Addison Disease
Hypoadrenocorticism
Also known as: Hypoadrenocorticism, Addison's disease, Adrenal insufficiency
Hypoadrenocorticism
Also known as: Hypoadrenocorticism, Addison's disease, Adrenal insufficiency
In short
Addison's disease is an uncommon endocrine disorder where the adrenal glands fail to produce vital hormones. This leads to severe gastrointestinal issues, weakness, and life-threatening electrolyte imbalances. While an Addisonian crisis is a veterinary emergency, the long-term prognosis is excellent with lifelong daily or monthly hormone replacement therapy.

TL;DR. Addison's disease is a serious but highly treatable hormonal disorder caused by underactive adrenal glands, requiring lifelong medication but offering an excellent quality of life once stabilized.

The adrenal glands are small but vital organs located just ahead of the kidneys.
Addison's disease, scientifically known as hypoadrenocorticism, is an endocrine disorder characterized by a deficient secretion of essential hormones from the outer layer of the adrenal glands (the adrenal cortex). These tiny glands, located near the kidneys, produce two primary types of hormones: glucocorticoids (such as cortisol) and mineralocorticoids (such as aldosterone). When these glands fail, your pet's body loses its ability to regulate hydration, blood pressure, electrolytes, and its response to stress.
Glucocorticoids are essential for regulating glucose metabolism, maintaining normal blood pressure, and helping the body cope with physical or emotional stress. Mineralocorticoids are responsible for maintaining the delicate balance of water and salts (electrolytes) in the body. Specifically, aldosterone signals the kidneys to keep sodium and excrete potassium.
As a leading veterinary internal medicine reference explains:
"Angiotensin I is then converted to angiotensin II by angiotensin-converting enzyme located in the lung, on endothelial cells throughout the body, and in many other organs. Angiotensin II stimulates the zona glomerulosa to release aldosterone, which stimulates cells of the renal collecting duct to reabsorb sodium and excrete potassium. Sodium reabsorption leads to water retention and thus augmentat" [2]
Without these hormones, potassium levels in the blood rise to dangerous levels, while sodium and water are rapidly lost through the urine. This leads to severe dehydration, low blood volume, and a dangerously slow heart rate. While Addison's disease is primarily diagnosed in dogs, it can occasionally occur in cats. Because feline cases are exceedingly rare, much of the diagnostic and treatment guidance for cats is extrapolated from canine medicine.
In most cases, Addison's disease is classified as idiopathic, meaning the exact trigger is unknown. However, the primary underlying cause is typically an immune-mediated destruction of the adrenal cortex. The pet's own immune system mistakenly attacks and destroys the hormone-producing cells of the adrenal glands. By the time clinical signs appear, more than 90% of the adrenal cortex has usually been destroyed.
Other less common causes include infections, tumors, or trauma to the adrenal glands. Additionally, Addison's disease can be caused "iatrogenically" (meaning caused by medical treatment). This can happen if a pet is receiving long-term steroid medications and the treatment is stopped too abruptly, or if medications used to treat Cushing's disease (the opposite of Addison's, where too much hormone is produced) over-suppress the adrenal glands.
While any dog or cat can develop hypoadrenocorticism, certain dog breeds have a strong genetic predisposition. In some breeds, the disease is known to be inherited as an autosomal recessive trait.
Addison's disease is often called "the great imitator" because its symptoms are vague, wax and wane, and mimic many other conditions, such as kidney disease or primary gastrointestinal disorders. A pet may seem sick for a few days, recover temporarily with basic veterinary care (like intravenous fluids), and then relapse later when exposed to stress.

Lethargy and weakness are common early signs of Addison's disease in predisposed breeds like the Standard Poodle.
Because the clinical signs of Addison's disease are so non-specific, your vet will need to perform several diagnostic tests to rule out other conditions and confirm the diagnosis.
Your vet will start with routine bloodwork, including a complete blood count (CBC) and a biochemistry profile. A key clue on the biochemistry panel is a low sodium-to-potassium ratio (Na:K ratio). Because aldosterone is missing, sodium levels drop while potassium levels climb.
According to a leading veterinary textbook:
"Clinical signs are often vague and easily ascribed to more common disorders involving the gastrointestinal and urinary... Clinicopathologic Abnormalities Associated with Primary Hypoadrenocorticism in Dogs and Cats... Biochemistry Panel: Hyperkalemia, Hyponatremia, Hypochloremia, Prerenal azotemia..." [1]
Your vet may also perform an electrocardiogram (ECG) to evaluate your pet's heart rhythm. High potassium levels (hyperkalemia) are toxic to the heart muscle and can cause severe, life-threatening electrical abnormalities.
As noted in a critical care reference:
"Hyperkalemia-related ECG changes are of immediate life-threatening importance and should be treated promptly and appropriately... There has been one report of atrial fibrillation in association with Addison's disease in a dog." [4]

An electrocardiogram (ECG) is crucial for identifying dangerous heart rhythms caused by high potassium levels.
To definitively confirm Addison's disease, your vet must perform the ACTH Stimulation Test, which is the gold standard diagnostic tool. During this test, your vet will draw a baseline blood sample to measure cortisol, inject a synthetic version of the brain hormone ACTH (which normally stimulates the adrenal glands to produce cortisol), and draw a second blood sample one to two hours later. In a healthy pet, cortisol levels will rise significantly. In a pet with Addison's disease, the adrenal glands are unable to respond, and cortisol levels will remain flat and extremely low.
Other supportive tests may include abdominal ultrasonography (to visualize abnormally small adrenal glands) and chest radiographs (to check for a microcardia, or small heart, which occurs due to low blood volume).
Treatment for Addison's disease is divided into two phases: emergency stabilization for pets in crisis, and lifelong maintenance therapy.
If your pet is admitted in a state of collapse or shock, this is a level-5 veterinary emergency. Your vet will immediately place an intravenous catheter to administer aggressive fluid therapy. This restores blood volume, improves blood pressure, and helps flush excess potassium out of the body. Your vet will also administer rapid-acting glucocorticoids, such as dexamethasone, which do not interfere with the ACTH stimulation test if it needs to be run concurrently. If potassium levels are dangerously high, treatments like insulin and glucose may be used to temporarily shift potassium back into the cells and protect the heart.
Once your pet is stable and eating, they will transition to lifelong hormone replacement therapy. This involves replacing both the missing mineralocorticoids and glucocorticoids.
Your vet will need to perform regular blood tests—especially in the first few weeks of treatment—to monitor sodium and potassium levels and adjust the medication doses accordingly.
The long-term prognosis for pets with Addison's disease is excellent. While the disease is lifelong and cannot be cured, it is highly manageable. Once the correct doses of medications are established, most dogs and cats live normal, active, and happy lives with a normal life expectancy.
As an owner, your primary responsibility will be administering medications consistently and monitoring your pet for any signs of relapse. You will also need to work closely with your vet to proactively increase your pet's glucocorticoid dose during anticipated times of stress, such as boarding, surgery, traveling, or veterinary visits, as their bodies cannot naturally produce the extra cortisol needed to cope with these events.
Because primary Addison's disease is an autoimmune condition with a strong genetic component, there is no known way to prevent it from developing. However, you can prevent iatrogenic Addison's disease by never abruptly stopping steroid medications (like prednisone) without your veterinarian's guidance. Steroids must always be tapered down slowly to allow the pet's adrenal glands time to wake up and resume natural hormone production.
For predisposed breeds, responsible breeders should screen their breeding lines and avoid breeding dogs that have been diagnosed with the disease or have close relatives affected by it.
If your pet has been diagnosed with Addison's disease, you should contact your veterinarian if you notice mild signs of a relapse, such as a sudden loss of appetite, mild lethargy, or a single episode of vomiting or diarrhea. These signs often indicate that your pet's medication doses need to be adjusted.
Seek emergency veterinary care immediately if your pet exhibits any of the following red flags:
These are signs of an impending or active Addisonian crisis, which can be fatal if not treated immediately with intravenous fluids and supportive medications.
If you own one of the following breeds, you should be especially vigilant for the vague, early signs of Addison's disease. Genetic research has identified different levels of heritability in these breeds:
Treatment must be prescribed by a licensed veterinarian based on your pet. Specific drug doses are intentionally not shown here.
Addison's disease is an uncommon endocrine disorder where the adrenal glands fail to produce vital hormones. This leads to severe gastrointestinal issues, weakness, and life-threatening electrolyte imbalances. While an Addisonian crisis is a veterinary emergency, the long-term prognosis is excellent with lifelong daily or monthly hormone replacement therapy.
Anorexia、Dehydration、Diarrhea、Lethargy、Vomiting、Weakness、Weight loss、Hematemesis
ACTH Stimulation Test、Abdominal ultrasonography、Baseline endogenous ACTH concentration、Electrocardiogram (ECG)、Low-dose ACTH stimulation test、Plasma aldosterone concentrations during ACTH stimulation test
Treatment must be prescribed by a licensed veterinarian based on your pet. Specific drug doses are intentionally not shown here.
This article is for general education and is not a substitute for professional veterinary advice. If your pet is unwell, please consult a veterinarian.
Peqaboo’s AI helps you track symptoms, understand lab reports, and know when to see a vet.
Get the Peqaboo app