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Healthier World with Quest Diagnostics
39 - Instant insights: How to screen for primary aldosteronism (updated guidelines) (9 min)
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Welcome to Healthier World with Quest Diagnostics. Our goal is to prompt action from Insight as we keep you up to date on current clinical and diagnostic topics to transform lives and illuminate a path to better health. Welcome to a special episode series called Instant Insights, a podcast episode designed to give you quick and highly impactful clinical pearls in just a few minutes. I'm Dr. Mason Latsko.
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Today we're dusting off your knowledge of primary aldosteronism or PA and flipping the script on the classical approach.
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So let's dive in. If you're a provider listening in today, you know that hypertension is one of the most common challenges in your daily practice. What if I told you that primary aldosteronism is far more common than we once thought? Up to 14% of hypertensive patients in primary care may have PA, and if a patient is being referred to specialty care, that number jumps to nearly 30%. And recognizing it can not only change the way that those hypertensive patients are managed, potentially getting them off multiple medications, but also change the understanding of their risk for conditions like cardiovascular disease, metabolic and renal disease. Patients with primary aldosteronism have elevated risk for these cardiometabolic conditions even compared to those with hypertension alone. And due to the increased prevalence and increased cardiometabolic risk associated with primary aldosteronism, the latest guidelines from both the Endocrine Society and the AHA and ACC strongly recommend expanding screening for primary aldosteronism. To understand why this condition carries such high risk and why screening is so vital, we need to look at the underlying mechanism.
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Primary aldosteronism is considered a condition that impacts the adrenal glands, a gland that releases a hormone called aldosterone. Under normal circumstances, renin is released from the kidneys to signal for aldosterone to be secreted from the adrenals, which in
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turn tells our kidneys to increase potassium excretion in the urine and retain sodium and water in the blood, which naturally raises our blood volume and increases our blood pressure. So high renin levels should mean high
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aldosterone signal, which increases our blood volume and subsequently increases our blood pressure.
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And this is a feedback loop. So low renin means low aldosterone and signals for the kidneys to stop retaining so much water and sodium in the blood so that our blood pressure doesn't continue to rise. However, in a patient with primary aldosteronism, the adrenals produce high amounts of aldosterone each, even in the absence of renin signal. Because of the high aldosterone, the Kidneys
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continue to increase blood volume and the cycle of high blood pressure continues. So in primary aldosteronism you can expect high aldosterone, low renin and high blood pressure.
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Unfortunately, historic tools to identify PA have
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fallen short, leading providers to believe that this condition affects very few individuals with high blood pressure. Fewer than 1% of patients are even being screened for PA. The traditional screening method is called the aldosterone renin ratio or the ARR, and
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this test has specific criteria for patient
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preparation, which requires withholding certain medications. And most importantly, the performance of the ARR varies widely, with some studies showing sensitivity below 50%.
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To address this and improve sensitivity, the latest guidance from the Endocrine Society has significantly lowered the ARR cut point. Historically, A ratio greater than 30 was often used to confirm PA, but now new guidance has dropped that threshold down to 15. Let's walk through how we can identify
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a patient with primary aldosteronism.
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Keep in mind primary aldosterone is characterized by low renin and high aldosterone, so first we look at suppressed renin. A low renin level can be the first and strongest signal pointing toward primary aldosteronism. Additionally, renin is suppressed by aldosterone itself, so if renin is low in a hypertensive patient, it's a red flag regardless of their aldosterone level.
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Once suppressed renin is confirmed, the next
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step is to assess whether or not aldosterone is inappropriately elevated for that suppressed renin. If plasma renin levels are low and aldosterone is high, you can calculate the ARR by dividing the level of aldosterone by the level of renin. This meets criteria for pa. So here's what to expect in a patient who is being assessed for PA using this one. Start with plasma renin activity. If you notice that the patient has plasma renin activity less than 1 nanogram per milliliter per hour, this is considered suppressed renin. 2. Look at the plasma aldosterone concentration. If the aldosterone is 7.5 nanograms per
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deciliter or greater, this indicates overt primary aldosteronism. To confirm that diagnosis, you should also look at the ARR. If the ARR is greater than 15, the patient meets criteria for primary aldosteronism.
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Also note that if your patient is already taking a mineralocorticoid receptor antagonist, they should withhold that medication for four to six weeks prior to checking the plasma renin activity level.
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Let's walk through an example. Say you have a patient with hypertension
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and you decide to screen them for primary aldosteronism, their plasma renin comes back at 0.8 ng per ML per hour, while the aldosterone comes back at 16 nanograms per deciliter. Under previous guidance, their aldosterone to renin ratio would be 20, which may have been considered a negative screen. However, using this updated algorithm, we first see that the renin is suppressed at 0.8 ng per ML hr. Next we see the aldosterone being elevated at 16 nanograms per deciliter, which is well above that 7.5 threshold, indicating overt primary aldosteronism. Furthermore, their ARR of 20 is greater than the new confirmation threshold of 15, confirming a diagnosis in that patient of primary aldosteronism. Using this new methodology, we're able to identify with greater sensitivity those patients who suffer from primary aldosteronism. Early detection of PA matters Untreated PA can worsen cardiometabolic and renal conditions compared to hypertension alone. This under screening is especially concerning in the chronic kidney disease population. Despite 39% of CKD patients having indications for screening, very few patients are actually being tested. It can be a challenge to diagnose PA in patients with hypertension and chronic kidney disease, where we often just assume that the high blood pressure is caused by the kidney disease itself. But we now know that excessive aldosterone actually accelerates kidney damage, leading to fibrosis and and reflected in proteinuria completely independently of high blood pressure. So proactively screening these patients for PA is a critical step to ensure a timely diagnosis and prevent further renal decline. But this damage, of course, is not limited to the kidneys. When left untreated, the excess aldosterone in PA puts patients at significant risk for severe cardiovascular events like atrial fibrillation, stroke and heart failure, and also drives metabolic complications like insulin resistance. And this is all far beyond what you would expect from high blood pressure numbers alone. To summarize, primary aldosteronism is no longer as rare as we once thought. By embracing these updated guidelines and using a clear stepwise approach, we can get to the root cause of countless patients, reducing their medication burden and ultimately protecting their long term health. That's a wrap on this episode of Healthier World with Quest Diagnostics. Please follow us on your favorite podcast app and be sure to check out Quest Diagnostics Clinical Education center for more resources, including educational webinars and research publications. Thank you for joining us today as we work to create a healthier world. One life at a time.
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SA.