Chapter 54 The term primary hyperaldosteronism (PHA) refers to the clinical consequences of mineralocorticoid excess arising from autonomous hyperfunction of the zona glomerulosa of the adrenal cortex. The first case of feline PHA related to an adrenocortical carcinoma was reported in 1983 (Eger, Robinson, and Huxtable, 1983). Since 1999, at least 40 additional affected cats have been described in individual case reports, case series, or book chapters. To date, the best-defined occurrences of PHA in cats are related to unilateral adrenocortical carcinoma or adenoma. Evidence for PHA related to idiopathic nodular hyperplasia of the zona glomerulosa was presented in a series of 11 cats with concomitant renal disease (Javadi et al, 2005). Increased awareness of the clinical manifestations has led to speculation that PHA may be the most common adrenocortical disorder in cats. This chapter summarizes the clinical features, diagnosis, and treatment of PHA in cats. In instances of reduced arterial blood volume, the RAAS can respond with sustained release of renin and aldosterone. Renin-stimulated aldosterone hypersecretion is referred to as secondary hyperaldosteronism, which usually occurs as a compensatory response to heart failure, gastrointestinal disease, water deprivation, or other causes of hypovolemia. Persistence of secondary hyperaldosteronism in an attempt to restore or maintain glomerular perfusion may contribute to the onset of hypokalemia or hypernatremia. In an experimental rat model, iatrogenic aldosterone excess promoted increased urinary loss of calcium and magnesium, with subsequent development of secondary hyperparathyroidism and reduced bone mineral content (Chhokar et al, 2005). Interestingly, cats with PHA and concomitant azotemia usually do not have hyperphosphatemia. It is possible that cats with PHA also have elevated parathyroid hormone levels, which would promote urinary excretion of phosphorus and allow serum phosphorus levels to remain normal (Graves, 2011). • Hypokalemic polymyopathy. This is the most common reported presentation for cats with adrenal neoplasia. Cervical ventroflexion is the most frequently encountered sign of muscle weakness, but hind limb weakness and ataxia or, less commonly, limb stiffness, dysphagia, respiratory failure, and collapse may also occur. Signs of muscular weakness may be mild and episodic or insidious in onset, whereas in other cats these signs can be severe and acute in onset. Hypokalemic polymyopathy is reported to be a much less common presenting sign in cases of adrenal hyperplasia • Ocular signs of arterial hypertension. These are a less common primary presentation in cats with adrenal neoplasia, but appear to be more common major presenting signs in cats with bilateral adrenal hyperplasia that tend to have more severe hypertension. Clinical signs may include intraocular hemorrhage or acute-onset blindness resulting from retinal detachment. This presentation is more likely in cats with systolic blood pressures above 200 mm Hg and can be the sole presenting sign. Subtle signs of hypertensive retinopathy evident on fundic examination (e.g., subretinal, intraretinal, and intravitreal hemorrhages, retinal edema) are more commonly observed. Less common clinical findings in adrenal neoplasia cases include polyuria and polydipsia, polyphagia, and a systolic heart murmur. An adrenal mass may also be detected as an incidental finding on abdominal ultrasound examination or palpation in a normokalemic cat that may develop additional signs of hyperaldosteronism some time later (Renschler and Dean, 2009).
Feline Primary Hyperaldosteronism
The Renin-Angiotensin-Aldosterone System: Regulation and Actions
Clinical Signs and Physical Examination Findings
