Case report: An Aldosterone-secreting Adrenal Tumor in a Cat

Elizabeth Appleman, VMD, DACVIM |  Fifth Avenue Veterinary Specialists
“Bennie,” a 9-year-old MC domestic shorthair was referred to Fifth Avenue Veterinary Specialists on June 16, 2009, for further evaluation of hyperaldosteronism and uncontrolled diabetes mellitus.
The initial work-up and treatment was performed by Dr. Dan Lauridia at Murray Hill Pet Hospital, in Manhattan. Previously in October 2008, Bennie was presented to Murray Hill for general weakness. He was subsequently diagnosed with hypokalemia (2.9 mmol/L), high baseline aldosterone level (2488 pmol/L, reference range 194-388 pmol/L), and persistent hypertension (200-240 mmHg). A full work-up was otherwise normal (including full bloodwork, sodium concentration, thyroid level, urinalysis, and acetylcholine antibody receptor level). An echocardiogram showed mild left ventricular hypertrophy, likely due to systemic hypertension. On abdominal ultrasound, both adrenal glands appeared normal in size and echotexture.

Due to the patient’s clinical presentation and clinicopathological abnormalities, an aldosterone-secreting adrenal tumor was suspected. However, the normal adrenal gland size precluded surgery, so the patient was managed medically with amlodipine and potassium supplementation at titrated doses. Bennie developed diabetes mellitus in February 2009, and his glucose levels remained uncontrolled despite steady increases in insulin. Shortly afterwards, the patient was referred to FAVS for a recheck abdominal ultrasound. At this time, a heterogenous and mineralized  mass (~2.8×2.8cm) associated with the right adrenal gland was identified. There was no invasion of the vena cava. The left adrenal gland and other abdominal organs were normal. Bennie had a right adrenalectomy performed several days later. Biopsies of the liver, pancreas, and omentum were normal. Histopathology of the right adrenal gland showed neoplastic epithelial cells with finely granular cytoplasm, consistent with a benign adenoma although malignancy could not be excluded. Surgical margins were clean. Within one month following surgery, Bennie’s diabetes mellitus had resolved, and he was also weaned off amlodipine and potassium supplementation.
Primary hyperaldosteronism (PHA), also called Conn’s disease, is an endocrinopathy characterized by excessive autonomous secretion of aldosterone. In cats, it is typically caused by either an adenoma or carcinoma of the adrenal gland. In a retrospective review of 13 cases, seven patients had adrenal adenomas (unilateral or bilateral), while the remaining six had unilateral carcinomas.1 Other less common etiologies in people include multiple endocrine neoplasia (MEN), familial, and idiopathic. A veterinary case report from 2005 documented MEN in a cat with an aldosterone-secreting adenoma, parathyroid gland adenoma, and pancreatic insulinsecreting tumor.2 In human medicine, hyperaldosteronism is also associated with insulin resistance and impaired betacell function, causing increased risk for development of diabetes mellitus.3
Animals diagnosed with PHA are usually older in age; there is no breed or sex predilection.3 The disease appears more common in cats versus dogs. Patients are typically presented due to side-effects from hypokalemia (weakness, respiratory distress, polyuria, polydipsia) or hypertension (erratic behavior, neurological signs, sudden onset of blindness). The diagnosis is confirmed through measurement of basal aldosterone levels (typically showing a marked elevation, i.e. 5-6 times higher than normal). In people, plasma renin activity should also be concurrently low, although this test is not clinically available in cats at this time. Aldosterone concentrations should be interpreted in combination with the serum potassium level (similar to the insulin:glucose ratio). If the aldosterone concentration is in the high-normal range, but the potassium level is concurrently low, PHA can still be considered as a differential.
dr-danAfter documentation of hyperaldosteronism, abdominal ultrasound is recommended to screen for an adrenal tumor. Failure to find an adrenal mass on ultrasound does not exclude underlying neoplasia, as some adrenal tumors can be small and are not visible until several months after initial diagnosis.4 Medical therapy consists of supportive care (potassium supplementation and control of hypertension with amlodipine), along with spironolactone, a competitive antagonist of aldosterone in the distal renal tubules. Adrenalectomy is the treatment of choice as hypertension and hypokalemia can be refractory to medical therapy. Aldosterone levels, potassium concentration, and hypertension often normalize shortly after surgery.1 Post-operative survival in these patients has been documented for up to five years, independent of tumor type.1 “Bennie’s” initial clinical signs and clinicopathologic abnormalities were diagnostic for PHA. However, no adrenal mass was documented at that time, likely due to his early diagnosis in the course of his disease process. On Bennie’s recheck abdominal ultrasound, performed nine months later, a right adrenal mass was identified. This progression in adrenal tumor size highlights the importance of repeating imaging at regular intervals, especially if neoplasia is a top concern. “Bennie” had a positive outcome post-surgery, with resolution of his clinicopathologic abnormalities and improvement in quality of life. In summary, PHA is characterized by concurrent hyperaldosteronism, hypokalemia, and hypertension. PHA should be considered as a differential diagnosis in older cats with unexplained hypokalemia and/or systemic hypertension. If an adrenal mass is identified, surgery is the treatment of choice, and postoperative prognosis is positive.
1 Ash R, Harvey A, Tasker S. Primary hyperaldosteronism in the cat: a series of 13 cases. J Fel Med Surg 2005;7:153-182.
2 Reimer SB, Pelosi A, Frank JD, et al. Multiple endocrine neoplasia type I in a cat. J Am Vet Med Assoc 2005;227:101-104.
3 Schulman R. Feline primary hyperaldosteronism. Vet Clin Small Anim 2010;40:353-359.
4 Shell L. Hyperaldosteronism. VIN database 2008.

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