteronism Clinical Practice Guideline. 2025.
2. Adler GK, et al. Primary Aldosteronism: An Endocrine Society Clinical Practice Guideline. Journal of Clinical Endocrinology & Metabolism. 2025;110(9):2453–2503.
3. American Heart Association. 2025 High Blood Pressure Guideline: Top Things to Know.
4. American Heart Association. When to Call 911 About High Blood Pressure.