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
Although most patients develop primary aldosteronism over many years, some may 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, Symptoms, and Comorbidities Associated with 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).
Primary aldosteronism affects potassium channels. 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 also affects calcium channels, and is associated with primary and secondary hyperparathyroidism (i.e., along with elevated PTH, some patients with PA develop hypercalcemia while others develop hypocalcemia). Many suffer from kidney stones and osteoporosis. Most have Vitamin D deficiency and/or sensitivity. Hyperaldosteronism and hyperparathyroidism share several signs and symptoms (e.g., polyuria, headaches, dizziness, muscle pain and wasting, bone pain and wasting, constipation, liver impairment, nasal congestion, and inner ear issues). Patients affected by both diseases can be quite sick as a result.
Because the diseases also share consequences, patients may find it even harder to control their hypertension. They also are at much higher risk of cardiorenal diseases, and must therefore be promptly and properly treated. Unfortunately, this may be quite challenging since hyperaldosteronism is seldom diagnosed, and in the presence of mildly abnormal values, hyperparathyroidism is often equally missed.
Since excess aldosterone is associated with cardiovascular and renal diseases, patients with PA often experience some of their signs and symptoms:
- Chest discomfort,
- Chest tightness,
- Dizziness,
- Flushing (i.e., skin becoming red and hot). Of note, in women, this 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.
Some patients with hyperaldosteronism develop allergies (e.g., to drugs and foods, or seasonal). As a result of relations between aldosterone production and the hypothalamus (i.e., the part of the brain that regulates body temperature), patients with PA often experience bouts of overheating and/or chills.
Most patients also complain of the following signs and symptoms:
- 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 account for many other disorders. While evidence supports the association of some of them with hyperaldosteronism (e.g., diabetes, hyperparathyroidism), research remains nonexistent with regard to many others. Because these diseases 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,
- Gallbladder disease (e.g., Cholecystitis, Cholelithiasis),
- Gastroesophageal Reflux Disease (GERD),
- Gastroparesis,
- Glaucoma,
- Grave’s disease,
- Hashimoto,
- Hidradenitis Suppurativa,
- Hyper- or Hypothyroidism,
- Livedo Reticularis,
- Lupus,
- Malignancy (e.g., adrenal glands, breast, kidney, liver, lung, thyroid),
- Mast Cell Activation Syndrome,
- Meniere’s disease,
- MEN Type 1,
- Nonalcoholic Fatty Liver Disease (NAFLD),
- Nephrolithiasis,
- Osteoporosis,
- Periodontitis,
- Pheochromocytoma,
- Pituitary disorders (e.g., prolactinoma),
- Polycystic Ovary Syndrome (PCOS),
- Postural Orthostatic Tachycardia Syndrome (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
