Feline hyperaldosteronism: Treatment and prognosis


Feline hyperaldosteronism: Treatment and prognosis

Now that you've diagnosed this disorder—which is more common than once thought—it's time to decide whether to treat it medically or surgically. Luckily, most cases have a good prognosis with proper therapeutic measures.
Mar 01, 2012

The previous article discussed how feline hyperaldosteronism is more common than we think and may be the more likely culprit behind hypertension and hyperkalemia in cats than chronic kidney disease. Once you have definitively diagnosed this disorder by using a combination of a patient's clinical signs and findings from laboratory testing and diagnostic imaging, you have two choices for treatment—medical or surgical.


Table 1
Medical management (Table 1) of the clinical abnormalities detected at the time of diagnosis is indicated in cats with primary hyperaldosteronism due to bilateral adrenal pathology, nonresectable unilateral adrenocortical neoplasia, or metastatic disease or in cases in which financial or comorbid conditions prohibit surgical intervention.

Spironolactone and potassium gluconate

Spironolactone is an aldosterone antagonist that binds to cytoplasmic receptor proteins in cells of the distal convoluted tubules and collecting ducts of the kidney, resulting in potassium retention and sodium excretion. It is necessary to use oral potassium gluconate in conjunction with spironolactone when hypokalemia is refractory to single-agent therapy.

Amlopidine besylate

Amlodipine besylate is a dihydropyridine calcium antagonist that inhibits the transmembrane influx of calcium ions and is an arterial vasodilator that reduces peripheral vascular resistance, thereby decreasing blood pressure.

Other alternatives

Amiloride or triamterene can be used in place of spironolactone therapy,1,2 but their use in cats, especially for this condition, has not been well-studied. These drugs block the sodium channels of the distal convoluted tubule, which decreases the availability of sodium for the sodium-potassium pumps, thereby decreasing kaliuresis.


Effective doses of each medication, especially potassium gluconate, will need to be determined for each individual patient. So serial electrolyte and blood pressure monitoring should be performed five to seven days after every dose adjustment until the cat is normokalemic and normotensive. Once ongoing testing and clinical assessment of the cat reveal apparent stability, recheck examinations can be performed every three months.

The goals of therapy include decreasing and ultimately eliminating clinical signs of myopathy and weakness secondary to hypokalemia and maintaining normal systolic blood pressure to minimize end-organ damage from persistent hypertension. Depending on the clinical abnormalities being treated at the time of diagnosis, disease progression may result in the need for increased doses of current medications (e.g. a hypokalemic cat treated with spironolactone and potassium gluconate may require higher doses of potassium gluconate to maintain normokalemia over time) or the addition of other drugs for newly developed signs (e.g. a cat that was hypokalemic but normotensive at the time of diagnosis may become hypertensive as the disease progresses).