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Feline Hyperaldosteronism

By Kiko Bracker, DVM, DACVECC


Feline hyperaldosteronism is likely the most common adrenocortical disease affecting cats.  It is rarely identified in dogs, with only a few sporadic case reports testifying to its existence in that species.  The eponym Conn’s syndrome is sometimes applied to primary hyperaldosteronism after Jerome Conn, who first identified the issue in humans in 1955.1  Tumors of the adrenal cortex or adrenal cortical hyperplasia can result in excessive aldosterone secretion.  Aldosterone is a hormone that balances sodium and potassium levels, with sodium being resorbed in the distal convoluted tubule of the loop of Henle, and potassium being excreted into the urine in the collecting ducts of the distal nephron.

Hyperaldosteronism can be a bit tricky to identify because it is not high on our radar of feline illnesses.  It does result in a fairly predictable collection of clinical and clinicopathological abnormalities that, when viewed together, can strongly suggest hyperaldosteronism as the cause of illness.

Figure 1: Cervical ventroflexion due to hypokalemia.

Profound hypokalemia (<3.0mEq/L) is often the first abnormality identified that triggers a suspicion of hyperaldosteronism.  Low potassium is seen in 90% of cats with this problem.  Interestingly, hypernatremia is not commonly seen since it is usually balanced by water being resorbed with the excess sodium.  Other clinpath irregularities include mild azotemia (50% of cases), creatine kinase elevation (95% of cases), and an elevated aldosterone level is seen in about 90% of cases.2,3,4  (A serum potassium of <3.0mEq/L on initial lab work in a patient that is not taking furosemide is almost always due to either potassium wasting from chronic kidney disease or hyperaldosteronism, in our experience.)

The clinical or historical signs of hyperaldosteronism are fairly non-specific.  These patients generally present with lethargy, weight loss, and historical PU/PD.  But if a patient also shows ventral neck flexion due to low potassium (image 1), or hypertension which can result in intraocular hemorrhage or retinal detachment – the leap to a suspicion of excessive aldosterone secretion is made more easily.

The next diagnostic steps will likely be an abdominal ultrasound and an aldosterone level.  But a serum potassium level of <3.0mEq/L does warrant some intervention often before those two tests can be accomplished.  If the potassium level gets near to 2.0mEq/L respiratory muscle weakness and hypoventilation can result.5,6   Profoundly weak or azotemic hypokalemic cats should be hospitalized for IV fluid therapy and aggressive IV potassium supplementation.  More stable patients can be supplemented with oral potassium gluconate at 2-6mEq/cat BID.3,4

An aldosterone level should be submitted prior to supplementation with potassium if at all possible.  Aldosterone secretion is directly related to the blood potassium level.  Aldosterone’s primary action is to reduce/excrete potassium.  If the blood potassium level is low, then aldosterone secretion should be maximally shut off in the normal patient.  Even an aldosterone level within the normal range in a hypokalemic patient would be considered too high, and suggestive of aldosterone hypersecretion.  Either a spun and separated EDTA plasma sample, or a clot tube can be used to evaluate an aldosterone level with a minimal sample requirement of 0.5-1.0ml of plasma or serum.  The turnaround time can be up to a week, so prompt submission of this sample is helpful.  Consult your lab about specific sample and shipping requirements.

Abdominal ultrasound is the most commonly used imaging modality to identify the source of suspected aldosterone secretion.  Single adrenal tumors are the most common finding, often with a small to normal contralateral adrenal gland.  Adrenal cortical hyperplasia may manifest itself as bilateral adrenal enlargement.  Bilateral adrenal adenomas have even been identified.3  Invasion of the vena cava is an uncommon occurrence, evident in only about 10% of cases.  Caval involvement is more critically evaluated with an abdominal CT scan.2

Figure 2: A unilateral adrenal adenoma in a cat.8

Once a diagnosis is made or is confidently suspected, medical treatment should be started.  Bilateral adrenal disease must be managed medically, and cats with unilateral disease who are contemplating surgical adrenalectomy should be stabilized medically for several weeks before surgery.  It can be very hard to achieve an adequate potassium level with potassium supplementation alone on an outpatient basis.2,3  Spironolactone, an aldosterone agonist and mild diuretic, at 1-2mg/kg BID should be used in conjunction with potassium supplementation.3,4  Although spironolactone has some mild diuretic effect, it is not potent enough to cause the mildly azotemic cat to worsen at home.  Sub-cutaneous fluid can easily be added at home to avoid this potential complication though.  A normal potassium level even when using spironolactone and potassium gluconate together is usually difficult to achieve – but normal should not be the goal.  Try to keep the serum potassium level 3.0-4.0mEq/L, which is usually enough to avoid any complications of hypokalemia.  Hypertension (>160mmHg) is best treated with amlodipine at 0.625-1.25mg/cat SID-BID.7  If retinal detachment is present, then BID dosing should be considered to control hypertension quickly and maximize the possibility of retinal reattachment.

The prognosis with medical management alone is very good, and survival times can be measured in years.3  Cats on medical management will need to remain on medication lifelong and have occasional BP and renal panel assessment. It is common for azotemia to gradually worsen over months to years due to imperfect control of hypertension and the profibrotic effects of aldosterone which further damages the kidneys.

If a unilateral adrenal mass or enlargement is identified, then surgical management is often the treatment of choice.  Left adrenal tumors are easier to access than right sided masses since the right kidney and adrenal gland are tucked up in the renal fossa of the liver making access challenging.  Once the affected adrenal gland is removed the prior hypertension and hypokalemia resolve quite quickly, and no further medication is needed.  The benefit of surgery for unilateral adrenal disease is that medications can be stopped and the gradually detrimental renal effects of excess aldosterone secretion can be avoided.  Survival times following adrenalectomy for an adrenal cortical adenoma or an adrenal carcinoma were not significantly different with a combined median survival time of 1,297 days.2  Carcinomas and adenomas are identified with about the same frequency.2,3



  1. JW Conn. Primary Aldosteronism. J Lab Clin Med 1955;45:661-664.
  2. AJ Lo, et al.  Treatment of aldosterone-secreting adrenocortical tumors in cats by unilateral adrenalectomy: 10 cases (2002-1012). J Vet Intern Med 2014;28:137-143.
  3. RA Ash, A Harvey, S Tasker. Primary hyperaldosteronism in the cat: a series of 13 cases. J Fel Med Surg 2005;7:173-182.
  4. S Djajadiningrat-Laanen, S Galac, H Kooistra. Primary hyperaldosteronism – expanding the diagnostic net. J Fel Med Surg 2011;13:641-650.
  5. TN Hammond, JL Holm. Successful use of short-term mechanical ventilation to manage respiratory failure secondary to profound hypokalemia in a cat with hyperaldosteronism. J Vet Emerg Crit Care 2008;18(5):517-525
  6. S Haldane, et al. Profound Hypokalemia Causing Respiratory Failure in a Cat with Hyperaldosteronism. J Vet Emerg Crit Care 2007;17(2):202-207.
  7. J Bisignano, DS Bruyette. Feline hyperaldosteronism: treatment and prognosis 2012. Vet Med;107(3):118-125.
  8. J Bisignano, DS Bruyette. Feline hyperaldosteronism: recognition and diagnosis 2012. Vet Med;107(3):118-125.