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Feline Hyperaldosteronism

Written by: Krista E.


Hyperaldosteronism is one of the most common adrenal gland disorders in cats, yet it is frequently underdiagnosed, often masked by corresponding kidney disease (Kooistra, 2015). First documented in felines in 1983, this relatively new disease process is still considered rare, but the number of case reports has risen considerably since (Kooistra, 2015). There are two classifications of hyperaldosteronism: primary and secondary. The primary form usually involves a tumor of one or both adrenal glands while the secondary form usually involves an abnormality somewhere besides the adrenal gland(s) causing reduced arterial blood volume such as heart failure, edema or ascites, or high blood pressure, in general (Nichols, 2016). For the purpose of this review, the primary form will be discussed. The anatomy of the adrenal gland is divided into a cortex and medulla. Each area produces different types of hormones that are essential to normal functioning of the body. The adrenal cortex is separated into three areas: zona glomerulosa, zona fasciculata, and zona reticularis. The zona glomerulosa produces the mineralocorticoid aldosterone, the zona fasciculata produces the glucocorticoids cortisol and cortisone, and the zona reticularis produces sex hormones. The adrenal medulla produces the catecholamines epinephrine and norepinephrine and will not be discussed in further detail in this review. In hyperaldosteronism, the overwhelming secretion of aldosterone from the zona glomerulosa tissue has major negative implications on the feline body. On physical presentation, the most significant findings presented are severe hypokalemia presenting as overwhelming muscle weakness, most distinctly cervical ventroflexion, and hypertension that can manifest retinal detachment and thus acute blindness in some instances.


The major function of aldosterone is in the Renin-Angiotensin-Aldosterone System, specifically by acting on the distal tubules and collecting duct, which helps to control blood pressure and maintain extracellular fluid volume in response to changes in renal blood flow and electrolytes (Nichols, 2016). It accomplishes this by resorbing sodium at the expense of potassium and naturally, water follows. Aldosterone has been found to play a major role in the control of vascular tone and mineralocorticoid receptors have been found in non-epithelial tissues such as the heart fibroblasts, endothelial cells, salivary and sweat glands, GI tract, and vascular smooth muscle cells (Bento et al., 2016). Experiments have also shown that increased aldosterone concentrations increases blood pressure, which is accomplished by the retention of sodium and water and the excretion of potassium into the urine. When excessive aldosterone is secreted, the blood pressure increases leading to hypertension and an increased urinary loss of potassium- so much so that the cat goes into a hypokalemic state.

Potassium is one of the three major electrolytes in the body, along with sodium and chloride, and is normally found in the extracellular fluids and plasma in the concentration of 3.2-5.7 mEq/L. In hypokalemic cats, the literature states that most are near 2.5 mEq/L which is considered severely low and leads to muscle weakness (Nichols, 2016). Potassium is the major determinant of cell resting membrane potential and has direct effect on the zona glomerulosa for the secretion of aldosterone. Both sodium and potassium are directly involved in establishing the resting membrane potential, which is the potential electrical difference across the cell membrane and allows consequent muscle movement to occur. The membrane threshold must be overcome by depolarization in which the membrane potential voltage becomes less negative to a certain degree. When this occurs, for a short period of time, sodium enters the cell and potassium leaves to maintain the balance. When serum potassium is low, the threshold potential is harder to reach and initiate meaning the action cannot occur and muscle weakness is seen as the nerve cell is essentially in an idle state (Bento et al., 2016). Cats show an overall systemic muscle weakness and in connection with this, cervical ventroflexion is observed.

Cervical ventroflexion indicates that the neck is positioned ventrally, toward the ground, and the cat is physically unable to lift it. Most domestic animals have a special anatomical structure called the nuchal ligament, with cats being the exception, which typically runs from the spinous process of the second cervical vertebrae to that of the

first thoracic vertebrae in the dog, for example. This ligament helps passively lift the head and neck and maintain its normal posture. Since cats lack this ligament, they cannot lift their head due to the overwhelming muscle weakness associated with the hypokalemia. In large domestic herbivores, such as horse and cattle, their nuchal ligament is much more impressive as they spend most of their time grazing and it actually attaches to the base of the skull.

As previously mentioned, hyperaldosteronism can cause hypertension and subsequent retinal detachment has been observed. When there is excessive aldosterone secreted, plasma renin is suppressed which is involved in controlling blood pressure. Since sodium and water are reabsorbed via aldosterone, the vascular volume increases and leads to an increase in systemic vascular resistance that helps propagate hypertension (Sahay & Sahay, 2012). It should be noted that not all cats with hyperaldosteronism also have hypokalemia and high blood pressure, but it is seen in most documented cases. The occular changes most commonly noted due to the hypertension were mydriasis (dilated pupils), hyphema (pooling of blood inside the anterior chamber of eye), and acute blindness due to retinal detachment and/or intraocular hemorrhages (Nichols, 2016). In a 2010 study of 40 cats diagnosed with hyperaldosteronism, 31 of 37 submitted for a blood pressure assessment had hypertension, 10 of 19 submitted for an ophthalmic exam had these ocular changes, and hypokalemia was observed in 19 of the 40 cats (Bento et al., 2016). There are also other less-specific symptoms documented with hyperaldosteronism including polyuria/polydipsia, anorexia, weight loss, and depressed mentation.


Cats diagnosed with primary hyperaldosteronism are largely geriatric, but it has been identified in those under five years (Bento et al, 2016). The best way to diagnose this condition, and to differentiate between the primary and secondary forms, is by measuring the aldosterone to plasma renin ratio. Cats with adrenocortical tumors have a very high plasma aldosterone concentration and a very low plasma renin concentration, which is usually almost completely suppressed since the secretion of aldosterone in this instance is independent of the Renin- Angiotensin-Aldosterone system. When the origin of the hyperaldosteronism is unknown or bilateral hyperplasia of the adrenal cortex is the cause, the aldosterone levels may only be slightly elevated and the renin levels slightly increased or within normal limits (Bento et al., 2016). Sample preparation is very important and only a few laboratories in the United States offer plasma renin testing, including the University of Tennessee and Michigan State University veterinary diagnostic laboratories.

An alternative diagnostic option is to measure the urinary aldosterone to creatinine ratio. This approach allows easier sample collection and is a good representation of the aldosterone circulating over a longer period of time. This may also be a more practical option when combined with suppression induced by salt or fludrocortisone acetate (Bento et al., 2016). The latter is the drug of choice for this test and significantly reduces the urinary aldosterone to creatinine ratio in healthy cats without hyperaldosteronism (Kooistra, 2015). In cats with hyperaldosteronism, this ratio was not lowered.

Yet another diagnostic test available is the adrenocorticotropic hormone (ACTH) stimulation test, which encourages the production of aldosterone (Bento et al., 2016). The administration of exogenous ACTH causes a notable increase in aldosterone secretion from the adrenal glands and in cats with primary hyperaldosteronism, the aldosterone response is usually reduced or absent. This test is extremely sensitive and many authors note that it is not the first choice in diagnosing hyperaldosteronism. In addition to these specific diagnostic tests, basic bloodwork including electrolyte levels and a complete urinalysis should be performed.

Diagnostic imaging is also highly recommended as an additional tool to assess any adrenal gland abnormalities and include ultrasonography, magnetic resonance imaging (MRI), and/or computed tomography (CT). These imagining options are also vital in determining if the disease is unilateral or bilateral which shapes the treatment protocol. Authors suggest utilizing these imagine methods in all cases of suspected hyperaldosteronism and especially when other diagnostic tests suggest abnormal aldosterone regulation (Bento et al., 2016). If imaging was used without corresponding laboratory testing, any adrenal abnormalities noted would not necessarily indicate hyperaldosteronism was to blame as other hormone producing or non-producing lesions could be present, such as cortisol or progesterone-secreting masses or other non-functional masses (Bento et al., 2016). Ultrasonography only

is perfectly acceptable after diagnostic testing and has often shown the presence of calcification and masses to differences in the echogenicity of the adrenal glands (Bento et al., 2016). Both MRI and CT could improve the images obtained from the cat, but are not required.

Treatment and Prognosis

The determination of unilateral vs bilateral hyperaldosteronism and the presence of any metastasis should be determined, if possible, as it shapes the treatment plan. The most common tumors associated are adenomas or adenocarcinomas, and in cats with unilateral primary aldosteronism, with no evidence of any metastasis, the gold- standard treatment of choice is a unilateral adrenalectomy. Before, during, and after operative treatment, the hypokalemia should be controlled with potassium supplementation. After the aldosterone-producing tumor has been removed, the prognosis is excellent with no medication required (Nichols, 2016). However, there have been documented complications with the surgery such as intra-abdominal hemorrhage, thromboembolism, acute renal failure, and sepsis. Although complications are possible, they are relatively uncommon and no risk factors for the surgery have been identified at this time.

Since at least one adrenal gland is required for normal endocrine functioning, a bilateral adrenalectomy is not an option if bilateral primary hyperaldosteronism is diagnosed. In this case, medical therapy is the best treatment option. It should be noted that there are other circumstances in which medical therapy is completely acceptable: financial constraints, bilateral adrenocortical hyperplasia, a tumor that cannot be completely removed with surgery, metastasis, and/or owner decision, to name a few. When medical therapy is chosen, there are three main drugs used: spironolactone, an antihypertensive drug, and potassium supplementation. Spironolactone is an aldosterone receptor blocker, which promotes potassium retention and sodium excretion (Bento et al., 2016). The antihypertensive drug of choice in this instance is amlodipine, which is a calcium channel blocker that dilates the blood vessels and improves blood flow. Finally, an oral potassium gluconate supplement should be used to combat the low potassium levels. In all, the prognosis for medical therapy is not as favorable as unilateral hyperaldosteronism, but has still reported a survival rate of several months to years even (Bento et al., 2016). It should also be noted that hyperaldosteronism due to bilateral adrenocortical hyperplasia is somewhat milder than that caused by a neoplastic tumor and can be maintained on long-term use of spironolactone and potassium supplementation. However, complete removal of an aldosterone-producing tumor offers the best prognosis.


Feline primary hyperaldosteronism is said to be one of the most common adrenocortical disorders in cats, yet it is still underdiagnosed. A veterinarian examining a geriatric, hypokalemic, hypertensive cat should place the condition high on their differential list; especially if the feline friend is very weak and displaying cervical ventroflexion. When the condition is suspected, the proper diagnostic and subsequent imaging tests should be performed to ensure a proper diagnosis. Upon diagnosis of primary hyperaldosteronism, surgical or medical treatment must be discussed and the best option chosen for the patient. While surgery is the gold-standard when unilateral hyperaldosteronism is to blame, medical therapy of spironolactone, amlodipine, and a potassium supplement still provide a favorable prognosis. Since the early 1980s, feline hyperaldosteronism has been on the rise and with growing knowledge of the condition, the number of diagnoses are also expected to keep rising. Treatment and diagnostics are continuing to improve with scientific advances, but the awareness of this condition still needs more widespread attention. Greater understanding of this disease process needs to be available to ensure the best options for our animal companions.


  • Bento, D. D., Zahn, F. S., Duarte, L. C., & Machado, L. H. (2016). Feline primary hyperaldosteronism: an emerging endocrine disease. Cie╠éncia Rural, 46(4), 686-693. doi:10.1590/0103-8478cr20141327
  • Kooistra, H. S. (2015). Feline Hyperaldosteronism. Retrieved July 6, 2017, from http://www.vin.com/doc/?id=6790463
  • Nichols, R. (2016). The Nuts and Bolts of Feline Hyperaldosteronism. Retrieved July 6, 2017, from http://www.vin.com/doc/?id=7126907
  • Sahay, M., & Sahay, R. K. (2012). Low Renin Hypertension. Indian Journal of Endocrinology and Metabolism, 16(5), 728-739. doi:10.4103/2230-8210.100665

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