Primary hyperaldosteronism is characterised by excessive autonomous secretion of aldosterone from one or both adrenal glands resulting in clinical signs relating to hypertension and/or hypokalaemia. Adrenocortical tumours are the most common cause of primary hyperaldosteronism in cats. There is an approximately equal incidence of adenomas and carcinomas affecting the right and left adrenal gland with almost equal frequency. Rarely, bilateral tumours have been reported. More recently, primary hyperaldosteronism has been recognized in association with adrenocortical hyperplasia.

Pathophysiology

Increased autonomous secretion of aldosterone has its primary effects on the mineralocorticoid receptors in the distal renal tubules, colon and salivary glands to stimulate sodium reabsorption and potassium and hydrogen excretion. Sodium retention results in an expansion of the extracellular fluid volume and resultant increase in blood pressure and excessive potassium excretion leads to hypokalaemia. The elevated plasma aldosterone and increased circulating blood volume have a negative feedback effect on renin release, resulting in reduced plasma renin activity.

Secondary hyperaldosteronism is used to describe other conditions, such as cardiac failure and hepatic cirrhosis, in which aldosterone release is a normal adrenal response to the activation of the renin-angiotensin-aldosterone system (RAAS).

Clinical Signs

 Primary hyperaldosteronism is a disease of middle-aged to old-aged cats with a mean age of 12 years. There is no breed or sex predisposition.

 The most common presenting sign is muscular weakness due to the hypokalaemia. The degree can range from mild weakness and lethargy to severe generalized weakness, ataxia, depressed spinal reflexes and flaccid. Ventroflexion of the neck may be noted.

 Blindness, which may be sudden or gradual in onset is due to systemic hypertension and is usually results from retinal detachment and intraocular haemorrhage. Systemic hypertension can also lead to left ventricular hypertrophy and cardiac murmurs. Most cats with primary hyperaldosteronism have blood pressure above 180 mmHg.

 Impaired renal function is common and many cats will exhibit polydipsia and polyuria.

Differential Diagnosis of Feline Systemic Hypertension

 Chronic renal disease

 Hyperthyroidism

 Diabetes mellitus

 Hyperaldosteronism

 Hyperadrenocorticism

 Chronic anaemia

 Liver disease

Diagnosis

Laboratory Findings

 Moderate to severe hypokalaemia is the typical and most consistent finding.

 The sodium concentration is usually normal or only slightly elevated, although total body sodium will be increased.

 Creatine kinase is elevated in cats with polymyopathy.

 Azotaemia with increased urea and creatinine is also a frequent, but non-specific finding.

 Definitive diagnosis requires demonstration of an inappropriately elevated aldosterone concentration (reference range 110-540 pmol/l) with a low plasma renin concentration (reference range 60-630 fmol/l/s). The latter is difficult to measure and the assay may not be available.

 Plasma aldosterone to renin ratios and urinary aldosterone to creatinine ratios before and after suppression with salt or fludrocortisone acetate have also been described.

Differential Diagnosis of Feline Hypokalaemia

 Decreased intake

 Anorexia

 Potassium-deficient intravenous fluids

 Potassium-deficient diet

 Potassium translocation

 Metabolic alkalosis

 Insulin administration

 Diabetic ketoacidosis

 Periodic hypokalaemia (Burmese cats)

 Increased gastrointestinal loss

 Vomiting

 Diarrhoea

 Increased renal loss

 Polyuria

 Chronic renal failure

 Acute renal failure (polyuric phase)

 Diuretic administration (loop or thiazide diuretics)

 Renal tubular acidosis

 Primary hyperaldosteronism

 Liver failure

 Congestive heart failure

Note: hypokalaemia in some diseases may have more than one mechanism

Diagnostic Imaging

 Ultrasonography, CT and MR are useful imaging techniques for localisation and staging of the tumour.

 Ultrasonography is the most available modality for identification of adrenal mass lesions or bilateral adrenal hyperplasia and may provide important information regarding adherence to surrounding organs, e.g., liver and kidney as well as possible extension into the lumen of the caudal vena cava.

 CT and MR may well provide additional information but these techniques do not always indicate the likely ease with which a mass may be surgically removed.

 In practice, primary hyperaldosteronism can be made by demonstrating an adrenal mass in a cat with hypokalaemia and/or hypertension and a markedly increased plasma aldosterone concentration.

Management

 Initial treatment should be directed at alleviation of hypokalaemia and controlling blood pressure.

Medical Management

 Medical management may also be used for non-surgical cases, for animals with metastases or in the rare case of bilateral hyperplasia.

 Treatment can be given using:

 Potassium supplementation e.g., potassium gluconate (Tumil-K) 2-6 mmol per os BID.

 Spironolactone (Prilactone), an aldosterone antagonist, 2-4 mg/kg per os SID.

 Amlodipine (Istin), a calcium channel blocker, to control blood pressure, 0.625-1.25 mg/cat per os SID.

 Those cases with polymyopathy will show clinical improvement despite the fact that the potassium concentration rarely returns to the normal range.

 In most, but not all cases of hypertension, the blood pressure can be controlled with amlodipine given SID or BID.

 Medical management has been used for long term control of signs.

Surgical Management

 Surgical intervention may be the treatment of choice for tumours with no detectable metastases, but post-operative morbidity and mortality can be high.

 Adrenalectomy is usually performed through a ventral midline celiotomy, so that both adrenals can be visualised. Care must be taken to keep the adrenal capsule intact during the dissection for adrenalectomy to avoid fragmentation of the tumour and possible seeding of neoplastic cells into the peritoneum.

 Complications of surgery include haemorrhage, anorexia, hypotension, renal failure and septicaemia.

 To reduce the peri-operative morbidity and mortality close monitoring of electrolytes and blood pressure should be performed.

 Intravenous fluid therapy with potassium supplementation and replacement mineralocorticoid therapy (fludrocortisone acetate at a dose of 15 mcg/kg per os SID) are given prior to surgery and continued for several days post-operatively.

 If the serum electrolytes and blood pressure remains normal, the treatment is phased out, but is re-introduced if the blood pressure falls below normal.

 Post-operative survival for over 5 years has been reported.