I had been to the emergency room 10 times in the past 6 months. 

Very scary!

Third time, I demanded a blood test. Doctor said high blood pressure is not an emergency! Since troponin I, EKG, chest X-ray, d dimer (later), CT scan with contrast — all normal.

I said — “but my potassium may be low.”

He ordered test.

Potassium: 3.1

Though most lab tests consider potassium as low as 3.5 to be normal, most doctors know that ideal levels should always be above 4.0 — preferably around 4.5.

I went home and looked up my potassium levels in the past 5 years.

They were all below 4.0

Which means my condition may have been going on all this time.

I went to my regular clinic. I seduced my primary care physician to think of all the reasons why I would have these scary symptoms along with a peculiar low potassium level. It worked.

She — my physician — thought of many tests. One of them was the Aldosterone-to-Renin Ratio (ARR). Renin is an enzyme produced by the kidneys that triggers aldosterone (produced) by the adrenal glands to retain sodium and water, which then raises blood pressure and excretes potassium.

So we ordered both renin and aldosterone together. One test is useless without the other.

Results:

Renin 0.01

Aldosterone 13.4

Which means renin is non existent since the lowest number is 0.01 — not 0.00.

Aldosterone-to-renin ratio should typically be less than 20.

Mine was 1340: hundreds of times disproportionately higher.

What that means is that my renin — which is used to raise aldosterone — is suppressed on purpose, yet aldosterone is being rogue — acting on its own, autonomously maintaining a disproportionately high level.

High aldosterone is well known for along raising blood pressure, also causing inflammation and fibrosis, and scarring of the blood vessel walls. And of course, potassium excretion through the kidneys.

A second test confirmed inappropriately high aldosterone-to-renin ratio, signaling a condition called Primary Aldosteronism. This condition is often simplified under the term, Conn’s syndrome, if only one adrenal gland is affected. These conditions are usually triggered by benign tumor or enlarged and overactive adrenal(s).

I was taking magnesium all this time, hoping it would help safeguard my potassium level.

It did not!

I did a carotid ultrasound: still pending after two weeks.

In two days, a echocardiogram. 

Another three days, discussion again with my endocrinologist about adrenal vein sampling (AVS): to confirm whether it’s one adrenal gland (unilateral) or both (bilateral) producing excess aldosterone; and whether operation or medication (spironolactone/eplerenone) is appropriate.

Up to 20 percent of the sudden or resistant blood pressure population has this condition, and they don’t know it.

In the meantime: kidneys are being destroyed, left heart ventricle thickening, vena cava narrowing, lowered hydrogen, low potassium, low magnesium, low ionized calcium, low zinc, and deregulation of blood pH. There may even be insulin resistance, leading to diabetes. There may even be risk factors for lacunar and hemorrhagic stroke.

Bottomline: if anyone has sudden or resistant high blood pressure, they should always test for primary aldosteronism aka hyperaldosteronism through testings for aldosterone-to-renin ratio.