What to do if you have drug-resistant hypertension.

There’s an article making the rounds of the online PA community that I think breaks things down really well, and bears repeating here. It’s based on the research of  Dr. Wanpen Vongpatanasin, of the University of Texas, who seems to be doing some pretty groundbreaking stuff – for instance, focusing on race and gender differences. (In the past, much of the research about hypertension focused on males, over 55, and mostly white or African American.)
If I had seen this information, say, five or six years ago, my life right now might be very, very different. This is a great checklist to bring to a primary care doctor if you’ve been diagnosed with hypertension and the typical meds they push these days – beta blockers, calcium-channel blockers, and ARBs – do not work for you. I’ve copied the main points directly from the article; my comments are in red.
  • Get tested for aldosterone. The starting point is a blood test that specifically checks your aldosterone level. If this test establishes that there is a problem, you will need to do a 24-hour urine catch to determine more precisely how high your aldosterone level is. This is called a salt-loading test because you consume a lot of dietary salt for five days beforehand. Why? Excess dietary salt normally shuts down aldosterone production, but this doesn’t happen in people who produce too much of the hormone. As a result, people with this problem tend to retain excess sodium. (Aldosterone level alone is not sufficient – they also need to check plasma renin activity and determine the aldosterone-renin ratio. And the salt loading test, as those of you who have been following me know, only requires three days of sodium loading and can be done via meds instead of diet – quicker, more controlled.)
  • Have a CT scan to learn whether you have an adrenal tumor. For reasons unknown, tumors on the adrenal gland trigger a hyperactive mode for aldosterone production. Ninety percent of the time, these tumors are benign and surgical removal of them solves the problem. Malignancies, of course, may require more complex treatment. (The statistics I’ve been given show that 90% of the time the tumors are benign, but the success rate of surgery is closer to 60-75%. Variables include other health problems, and how long the patient’s blood pressure has been uncontrolled.)
  • Consider whether you need medications to control aldosterone. In people who don’t have a tumor, the drug spironolactone (Aldactone), which blocks aldosterone from its receptors in the brain and the kidney, is useful, says Dr. Vongpatanasin, noting that it’s also helpful for those with a tumor who aren’t candidates for surgical removal. (Additionally, there is another drug, eplerenone, which also goes by the brand name Inspra, that works with fewer side effects. There is no generic, and it is expensive, and most insurance companies will not cover it without a preapproval process. But spironolactone has some really extreme side effects in some,, so it’s good to be aware that there is another option – I’m one of these people, and I’ll address this in a future post.)
  • Reduce dietary sodium, and increase fruits and vegetables in your diet. Cutting sodium helps bring aldosterone levels back in line. For most people, the general guideline for salt intake is now about one teaspoon per day, according to the National Institute of Medicine, but for those who are more sensitive (including people who have high aldosterone), the recommended upper limit should be no more than half that amount. And Dr. Vongpatanasin’s research shows that while people who live in places without lots of processed foods have high aldosterone levels at the same rate as the rest of the world, they don’t tend to develop elevated blood pressure. It’s likely that the lower sodium intake from their fresh- and whole-food diets deters hypertension. (I’m a huge skeptic when it comes to conventional Western medicine’s dietary cure-alls – for instance, the government-recommended 9-11 servings of grain a day would make me sick as a dog and big as a house! – but this one makes sense. Except for one thing – I’ve never been a huge eater of processed foods, and I’ve been salt-averse since childhood, and I still developed the dang tumor. But the takeaway message – put the processed foods back on the shelf, eat real food, and don’t add salt – is one that applies to everybody who is interested in being in optimal health.)

What’s it called again?

Like most sites dealing with primary aldosteronism, I’ll probably use several terms to describe the same condition: PA, hyperaldosteronism, and Conn’s Syndrome*. The latter term seems somewhat antiquated, but some people still use it. I think it breaks down this way, broadest to narrowest:

Hyperaldosteronism means a person produces too much aldosterone. The cause can be primary or secondary. I believe the most common cause of secondary aldosteronism is renal artery stenosis (which, for the record, I’ve been screened for and don’t have). On this site, I’ll be dealing with primary aldosteronism.

Primary aldosteronism (PA), sometimes called primary hyperaldosteronism, is what I have. It means that for one reason or another, the adrenal glands produce too much aldosterone. One cause is a unilateral adenoma (which is what my doctor believes I have), in which case surgery is the treatment of choice, as only one adrenal gland is affected. Other causes affect both glands, and surgery is usually not done; these causes include bilateral adenomas – one or more in each gland – or bilateral hyperplasia, which is an enlargement of both adrenal glands. Unilateral hyperplasia can also occur; I don’t know too much about this as it seems to be less common and it’s not what I’m dealing with. The distinction to make is that when it’s unilateral, surgery can be an option; when it’s bilateral, the only treatment is medication for life.

Conn’s Syndrome was named after endocrinologist Jerome W. Conn, who was the first to make the connection that an aldosterone-producing adenoma (APA) was associated with a collection of specific symptoms. There is a brief Wikipedia article about him here. Conn’s Syndrome (sometimes just called Conn Syndrome) originally meant hyperaldosteronism caused by a unilateral APA, but is sometimes used to describe hyperaldosteronism of any variety now. I haven’t heard any of my medical team use this term, but on the support sites dealing with hyperaldosteronism, other patients use it so I assume their doctors do too.

*Truth be told, I’ll probably most often just call it PA, because really, I’m lazy and it’s short!

Aldosterone suppression test, day three.

Today started with a blood draw, bright and early. The phlebotomist asked me what I was doing with the rest of my day. I’ll bet he didn’t expect my answer would be, “Staying home and peeing in a bottle!” but hey, I speak the truth. We both had a good laugh about that one.

When I got back from the lab, I measured my blood pressure and it was 165/125. For reference, that second number? Shouldn’t really ever be higher than 80. Mine’s usually in the high 80s, low 90s at most, but that’s because of the PA. For a brief moment I panicked and almost called 911, since a diastolic reading of over 110 is considered hypertensive crisis and holy crap 125?! Then I thought I should check it again: 165/100. Which is ballpark for where it’s been throughout the past three days, and where it should be while taking the sodium. Then just to be certain, a few minutes later, 155/95. Whew. Crisis averted.

Second moment of panic came while I was on the phone dealing with an insurance issue. My network of friends checking up on me called, and I didn’t know how to use the call waiting. (Yes, I’m an old fart who doesn’t really know how to use her smartphone! In fact, I thought I had call waiting disabled. Oops.) When I hung up I had a couple of panicked texts and voice mails and – I felt kinda dumb about the whole thing. But I suppose it was a good test of the emergency support system – at least we know it works!

Anyway, I’ve got one more dose of the NaCl, then tomorrow morning I get to pee in the bottle one last time, and then drop my little offering at the lab, and I’m done. And as long as nobody at the lab screws up*, I don’t have to do it again.

So now that all is said and done? The scary stuff out there about the risks of this test, including potassium dropping too low and stopping the heart, or stroke or aneurysm due to the elevation in blood pressure from the sodium, seem to me to be a bit exaggerated. I think I got lucky on this one – since my “normal” blood pressure, unmedicated, is on the low end of high, the sodium didn’t cause too much of an increase. The other expected side effects – nausea, headache – were only during the first day, and were really minimal. This test seems to have a really bad reputation, but all in all it was pretty unremarkable.

*This morning I had to tell the phlebotomist how to correctly do the blood draw for renin, although there seems to be several schools of thought contradicting each other on this one.

Aldosterone suppression test, day two.

So far, so good. Today’s job was to take 2mg NaCl three times – the first two are already a done deal. The side effects have been absolutely minimal – a little bit of nausea about an hour after taking it. I did wake up at 3am with a crazy bad headache, but fortunately it’s okay to take super double extra strength aspirin/caffeine/acetaminophen cocktails during this test – I popped one of those and went back to sleep and woke up magically headache-free. The worst thing so far is that my potassium dropped to 3.2, so I’m taking extra doses of the giant pills.

Tomorrow: more blood-letting, and, whee, big fun – it’s the day I get to pee in a jug all day. Then Thursday I take that in to the lab, submit myself to even more blood-letting, and then I’m on my merry way, unless tomorrow’s labs show even lower potassium, in which case I may end up being subjected to potassium infusion. Um, let’s hope not, okay?

I consider myself really, really lucky that I’m almost 2/3 done with this thing and – fingers crossed – nothing scary-bad has happened. There’s a bit of negative information out there about the risks of this test, and while I’m sure the risks are all very real, I almost think Dr. Google had me unnecessarily worried.

Also? I consider myself really, really lucky that I’ve got a nice little group of friends looking out for me right now. You know who you are. Thank you.

22 February 2011

Dr. Brent Michael

2001 Santa Monica Blvd., Ste. 1260W
Santa Monica, CA 90404

cc: Bay Area Community Medical Group

Dear Dr. Michael:

You may recall I was your patient from 2009-2010. During that time, you treated me for a trapezius muscle spasm, drug-resistant hypertension, and low potassium.

The last time I visited your office, I presented with heart palpitations and a racing pulse. Your assistant, Anita, noticed this and did an EKG, which indeed showed tachycardia. Even though I had been concerned enough to pay a visit to your office, you appeared unconcerned, told me it was “anxiety,” and dismissed it as being a typical problem for a woman my age.

I found this response to be both ageist and sexist, which angered me enough to take my business elsewhere. I sought recommendations for another primary care physician and chose Dr. Rob Kassan. Within mere minutes of hearing my medical history, Dr. Kassan asked if I had ever had my aldosterone level checked. I told him to the best of my knowledge I had not; in the copies of my labs I have from the time I was your patient there is no evidence that this was ever considered.

Dr. Kassan referred me to Dr. Earl Gordon, a nephrologist and hypertension specialist. Again, within a few minutes of hearing my history, Dr. Gordon asked if I had had my aldosterone levels checked. Again, I told him I had not.

Dr. Gordon took me off of the medications you had prescribed – Diovan 360mg and Cardizem 180mg – as they can interfere with the testing. Interestingly, within days of being off of antihypertensives, my blood pressure went down rather than up. Blood tests revealed the following: Potassium 2.9, aldosterone 42.3, renin .5. As I hope you know, this is indicative of primary aldosteronism rather than essential hypertension.

Dr. Gordon ordered a CT scan, which revealed I have a 1cm nodule in my left adrenal. I am currently undergoing further testing to confirm that this is the source of the excess aldosterone, but given my other symptoms, it is probable that it is. Other complaints that I mentioned during my time as your patient, including frequent headaches and that muscle spasm, are consistent with the condition.

During the time I was your patient, rather than get to the cause of my problems, only my symptoms were treated. For a year and a half, I took numerous expensive and unnecessary medications that you prescribed, none of which did anything to help, as they were designed to treat essential, rather than secondary, hypertension.

I am writing this in order to educate you to avoid something like this happening to another of your patients. Enclosed are two articles that cover some of the basics of primary aldosteronism. I realize this is an uncommon condition and that you may not ever encounter another case in your practice, but please take a moment to educate yourself so that you will know what to do the next time a patient presents with hypertension and low potassium.


The Wayward Bus

Aldosterone suppression test, day one.

Today’s routine: early morning blood draw, 2mg of sodium chloride 3x/day. So far, so good – I took the first dose at 7am and felt fine, although I got a couple of blood pressure readings that bordered on the lowest end of what my doctor described as dangerous. I fully expected it to go into the “dangerous” zone after I took the second dose this afternoon, but – nothing. It actually went down a bit. About an hour after the second dose I got pretty nauseated, but it was over with pretty quickly.

I’m feeling a bit optimistic that this is going to go well. One day (almost) down, two to go…

What the hell is an adrenal gland, anyway?

Glad you asked! Rather than relying on my memory of college biology, I’ll share a concise definition that pretty much accounts for all of the health issues I’ve been trying to figure out for the past decade or so.

They kinda look like eggplants to me. Mmmmm, eggplant.

Courtesy of the University of Maryland Medical Center:

The adrenal glands are small yellow-bronze organs found in the retroperitoneum, (the back of the abdomen behind the abdominal lining) usually near the top of each kidney.

They provide essential hormones that control the body’s fluid and salt regulation, blood pressure, muscle development, sexual drive and development and sugar metabolism, as well as serving as the source for epinephrine, also called adrenaline.

Those things that they control? It’s like a laundry list of the reasons I’ve sought the expertise of doctors for the past 10+ years. Every. Single. One. Of them:

Fluid and salt retention: I eat in a restaurant, I gain two to five pounds. When I cook at home, I don’t use salt, and I don’t gain weight. Hmmm.

Blood pressure: Well yeah, you already knew that. It’s messed up.

Muscle development: I’ve had a muscle spasm in my left trapezius for over 10 years. I’ve had it MRI’d, X-rayed, and nerve tested. I’ve been prescribed physical therapy, Vicodin, Norco, and Oxycontin. I had an orthopedist recommend surgery for a herniated cervical disk. Guess what? WRONG. It’s the potassium, which is regulated by the adrenals. If my potassium gets too low, the spasm starts up. When it comes back to normal, the spasm goes away.

Sexual drive: Not much to say here other than when you feel crappy, it’s typically the last thing you’re interested in. That there could be a biological component here never really crossed my mind.

Sugar metabolism: DING DING DING DING DING! We have a winner here. I’ve had reactive hypoglycemia for at least half of my life. In early 2003, after mysteriously gaining 50 pounds (when I had been skinny/underweight my whole life) I was diagnosed with insulin resistance at the same time that I learned I was fructose intolerant. Because of the latter, I dumped all sugars and wheat from my diet and, bingo, dropped those 50 pounds within three months. Problem solved, right? No, here’s where it gets interesting: I don’t test positive for IR on paper. As IR is a precursor to Type 2 diabetes, and my entire maternal family has T2 diabetes, it seemed a logical conclusion that I would have IR too. I have all the symptoms of it – sleepy after eating, inability to eat carbs without instantly puffing up like a balloon – but my labs are all normal. This has been a mystery to me and to several doctors. However, after talking with other PA patients, I’m learning that this pattern – sudden weight gain, reactive hypoglycemia – is often the first sign that something is wrong. While the inability to digest fructose (and fructans, a fiber found in wheat) is a completely separate issue which I know will not go away, I’m suddenly hopeful – and excited! – at the prospect that if I can get the adrenalectomy, some of my food-related problems will be gone. I mean – HELLO, RICE NOODLES. A girl can dream, yeah?

Anyway. I’m told the adrenal gland is the size of a peanut. It kind of amazes me that something so tiny can control so much, but there you go.