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 hyperaldosteronism, 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
Most patients develop primary aldosteronism progressively over many years. Some, however, experience severe forms of the disease as early as or even before the age of 30.
The hallmark of hyperaldosteronism is “difficult to control” and labile hypertension: blood pressure remains elevated despite taking multiple antihypertensives, and can vary greatly and abruptly over short periods of time (e.g., from normal to hypertensive crisis requiring an ER visit).
In the earlier stages of the disease, excess aldosterone can also be seen in normotensive individuals.
Few of the signs and symptoms of primary aldosteronism have been formally established. As a result, primary care physicians and specialists do not know how to recognize the disease in their patients. Instead, they either dismiss their complaints as hypochondriasis or erroneously attribute them 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 hyperaldosteronism remains ignored.
In many patients, and particularly those with resistant hypertension, the following signs and symptoms are highly indicative of primary aldosteronism:
- Cognitive impairment or “brain fog” ranging from memory loss to difficulty focusing, confusion, and sometimes even seizures,
- Easy bleeding,
- Easy bruising,
- Edema,
- Exhaustion and fatigue (which can be debilitating, and do not improve with sleep),
- Irregular heartbeat,
- Itching
- Nocturia,
- Polyuria,
- Reduced physical endurance,
- Reduced resistance to stress, and
- Weight gain (can be significant, and is usually associated with dietary salt intake above 1,500 mg/day).
The sodium reabsorption caused by excess aldosterone is accompanied by potassium loss. The greater the loss, the more intense symptoms are:
- Muscle cramps, or even spasms and paralysis,
- Muscle fatigue, and
- Palpitations (i.e., irregular, strong or fast heartbeat).
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.
Primary aldosteronism can also cause calcium malabsorption. At the recommended daily allowance of 1,000 mg, some patients experience irregular heartbeat and palpitations. It is not uncommon for patients with PA to develop primary or secondary hyperparathyroidism with early onset or severe osteoporosis, as well as Vitamin D deficiency or sensitivity, 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:
- Chest discomfort,
- Chest tightness,
- Dizziness,
- Flushing which, in women, is nearly always mistaken for perimenopause and menopause,
- Headaches,
- Lightheadedness,
- Pain, numbness, tingling in the extremities, and
- Shortness of breath.
Excess aldosterone is 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:
- Digestive issues, including constipation, acid reflux, and liver impairment,
- Dry eyes and/or blurry vision,
- Dry mouth,
- Dysgeusia (i.e., a metallic taste in the mouth),
- Hyperhidrosis (i.e., excessive sweating),
- Insomnia,
- Nasal congestion,
- Thirst, and
- Tinnitus.
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 anxiety and/or irritability, and are erroneously diagnosed with depression while these symptoms are in fact also caused by excess aldosterone.
Comorbidities
Comorbidities designate the presence of more than one condition in an individual. Only cardiorenal diseases are formally associated with PA. However, patients’ lived experiences indicate other diseases co-occur with PA. Because some of them can be severe and/or further increase aldosterone, it is critical that patients seek prompt and appropriate diagnosis and treatment when they suspect they may have one or more of the following diseases:
- Colitis
- Diabetes
- Diverticulosis
- Dysautonomia
- Dyslipidemia
- Ehlers Danlos Syndrome
- Fuchs’ Dystrophy
- Gastroparesis
- GERD
- Glaucoma
- Grave’s disease
- Hashimoto
- Hidradenitis Suppurativa
- Hyper- or Hypothyroidism
- Livedo Reticularis
- Lupus
- Malignancy (adrenal glands, breast, kidney, liver, lung, thyroid)
- Mast Cell Activation Syndrome
- Meniere’s disease
- MEN Type 1
- NAFDL
- Nephrolithiasis
- Osteoporosis
- PCOS
- Periodontitis
- Pheochromocytoma
- Pituitary disorders (e.g., prolactinoma)
- POTS
- Preeclampsia
- Primary or Secondary Hyperparathyroidism
- Raynaud’s Syndrome
- Sleep Apnea
- Urinary Tract Infection.
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
