Do I Have PA?

You may have come to this website because you are concerned about your hypertension, and are searching for answers. Perhaps it has become difficult to control or you are “just not feeling quite right,” and are worried that something else might be going on. One in four patients with resistant hypertension has primary aldosteronism, and up to 50% of those with essential hypertension may be affected. Thus, it is reasonable to ask: “do I have PA?”

Primary Aldosteronism is Commonly Missed or Misdiagnosed

Since primary aldosteronism is a syndrome, multiple signs and symptoms are associated with it. While most patients develop the disease over many years, if not decades, some experience severe forms as early as age 30 or before. Although hypertension is usually present, excess aldosterone has also been found in patients without hypertension.

To make matters worse, only a limited number of signs and symptoms are commonly linked to the disease. This lack of actionable evidence largely contributes to underdiagnosis: physicians, particularly in primary care, do not know how to recognize the disease.

Patients lived experiences account for diffuse symptoms such as itching, tingling, poor vision, confusion, stress, malaise and pain. Although part of the syndrome, none of them have ever been formally associated with the disease. As a result, such complaints are usually either dismissed as hypochondriasis or erroneously attributed to other diseases.

It is thus critical that patients advocate for themselves, ask more questions of their physicians, and request screening for primary aldosteronism.

Symptoms vs. Signs

Symptoms are noticed by the patient alone. They represent what a person experiences as a result of a health issue. They are subjective (e.g., feeling tired). There are three types of symptoms:

  • Chronic: persist over long periods of time,
  • Relapsing: reoccur after having disappeared,
  • Remitting: improve or resolve completely.

Signs are observed (felt, heard, seen) by a physician. They are objective (e.g., swelling). They are used to get factual information about a particular disease during a consultation, via patient’s history, and by getting measures from tests. There are three types of signs:

  • Anamnestic: refer to past experiences,
  • Prognostic: predict disease occurrence,
  • Diagnostic: show the actual disease.

Signs and Symptoms of Primary Aldosteronism

As the disease progresses, your blood tests may show elevated blood sugar when fasting (i.e., impaired fasting glucose), or other early signs of diabetes. You may have an abnormal EKG, or an echocardiogram may indicate Left Ventricular Hypertrophy (LVH). Your kidney functions may decline, and you may develop chronic kidney disease.

Since each of these conditions are relatively common and can have other causes, they are usually treated separately without any connection to primary aldosteronism. Patients are sent to separate specialists without team-based coordination of their care, and on the long road to a belated diagnosis of PA, they are unsuccessfully treated for widely differing disorders while primary aldosteronism remains ignored.

In many patients, and particularly those with resistant hypertension, the following signs and symptoms are highly indicative of primary aldosteronism:

  • Fatigue, which can be debilitating and does not improve with sleep,
  • “Brain fog” or cognitive impairment ranging from memory loss to difficulty focusing,
  • Polyuria,
  • Nocturia,
  • Edema,
  • Significant weight gain,
  • Reduced resistance to stress, and
  • Reduced physical endurance.

The sodium reabsorption caused by excess aldosterone is accompanied by potassium loss. The greater the loss, the more intense symptoms are:

  • Palpitations (i.e., irregular, strong or fast heartbeat),
  • Muscle fatigue,
  • Muscle cramps, or even spasms and paralysis.

Some patients report difficulty maintaining sufficient magnesium levels, and find that increasing their magnesium intake improves their potassium levels. In response to sodium reabsorption, the kidneys also release hydrogen. Because hydrogen must be tightly controlled to maintain optimal acid balance, the body compensates for the loss of hydrogen with an increase in bicarbonate. The mechanism is called alkalosis, and patients with PA who are subject to it often experience shallow breathing.

Since calcium channels are also involved in aldosterone production, primary aldosteronism is also found to cause calcium malabsorption. At the recommended daily allowance of 1,000 mg, some patients experience irregular heartbeat and palpitations. A lot of patients develop early onset and/or severe osteoporosis, others experience Vitamin D deficiency and kidney stones.

Since excess aldosterone is associated with cardiovascular and renal disease, patients with PA often experience some of the signs and symptoms of these diseases:

  • Headaches,
  • Dizziness,
  • Flushing which, in women, is nearly always mistaken for perimenopause and menopause,
  • Shortness of breath,
  • Lightheadedness,
  • Chest tightness, chest discomfort,
  • Pain, numbness, tingling in the extremities,
  • Fatigue,
  • Edema,
  • Polyuria,
  • Nocturia, and
  • Kidney stones.

Excess aldosterone is known to be associated with eye diseases — particularly those affecting the retina. In those instances, patients with PA will experience floating specks or webs, as well as blurred or distorted vision.

With primary aldosteronism, some patients develop sudden allergies (e.g., to drugs and foods, or seasonal), others frequently experience:

  • Dysgeusia (i.e., a metallic taste in the mouth),
  • Dry eyes,
  • Dry mouth,
  • Nasal congestion,
  • Hyperhidrosis (i.e., excessive sweating),
  • Thirst, and
  • Digestive issues, including constipation.

Overall, excess aldosterone triggers inflammation processes which, in most patients with PA, manifest as generalized pain and unwellness, and is usually mistaken for fibromyalgia. Similarly, patients with PA often experience sleep disorders and/or sleep apnea, anxiety and/or irritability, and are erroneously diagnosed with depression while the condition is in fact also caused by excess aldosterone.

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References

  • John W. Funder, Robert M. Carey, Franco Mantero, M. Hassan Murad, Martin Reincke, Hirotaka Shibata, Michael Stowasser, William F. Young, The Management of Primary Aldosteronism: Case Detection, Diagnosis, and Treatment: An Endocrine Society Clinical Practice Guideline, The Journal of Clinical Endocrinology & Metabolism, Volume 101, Issue 5, 1 May 2016, Pages 1889–1916, DOI: 10.1210/jc.2015-4061
  • William F. Young, Jr. Diagnosis and treatment of primary aldosteronism: practical clinical perspectives. The Journal of Internal Medicine, Volume 285, Issue 2, February 2019, DOI: 10.1111/joim.12831

©2021 Primary Aldosteronism Foundation — All Rights Reserved

The Primary Aldosteronism Foundation is a registered 501(c)(3) public charity. Donations are tax deductible in the US.

©2021 Primary Aldosteronism Foundation

The Primary Aldosteronism Foundation is a registered 501(c)(3) public charity. Donations are tax deductible in the US.