HYPERALDOSTERONISM   
Doug Brum, DVM                                                          

One of the most common problems seen in older cats is chronic renal disease and hypertension. Some of these cats also have a mild to moderate hypokalemia. An emerging diagnosis in a number of them is hyperaldosteronism, and it is one that can be easily missed. As of 2003, only 5 cases of primary hyperaldosteronism had been reported in veterinary literature. It was considered a very unusual condition. However, in the past several years, numerous publications have described the syndrome, and it is being identified with more frequency by clinicians around the country. It definitely should not be considered a rare condition anymore. 

Excess production of aldosterone may be the result of primary or secondary causes. Primary hyperaldosteronism is due to the autonomous secretion of aldosterone by abnormal cells in the adrenal gland. This can either be due to an adrenal tumor or from bilateral adrenal hyperplasia. In people, this is a very important condition (Conn’s syndrome), as it is a potential curable cause of hypertension. Secondary causes are rarer and are the result of some other condition in which excessive aldosterone production is a normal adrenal response to the activation of the renin angiotensin system (RAS). These include: kidney, liver (cirrhosis) or cardiac disease-states associated with peripheral edema.

The main function of aldosterone is the regulation of serum sodium and potassium homeostasis while maintaining normal vascular fluid volume. When aldosterone levels increase, potassium is lost through the kidneys and sodium is retained. In causing sodium conservation, aldosterone indirectly causes conservation of water, which raises blood volume and increases blood pressure. This expansion of the extracellular fluid volume and the conservation of sodium leads to suppression of the RAS, decreased renin plasma levels and hypertension. Additionally, chronically elevated aldosterone levels may also contribute to the progression of kidney damage by promoting thrombosis and fibrosis. The disease occurs much more commonly in cats, and it is very rare in dogs. It has been reported in cats between six and 20 years of age. The main clinical signs are related to the hypokalemia and hypertension that occurs with excessive aldosterone levels. Weakness and a polymyopathy causing cervical ventroflextion are commonly seen. Retinal detachments and blindness are also common clinical signs. Other less common clinical presentations include polyuria, polydypsia, polyphagia and rarely respiratory failure. Occasionally it is diagnosed in asymptomatic cats.

Diagnosing the disease can be challenging as it is often overlooked in cases of unexplained hypertension or hypokalemia. Primary hyperaldosteronism should be considered as a differential diagnosis in middle-aged and older cats with hypokalemic polymyopathy and/or systemic hypertension. If the disease is suspected, an abdominal ultrasound should be performed. Unilateral adrenal masses may be seen. More commonly, only very subtle changes in the adrenals compatible with nodular hyperplasia may be noted. Ideally, plasma aldosterone levels should be measured, and significant elevations are generally seen. In primary hyperaldosteronism with elevated aldosterone levels, there is a corresponding decrease in plasma renin activity demonstrating a renin-aldosterone dissociation. This decreased plasma renin level in light of an elevated aldosterone level (or the plasma aldosterone/renin ratio) is the human standard for diagnosis. Unfortunately, there is no commercially-available assay for plasma rennin activity available at this time in North America

When hyperaldosteronism is diagnosed, treatment is either surgical removal of the affected adrenal gland if a tumor is present, or medical management. Medical management is the treatment of choice in bilateral adrenal hyperplasia, or when the cat’s clinical condition makes surgery a poor option. Medical treatment is based on controlling the hypokalemia and hypertension. Initially, IV potassium chloride may be needed to correct the electrolyte abnormalities (not to exceed 0.5meq/kg/hr) in cases of severe hypokalemia. Once stable, oral potassium gluconate should be started at 2-6mg/kg/day. The dose may then be adjusted as indicated. 

Hypertension is treated initially with Spironolactone (2-4mg/kg/day), a potassium-sparing diuretic. Spironolactone should be the treatment of choice as it is a synthetic homologue and competitive antagonist of aldosterone. If further blood pressure control is needed, then amlodipine (0.625-1.25mg/day) can be added. The prognosis is variable, but some cats survive for years with just medical management. The clinician should always consider hyperaldosteronism as a diagnosis in any middle-aged to older cat with hypokalemia (especially if associated with a polymyopathy) and/or systemic hypertension.

For more information or to refer a client to the Internal Medicine service at Angell, please call Referral Coordinator, Eleanor Cousino, at 617 522-5011 or visit www.mspca.org/internalmedicine.

Powered By Convio