Is It Primary Aldosteronism What Not to Miss скачать в хорошем качестве

Is It Primary Aldosteronism What Not to Miss

Low renin and high aldosterone levels should tip you off, especially if the patient has resistant hypertension. But how to confirm the diagnosis and make sure it's not something else? https://www.medscape.com/viewarticle/... -- TRANSCRIPT -- Matthew F. Watto, MD: Welcome back to The Curbsiders. I'm Dr Matthew Watto, here with my great friend, Dr Paul Nelson Williams. Today we're going to be talking about primary aldosteronism and the mineralocorticoid receptor antagonists (MRAs). Low renin and high aldosterone levels, checked in the morning, should tip you off to this diagnosis, especially if the patient has resistant hypertension. But if we think we have a case, what else should we do to confirm the diagnosis and make sure we're not missing something else? Paul N. Williams, MD: Primary aldosteronism is more prevalent than had previously been recognized. If you think a patient may have it, a good thing to order, even with central hypertension, is an EKG to look for indirect evidence of structural heart disease. If that is found, then get an echocardiogram. Our expert, Dr J. Matthew Luther, checks a urinalysis, which is good form in any case. In essential hypertension you won't necessarily find proteinuria, and in hyperaldosteronism you won't see hematuria. You want to make sure you aren't missing glomerulonephritis, or something intrinsic to the kidney that could be averted. Dr Luther does his due diligence with urinalysis to make sure he's not missing another renal cause of hypertension. Watto: With a rapid rise in creatinine, hypertension, and hematuria, you worry about glomerulonephritis. You don't want to miss Cushing syndrome. We talked about sending a DHEA sulfate as a first-line test, and then doing the dexamethasone suppression test if the DHEA sulfate is suggestive. Should we freak out if the creatinine goes up once we start the patient on treatment for primary aldosteronism? Williams: Dr Luther explained that it's not uncommon to see an increase in the creatinine level once you have the blood pressure under control — you're reversing some of the hyperfiltration. You might have an artificially preserved creatinine, and once you manage the patient's blood pressure appropriately, this can unmask the underlying chronic kidney disease that was probably there in the first place. Patients don't progress as much to hemodialysis once their blood pressure is controlled. So you might see an initial creatinine bump, but then it stays there. That's the overarching pattern he sees. Watto: The numbers he quoted were a creatinine of 1.5 or 2 that increases to 3 and then stays there. He has had patients who remain at that level for years. If I have a patient whose creatinine goes up by 1 or almost doubles, I'm definitely going to be having a nephrologist holding my hand. But it's good to know that this is expected to happen. And he made the point that, even with your run-of-the-mill high blood pressure, when you control it, you will often see a creatinine bump and then it will stabilize. This shouldn't cause us to pull everyone off these first-line medications because they are going to need them for primary aldosteronism in addition to the MRAs. It can be very difficult to treat. The last topic is treatment, and our main choices are the MRAs spironolactone and eplerenone. The dosing he gave us for spironolactone was 12.5 mg daily, going up to 25 mg or 50 mg, and in some cases, 100 mg might be needed, especially if patients have bilateral adrenal hyperplasia and are not candidates for surgery. In that case, you might have to have them on the frontline meds and spironolactone, and keep a close eye on their creatinine and potassium levels. Anything else you wanted to mention about spironolactone? We should talk about eplerenone as well. Williams: This is not a recommendation, by the way, just to be explicit. They talk about doses of spironolactone as high as 400 mg back in the day, which would actually suppress aldosterone secretion. But in practicality, you would be limited by side effects. The doses can go really high, which you probably wouldn't do except in concert with a nephrologist or hypertension specialist. Watto: Patients with cirrhosis are on the highest doses of spironolactone I've seen nowadays. But he did make the point that you can actually follow the renin because the renin is suppressed, because there's so much endogenous aldosterone. When you have the dose of the MRA high enough, you actually start to see the renin become unsuppressed, and you can track that over time. If they had a low potassium, the potassium will also start to rise as you suppress the aldosterone. Eplerenone is the other MRA. It tends to have fewer of the antihormonal side effects, such as gynecomastia in men, which starts at doses of 100 mg and can be a limiting factor. https://www.medscape.com/viewarticle/...