Feline hyperaldosteronism: Recognition and diagnosis - Veterinary Medicine
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Feline hyperaldosteronism: Recognition and diagnosis
Have a cat presenting with hypertension? Hypokalemia? Here's why you should add this disorder to your differential diagnosis list.



Aldosterone:renin ratio

The gold standard for screening for feline primary hyperaldosteronism is the aldosterone:renin ratio.5,6,21 This test will allow determination and differentiation of primary vs. secondary hyperaldosteronism. The plasma renin activity (PRA) is taken into account, as an elevated plasma aldosterone concentration (PAC) with low PRA is indicative of aldosterone secretion independent of stimulation from the renin-angiotensin-aldosterone system.6 These patterns are consistent with primary hyperaldosteronism and the autonomous secretion of aldosterone by the adrenal glands.6,10 In cases of either unilateral or bilateral adrenal tumors, the PAC is typically markedly elevated, and the PRA is usually completely suppressed.5,6,10

This test has some disadvantages, mainly attributable to the sensitivity of the renin assay. The accuracy of the aldosterone:renin ratio depends on preservation of renin activity during sample collection and storage.5 A large volume of blood (4 ml) and instant freezing of separated plasma are necessary, and reference intervals for PRA differ markedly among laboratories, making comparison difficult.5 Thus clinicians are often left to rely on PAC alone.10 It is important to interpret the PAC concurrently with the cat's potassium concentration, since potassium is the main determinant of aldosterone secretion.6 A PAC within or above the laboratory's reference interval is inappropriate in a cat that is volume-overloaded or hypokalemic.

ACTH stimulation

ACTH is an additional stimulant of aldosterone production and can also be used to evaluate adrenal mineralocorticoid production.9 Exogenous ACTH administration causes a reliable increase in aldosterone secretion. A standard dose of cosyntropin (125 μg/cat intravenously) has been used for ACTH stimulation tests traditionally.8 However, a recent study has determined that a cosyntropin dose of 2.5 μg/kg given intravenously will cause a peak aldosterone response analogous to that obtained with the 125-μg/cat intravenous dose, and blood sample collection after cosyntropin administration can be obtained 15 to 75 minutes after administration with no significant difference in aldosterone concentration.8

If it is necessary to evaluate plasma cortisol response simultaneously, then a cosyntropin dose of 5 μg/kg given intravenously is recommended, with a sample collected 60 to 75 minutes after stimulation.8 When evaluating a cat for primary hyperaldosteronism, an ACTH stimulation test is typically unnecessary, and diagnosis can usually be made from the PAC alone.

Future alternative testing

Ideally, a test using an agent that will suppress aldosterone production in healthy cats but have little to no effect in those with primary hyperaldosteronism would be the best method to confirm a suspected diagnosis and prove that hyperfunction of the zona glomerulosa is the cause of an elevated PAC. In people, several tests have been developed to show that an elevated aldosterone:renin ratio is due to primary hyperaldosteronism, including a captopril stimulation test, oral sodium loading, saline infusion, and a fludrocortisone suppression test.5 Since such diagnostic tests have yet to be developed and validated in cats, the patient's clinical presentation, electrolyte concentrations, PAC, and diagnostic imaging all need to be taken into consideration to make a diagnosis.


Imaging should be performed in all cats that you suspect have primary hyperaldosteronism, and it is a necessity in those cats whose screening tests indicate abnormal regulation of aldosterone production. Determining the laterality of disease is important to direct proper treatment, as unilateral primary hyperaldosteronism can potentially be cured surgically, while bilateral or confirmed metastatic disease should be managed medically.

Abdominal ultrasonography, magnetic resonance imaging (MRI), and computed tomography (CT) can be used to identify adrenal abnormalities and potentially evaluate distant metastases to other abdominal organs and local invasion of the tumor into the caudal vena cava and surrounding structures. Thoracic radiography can be used to detect the presence of pulmonary metastases.


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