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Help cats with hyperaldosteronism hold their heads high

VettedVetted April 2019
Volume 114
Issue 4

What you need to know when it comes to recognizing, diagnosing and managing this endocrine disease in cats.

Aldosterone is secreted by the zona glomerulosa of the adrenal cortex and is the endpoint of the renin-angiotensin-aldosterone system (RAAS). This hormone promotes the reclamation of sodium from the renal filtrate, thereby increasing extracellular fluid volume and blood pressure. Hyperkalemia also triggers the release of aldosterone; secretion is inhibited by the natriuretic peptides and by hypokalemia.1

Primary hyperaldosteronism (PHA; aka Conn's syndrome) is the inappropriate release of aldosterone by one or both adrenal glands and is the most common cause of endocrine hypertension in people. Bilateral idiopathic hyperplasia accounts for more than 60% of cases in people, and a unilateral adenoma is identified in about 35%.2 PHA is uncommonly reported in cats and dogs and is traditionally associated with a functional adrenocortical tumor.3,4 However, PHA with bilateral hyperplasia of the zona glomerulosa was described in cats with chronic kidney disease, hypertension and hypokalemia.5

Signalment, history, physical examination

Most cats with PHA are > 10 years of age.3-5 Very few canine cases have been reported, but all were > 10 years old.6-8

Most patients present with signs related to systemic hypertension, hypokalemia, or both. Hypertension may cause vision loss or acute neurological compromise; ocular lesions such as hyphema, mydriasis, anisocoria, retinal hemorrhage or detachment may be noted. Hypokalemia will result in muscle weakness; this may initially manifest as an intermittent plantigrade stance or difficulty jumping but will progress to collapse as potassium concentrations drop below 2.5 mmol/L. Cats with severe hypokalemia have cervical ventroflexion (Figure 1) and feel ‘floppy' when handled.

Figure 1. A cat with hypokalemia and cervical ventroflexion. (Image courtesy of Dr. Jimmy Barr)

Polyuria and polydipsia are also routinely reported and appear to be the most common clinical complaint in dogs with PHA.6-8  

Routine laboratory findings

Hypokalemia may be marked or borderline. Serum sodium concentration are often normal, as the excess sodium is accompanied by water. A metabolic alkalosis may be noted due to exchange of sodium for hydrogen ions in the distal nephron. Creatinine kinase (CK) concentrations are increased in patients with overt myopathy. Serum creatinine and urea nitrogen concentrations may be increased; interestingly, concurrent serum phosphorus concentrations may be borderline low.

Urine is often poorly concentrated; this is due to a combination of hypertension, renal compromise and hypokalemia (low potassium causes a secondary nephrogenic diabetes insipidus). Proteinuria may be noted and should be quantified by measurement of the urine protein:creatinine ratio.

The results of a complete blood count are expected to be essentially normal, although dogs may manifest a stress leukogram. Concurrent renal disease may result in anemia, particularly in cats.  


Abdominal ultrasonography should be performed in any patient with a clinical suspicion of PHA. PHA is traditionally associated with a unilateral adrenal mass, although a small number of cats with bilateral tumors have been described.3 However, bilateral hyperplasia may not be easily detected during abdominal ultrasonography.5 Conversely, finding an adrenal mass is not sufficient to diagnosis PHA, as it may be nonfunctional, or secreting catecholamines (a pheochromocytoma), cortisol or sex hormones. Cats with tumors secreting both progesterone and aldosterone have been reported, with a confusing constellation of clinical signs; similarly, a multifunctional cortical tumor has been reported in a dog.6

Thoracic radiographs may identify metastatic lesions or evidence of cardiomegaly.


Baseline aldosterone measurement. Serum aldosterone concentrations should be interpreted in light of the concurrent potassium status, as hypokalemia should suppress aldosterone release. Generally speaking, a single aldosterone measurement > 1,000 pmol/L is enough to establish a diagnosis in a euvolemic patient with an adrenal mass, but further testing will be necessary if resting aldosterone concentrations are not dramatically elevated.1

Plasma renin activity and aldosterone:renin ratio. Comparison of serum aldosterone concentrations to plasma renin levels is ideal, as this helps to differentiate PHA (low renin) from secondary hyperaldosteronism (increased renin).1 Unfortunately, measurement of plasma renin activity is not routinely available for veterinary patients.

Urine aldosterone:creatinine ratio. This test has recently been proposed as a suitable screening test for PHA in cats. It's superior to simply measuring aldosterone in serum or plasma, as it reflects events over several hours and not just one time point.9 However, the reference range is quite wide, and the test may lack sensitivity when used alone.

Fludrocortisone suppression test. Failure of an exogenous aldosterone analogue (i.e., fludrocortisone) to suppress aldosterone production suggests autonomous or inappropriate secretion and supports a diagnosis of PHA.9,10 The protocol is as follows:

1. Determine the baseline urine aldosterone:creatinine ratio.

2. Administer fludrocortisone for four days (0.05 mg/kg orally twice daily).

3. Determine the urine aldosterone:creatinine ratio.

Failure to suppress aldosterone production (defined as > 50% decrease in urine aldosterone:creatinine ratio) indicates PHA.


Hypokalemia. Hypokalemic animals can become acutely compromised with cardiac arrhythmias and compromised ventilation.11 Even if the patient is substantially dehydrated, it's more important to manage the hypokalemia than replace crystalloid losses. Bear in mind that even modest amounts of volume restoration may markedly exacerbate hypokalemia and result in death. The best way to provide potassium is by an infusion of potassium chloride (KCl); this is caustic to veins but is well-tolerated if diluted appropriately. Most clinicians regard 0.5 mEq/kg/hr as the maximum rate of administration of parenteral potassium (see example below). Oral potassium supplementation can be started concurrently and repeated every four to six hours until serum concentrations are back in the reference range. Fluid losses can be cautiously replaced over 24 hours using an appropriate replacement fluid such as lactated Ringer's solution (LRS).

Example: Patient weight: 5 kg

“K-max” = 0.5 mEq/kg/hr = 0.5 x 5 = 2.5 mEq/hr

Volume of KCl at 2 mEq/ml/hr = 1.25 ml KCl/hr

Via a peripheral catheter:

  • Dilute 1:9  = 1.25 ml KCl and 11.25 ml D5W or LRS (add 25 ml of KCl to 225 ml D5W or LRS)
  • Administer 12.5 ml of the mixture/hr
  • Via a central line:
  • Dilute 1:4 = 1.25 ml KCl and 5 ml D5W or LRS (add 50 ml of KCl to 200 ml D5W or LRS)
  • Administer 6.25 ml of the mixture/hr

.Chronic management includes oral potassium supplementation (2 mEq/kg orally twice daily), along with spironolactone (starting at 2 mg/kg orally twice daily). This agent is an aldosterone receptor antagonist and directly inhibits the action of the hormone. It should be used cautiously in azotemic patients.

Hypertension. Prompt control of systemic hypertension is essential to protect the retina, central nervous system and kidney. Amlodipine is a good choice if spironolactone alone is not effective; angiotensin-converting enzyme inhibitors (e.g., enalapril) are unlikely to be helpful, as renin is suppressed. 

Surgical. In patients with a nonmetastatic unilateral adrenal mass, adrenalectomy is the treatment of choice. Reported outcomes are fairly positive, although a high level of surgical expertise and careful postoperative management is needed.3,4,12

Simpson (Image courtesy of Dr. Audrey Cook)

Simpson (Image courtesy of Dr. Audrey Cook)

Case example

Simpson is a 14-year-old castrated male domestic shorthaired cat.

Chief complaint: Intermittent weakness for 2 months, with difficulty walking; events often noted after vomiting episode.

Past history: Diagnosed with hyperthyroidism 2 years ago; controlled with oral methimazole 2.5 mg PO q12h.

Physical examination: T=101.0F; P=172 bpm; R=36 bpm; Wt=4.2 kg; BP=178 mmHg;

1 cm nodule noted in left thyroid gland; remainder of examination unremarkable

Chemistry profile: All parameters within normal limits, except potassium which was 3.2 mmol/L (ref range: 3.5-5.1 mmol/L)

Abdominal ultrasonography: A 12.4-mm mass associated with the right adrenal gland

An ultrasonographic image of Simpson's right adrenal gland. (Image courtesy of the Radiology Section at Texas A&M University)

Serum aldosterone concentration: > 4,000 pmol/L (ref range: 194-388 pmol/L)

Initial treatment: Spironolactone 6.25 mg orally q12h; potassium gluconate 2 mEq orally q12h; methimazole orally, as before

Outcome: Owner declined adrenalectomy. Managed effectively with increasing doses of spironolactone (up to 12.5 mg PO q12h) and potassium gluconate (up to 4 mEq PO q12h) for more than 2 years. Euthanized for refractory hypokalemia after 25 months.


1. Djajadiningrat-Laanen SC, Galac S, Kooistra. Primary hyperaldosteronism; Expanding the diagnostic net. J Feline Med Surg 2011;13:641-650.

2. Fagugli RM, Taglioni C. Changes in the perceived epidemiology of primary hyperaldosteronism. Int J Hypertens 2011; http://dx.doi.org/10.4061/2011/162804

3. Ash RA, Harvey AM, Tasker S. Primary hyperaldosteronism in the cat: a series of 13 cases. J Feline Med Surg 2005;7:173-182.

4. Lo AJ, Holt DE, Brown DC, et al. Treatment of aldosterone-secreting adrenocortical tumors in cats by unilateral adrenalectomy: 10 cases (2002-2012). J Vet Intern Med 2014;28:137-143.

5. Javadi S, Djajadiningrat-Laanen SC, et al. Primary hyperaldosteronism, a mediator of progressive renal disease in cats. Dom Anim Endocrinol 2005;28:85-104.

6. Behrend EN, Weigand CM, Whitley EM, et al. Corticosterone- and aldosterone-secreting adrenocortical tumor in a dog. J Am Vet Med Assoc 2005;266;1662-1666.

7. Rijnberk A, Kooistra HS, van Vonderen IK, et al. Aldosteronoma in a dog with polyuria as the leading symptom. Dom Anim Endocrinol 2001;20:227-240.

8. Frankot JL, Behrend EN, Sebestyen P, et al. Adrenocortical carcinoma in a dog with incomplete excision managed long-term with metastasectomy alone. J Am Anim Hosp Assoc 2012;48:417.

9. Djajadiningrat-Laanen SC, Galac S, Cammelbeeck SE, et al. Urinary aldosterone to creatinine ratio in cats before and after suppression with salt or fludrocortisone acetate. J Vet Intern Med 2008;22:1283-1288.

10. Djajadiningrat-Laanen SC, et al. Evaluation of the oral fludrocortisone suppression test for diagnosing primary hyperaldosteronism in cats. J Vet Intern Med 2013;27:1493-1499.

11. Haldane S, Graves TK, Bateman S, et al. Profound hypokalemia causing respiratory failure in a cat with hyperaldosteronism. J Vet Emerg Crit Care 2007;17:202-207.

12. Daniel D, Mahoney OM, Markovich JE, et al. Clinical findings, diagnostics and outcome in 33 cats with adrenal neoplasia (2002-2013). J Fel Med Surg 2016;18;77-84.

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