Amanda Mansz   

Animal Health Laboratory, University of Guelph, Guelph, ON

AHL Newsletter 2026;30(2):23.

A 14-year-old male neutered cat was submitted to the AHL for postmortem examination following euthanasia with a clinical history of drooling, flaccid paraparesis of all four limbs with muscle tremors, and low serum potassium (2.3 mmol/l; ref 3.4 – 5.3).  There was a mild increase in glucose and ALT; however, all other biochemical parameters were within reference range.

Postmortem examination revealed neoplasia of the right adrenal gland, surrounded by mild hemorrhage. There was no distinguishable adrenal cortex or medulla, and the entire gland was replaced by a 2.5 cm x 2.0 cm x 1.1 cm soft, marbled light yellow to tan, encapsulated, rounded mass (Fig. 1).

Microscopic examination highlighted virtually complete obliteration of the normal adrenal gland parenchyma by an expansile nodule of highly vacuolated polygonal cells, resembling epithelial cells of the adrenal cortex (Fig. 2). The neoplastic cells focally invaded through the adrenal capsule (Fig. 2b). The left adrenal gland showed a thinned cortex (contralateral adrenal cortical atrophy) (Fig. 2d).  Based on the combination of the clinical findings, gross and microscopic findings, a functional, aldosterone secreting adrenocortical carcinoma was diagnosed. 

Aldosterone-secreting tumors are rare but are most often reported in cats. Feline primary hyperaldosteronism (AKA Conn’s syndrome) is an endocrine disorder characterized by the excessive, autonomous secretion of aldosterone from the adrenal cortex, most commonly caused by adrenal neoplasia. This primary hyperaldosteronism leads to hypokalemia and systemic hypertension. As in this case, hypokalemic polymyopathy is one of the most common presenting signs in cats with adrenal tumors causing hyperaldosteronism.

Figure 1. Formalin-fixed adrenocortical carcinoma in a 14-year-old cat. Distinctive cortex and medulla are replaced by a 2.5 cm x 2.0 cm x 1.1 cm soft, marbled light yellow to tan, encapsulated, rounded mass.

Figure 2. Histologic lesions of right adrenocortical carcinoma and left adrenal cortical atrophy. H&E stains. a. Right adrenal gland: multinodular masses replace the normal corticomedullary architecture. 4x. b. Right adrenal gland: neoplastic cells extend through the capsule (black arrow pointing to the fibrous capsule). 10x. c. Right adrenal gland: packeted, highly vacuolated neoplastic polygonal cells resembling epithelial cells of the adrenal cortex with a mitotic figure (blue arrow) and variation in nuclear size with some enlarged nuclei (black arrow). 20x. d. Left adrenal gland: a thinned (atrophic) contralateral cortex (double headed black arrow). 10x.

Reference

1. Rosol TJ, Grone A. Endocrine Glands. In: Jubb, Kennedy, and Palmer's Pathology of Domestic Animals, 7th ed. Maxie MG, ed. Elsevier, 2026; 1: 353-355.