Feline hyperaldosteronism: Treatment and prognosis

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.

MEDICAL MANAGEMENT

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.

Table 1

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.

Monitoring

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).

SURGICAL TREATMENT

For cats with unilateral aldosterone-secreting adrenal masses and no detectable metastatic disease, the preferred treatment is surgical excision3,4 based on reports with successful interventions (Figures 1 & 2).1,5-7 Successful surgery can be curative for both adenomas and adenocarcinomas, and signs of hypokalemia and hypertension often resolve without further treatment or medical management.1,5-7

1. An adrenal tumor. Note the large size, coarse appearance of the capsule, and invasion of the gland into surrounding structures.

Preoperative medical therapy

Correcting hypokalemia and controlling hypertension with medical management (Table 1) are recommended to increase anesthetic, perioperative, and postoperative stability. In one case report, all cats that underwent surgery (n=10) had a successful preoperative stabilization period ranging from 14 to 149 days of medical management.5 All cats meeting the criteria for surgical managment that were hypertensive at presentation became normotensive when treated before surgery.5 Potassium concentrations of hypokalemic cats receiving oral supplementation before surgery increased in all cases but did not normalize by the time of surgery; however, cats that presented with a myopathy showed resolution of these clinical signs despite the persistent hypokalemia.1,5,8

2. A unilateral adrenal adenoma. The well-circumscribed tan-colored tissue is the adenoma, which was confirmed with histopathologic examination. The rest of the adrenal tissue architecture was normal.

Perioperative complications

Reported perioperative complications include six cases of intra-abdominal hemorrhage, one case of acute renal failure, one case of sepsis, and one case of suspected thromboembolism.5,6,8,9 Sepsis and thromboembolism have been reported after adrenalectomy for other conditions, but hemorrhage has been reported more frequently in cats undergoing adrenalectomy for primary hyperaldosteronism.5,6,9 Further studies are necessary to assess risk factors associated with poor outcomes.

Postoperative care

After surgery, blood pressure measurements and potassium concentration monitoring should be evaluated upon recovery and repeated at least once a day for the initial 48 hours after surgery. Ideally, the potassium concentration should be checked every six hours for the first 24 hours after surgery until values stabilize or the patient begins to eat, in which case, oral supplementation can replace intravenous replacement.

Adjustments to the antihypertensive therapy and potassium replacement therapy (potassium concentration in intravenous fluids or oral supplementation dose) should be made according these results. If the patient remains hypertensive or hypokalemic by the time of discharge, oral therapy to correct the condition should be continued, and the patient should be rechecked within five days.

In reported cases in which cats survived surgical intervention, spironolactone and amlodipine therapy were discontinued the day of surgery without the need to reinstitute therapy postoperatively.1,5 Normokalemia after successful adrenalectomy was documented within six days in most cases5,6 and on postoperative day 13 in one case.1 Oral potassium supplementation doses should be tapered until and ultimately discontinued when the serum concentration normalizes. Once blood pressure and potassium concentrations are stable without the need for medical intervention and the owner reports resolution of clinical signs associated with hypertension or hypokalemia, no further rechecks or follow-up are necessary.

PROGNOSIS

The prognosis in cats with completely excised unilateral nonmetastatic adrenocortical neoplasia that survive the perioperative period without complication is excellent without the need for life-long medication in most cases.3-5,7 In cats, adrenal adenocarcinomas do not appear to be associated with a poorer prognosis than adrenal adenomas.5 The reported survival time for medically managed cats with primary hyperaldosteronism ranges from several months to many years.1,4,5

SUMMARY

Whether you choose medical or surgical treatment of feline hyperaldosteronism often depends on the laterality of the disease and whether metastasis has occurred. Cats with primary hyperaldosteronism caused by a nonmetastatic unilateral adrenal tumor have a good prognosis with surgical excision. Medical management with potassium supplementation, antihypertensive agents, and spironolactone therapy can be implemented for stabilization before surgery and in cases in which surgery is prohibitive. The expected survival time for these cats ranges from months to years with a good to excellent quality of life. See Hyperaldosteronism case report: Reviving a senior cat's verve for an overview on how to handle this adrenocortical disorder in cats.

Joseph Bisignano, DVM

Department of Veterinary Clinical Sciences

College of Veterinary Medicine

University of Minnesota

St. Paul, MN 55108

David S. Bruyette, DVM, DACVIM VCA

West Los Angeles Animal Hospital

1818 S. Sepulveda Blvd.

Los Angeles, CA 90025

Veterinary Diagnostic Investigation and Consultation

26205 Fairside Road

Malibu, CA 90256

REFERENCES

1. Flood SM, Randolph JF, Gelzer AR, et al. Primary hyperaldosteronism in two cats. J Am Anim Hosp Assoc 1999;35(5):411-416.

2. Ahn A. Hyperaldosteronism in cats. Semin Vet Med Surg (Small Anim) 1994;9(3):153-157.

3. Djajadiningrat-Laanen S, Galac S, Kooistra H. Primary hyperaldosteronism: expanding the diagnostic net. J Feline Med Surg 2011;13(9):641-650.

4. Schulman RL. Feline primary hyperaldosteronism. Vet Clin North Am Small Anim Pract 2010;40(2):353-359.

5. Ash RA, Harvey AM, Tasker S. Primary hyperaldosteronism in the cat: a series of 13 cases. J Feline Med Surg 2005;7(3):173-182.

6. MacKay AD, Holt PE, Sparkes AH. Successful surgical treatment of a cat with primary aldosteronism. J Feline Med Surg 1999;1(2):117-122.

7. Rose SA, Kyles AE, Labelle P, et al. Adrenalectomy and caval thrombectomy in a cat with primary hyperaldosteronism. J Am Anim Hosp Assoc 2007;43(4):209-214.

8. DeClue AE, Breshears LA, Pardo ID, et al. Hyperaldosteronism and hyperprogesteronism in a cat with an adrenal cortical carcinoma. J Vet Intern Med 2005;19(3):355-358.

9. Rijnberk A, Voorhout G, Kooistra HS, et al. Hyperaldosteronism in a cat with metastasised adrenocortical tumour. Vet Q 2001;23(1):38-43.