The Case of the Feeble Feline

1. Referral:
“Doubie,” a 15yr old castrated male domestic short hair*, was referred for further evaluation of progressive weakness, lethargy and decreased appetite. Prior to referral, abdominal radiographs performed by the referring veterinarian revealed bilateral coxofemoral and spinal arthritis. A complete blood chemistry and electrolyte panel revealed a moderate hypokalemia (2.2 mmol/L) but was otherwise unremarkable. A CBC revealed a mild normocytic, normochromic anemia (26%).
2. Exam:
On physical examination, Doubie had a BCS of 2/5. A soft grade II systolic heart murmur was ausculted. When Doubie ambulated around the exam room, he demonstrated marked hind limb weakness with bilaterally dropped hocks. The rest of his physical exam was within normal limits.
3. Procedures:
A urinalysis revealed a USG of 1.024 with trace proteinuria. A systolic blood pressure measured 230mmHg. A venous blood gas and repeat electrolytes revealed a metabolic alkalosis (pH 7.44), moderate hypokalemia (2.4mmol/L) and hypernatremia (167mmol/L). Abdominal ultrasound revealed a mass associated with the cranial pole of the left adrenal gland- measuring approximately 14mm. Echocardiogram revealed marked left ventricular thickening and left atrial enlargement (20mm). An aldosterone level was markedly elevated at 1,318.3 pg/ml (normal range = 11.3-294.3 pg/ml)
4. Diagnosis:
Hyperaldosteronism AKA Conn’s Syndrome
5. Discussion:
The primary function of aldosterone is the regulation of serum sodium and potassium and maintenance of normal vascular fluid volume. Aldosterone is the principle mineralocorticoid synthesized and secreted by the zona glomerulosa of adrenal cortices and is mainly controlled by serum potassium concentrations and the renin angiotensin system. After synthesis and secretion, aldosterone promotes potassium excretion and stimulates conservation of sodium. In causing conservation of sodium, aldosterone indirectly causes conservation of water, which raises blood volume and increases blood pressure. Primary hyperaldosteronism is defined as the autonomous secretion of the hormone by abnormal cells with the adrenal cortex.
6. Treatment:
Doubie was sent home on oral medications including spironolactone (an aldosterone antagonist) and potassium gluconate (potassium supplement) to manage the hypokalemia. Additionally, therapy with atenolol and low dose aspirin was initiated for the hypertrophic changes to Doubie’s heart. These changes were suspected to be secondary to sodium retention and thus resultant elevated blood pressure. A low sodium diet was also recommended (a prescription renal diet was felt to be appropriate).
7. Follow Up:
At Doubie’s one week recheck his blood pressure and potassium levels were within normal range. Ultimately, a surgical consult was recommended in order to discuss adrenalectomy, the only potential definitive treatment for such aldosterone secreting tumors.
8. Take Home Point:
This endocrine disorder, although rare, should be included among the differential diagnoses for cats with undefined hypokalemia, hypertension and/or adrenal masses.
by Mickila Collins, DVM,
Practice Limited to Internal Medicine
*Photo of Cat is not “Doubie.”

