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.



Excessive aldosterone production can be the result of primary or secondary causes.5,10-13 Primary hyperaldosteronism results from a neoplastic adrenal mass—either an adenoma or an adenocarcinoma that could be unilateral or bilateral—or from hyperplasia of the zona glomerulosa of the adrenal cortex, often termed idiopathic or nontumorous primary hyperaldosteronism.5,11 Congestive heart failure, renal failure, and hepatic failure can each be responsible for secondary hyperaldosteronism because of activation of the renin-angiotensin-aldosterone system. The consequences of excessive aldosterone production are related to increased sodium and water retention, causing systemic arterial hypertension and increased renal potassium excretion, resulting in hypokalemia.5,10,14,15

1. A unilateral adrenal adenoma from a cat. (The shiny layer is the peritoneum, and the cat's head is to the right.)
Histopathologic findings in reported cases of cats with primary hyperaldosteronism include unilateral adrenocortical adenocarcinomas, unilateral and bilateral adenomas (Figure 1), and bilateral nodular hyperplasia of the adrenal glands.5,6,11,12,14,16,17 Since histopathologic examination of adrenal tissue is required to determine the cause of primary hyperaldosteronism, and cats with hyperplasia of the zona glomerulosa are typically treated medically, bilateral nodular hyperplasia likely occurs more frequently than is represented by current data. The etiology of this idiopathic form of hyperaldosteronism in cats is unknown at this time, but a circulating stimulatory factor is thought to be responsible for hyperfunction of the zona glomerulosa.6 This factor has not been identified, but one theory suggests it is a pituitary peptide that may be a fragment of pro-opiomelanocortin.6

With respect to cases of primary hyperaldosteronism, nontumorous or idiopathic bilateral nodular hyperplasia of the zona glomerulosa may lead to incomplete suppression of renin, while unilateral or bilateral neoplasia of the zona glomerulosa typically results in complete renin suppression.4-6,11,12,14,16,17 In disease with incomplete renin suppression, hyperaldosteronism is an important mediator of progressive renal disease in cats because of the presence of two mediators of vascular change and fibroproliferative destruction—aldosterone and angiotensin II.6

CKD has been linked to glomerular and tubulointerstitial injury as well as excessive accumulation of the extracellular matrix of the kidney.6 Extracellular matrix accumulation can be mediated by several growth factors including angiotensin II.6 Its actions may be involved in the upregulation of hyperplasia or hypertrophy of mesangial, glomerular endothelial, tubular epithelial, and renal interstitial fibroblasts.6 Angiotensin II is also a peripheral vasoconstrictor and a regulator of glomerular filtration and is considered a proinflammatory cytokine responsible for the onset of and progressive damage associated with CKD.6

Aldosterone can also contribute to the progression of renal damage by promoting vascular thrombosis and fibrosis.6 Thus both aldosterone and angiotensin II are instrumental in sustaining hypertension and further fibroproliferative destruction of the kidney.6 It is important to be aware of the role these factors play in the progression of renal disease, as systemic hypertension, hypokalemia, or both in geriatric cats are often clinical signs attributed to CKD as the causal disorder, as opposed to the direct effect of primary hyperaldosteronism. This association tends to delay or often preclude further diagnostic tests or screening for this disease in cats.

Many cats with hyperaldosteronism can also have evidence of cardiovascular disease indicated by the presence of a heart murmur, cardiomegaly on thoracic radiographic examination, or ventricular hypertrophy on echocardiographic examination.11,14,16-18 These cardiac changes are consistent with organ damage caused by hypertension secondary to increased intravascular volume.15


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