Feline hyperaldosteronism: Recognition and diagnosis
The first case of primary hyperaldosteronism in a cat was described in 1983.4 The disease is not often diagnosed in veterinary practice despite the thought that it is likely one of the most common adrenocortical disorders in cats.5 Many cases of arterial hypertension, hypokalemia, or both are attributable to chronic kidney disease (CKD) as the primary disorder, but primary hyperaldosteronism itself has been shown to be a mediator and associated with the progression of CKD.6
This article reviews the physiology and actions of aldosterone and the pathophysiology of primary hyperaldosteronism, and it describes the typical presentation and clinicopathologic abnormalities. Primary hyperaldosteronism should be included as a differential diagnosis in cats presenting with hypokalemia, hypertension, or both and should no longer be regarded as a rare condition.ALDOSTERONE PHYSIOLOGY
Potassium ions also regulate aldosterone secretion independent of the renin-angiotensin-aldosterone system by directly depolarizing the membranes of the zona glomerulosa cells in cases of hyperkalemia.7 Adrenocorticotropic hormone (ACTH) also acts as a third stimulant of aldosterone production, and studies have shown significant differences between plasma aldosterone concentrations before and after synthetic ACTH administration.8,9
Circulating aldosterone targets tissues of the kidney, colon, and salivary gland and passes through the plasma membranes of these epithelial cells, binding to cytoplasmic mineralocorticoid receptors. In response to circulating aldosterone, the epithelial cells of the distal convoluted tubules and collecting ducts of the kidney reabsorb sodium, thereby increasing water retention, and excrete potassium. Plasma and extracellular fluid volume are increased along with total peripheral resistance because of vasoconstriction from angiotensin II, thus causing an increase in blood pressure. Potassium is excreted into the urine, decreasing plasma potassium concentrations.
The increase in extracellular fluid volume results in an increased blood flow to the kidney, thereby decreasing renin secretion.5,10 Hyperkalemia resolves through kaliuresis, and repolarization of the zona glomerulosa cells occurs.7 These two mechanisms make up the negative feedback loop for aldosterone secretion.