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Keywords:

  • Conn's syndrome;
  • Feline;
  • Hypertension;
  • Hypokalemia

Background

Primary hyperaldosteronism (PHA) in cats is suggested by clinical signs and an elevated plasma aldosterone-to-renin ratio (ARR), but a test to confirm the diagnosis is lacking.

Hypothesis

Fludrocortisone does not suppress urinary aldosterone excretion in cats with PHA, but does so in cats with arterial hypertension because of other causes.

Animals

Nineteen client-owned cats with arterial hypertension because of PHA (n = 9) or other causes (n = 10).

Methods

Prospective clinical study. The urinary aldosterone-to-creatinine ratio (UACR) was determined in morning urine before, during, and after 4 days of oral fludrocortisone administration in a dose of 0.05 mg/kg q12h. Arterial blood pressure and plasma potassium concentration were measured before and after fludrocortisone administration.

Results

A basal UACR above 46.5 × 10−9, the upper limit of the reference range, was found in 3 cats with PHA. All PHA cats had basal UACRs >7.5 × 10−9. In all non-PHA cats with a basal UACR >7.5 × 10−9, fludrocortisone administration induced >50% suppression. In contrast, fludrocortisone administration resulted in <50% suppression in 6 of the 9 PHA cats. Neither basal UACR, nor UACR after suppression testing, correlated with the etiology of PHA (adenoma, adenocarcinoma, or suspected bilateral hyperplasia of the zona glomerulosa). Fludrocortisone induced hypokalemia in 7 cats, but did not induce or exacerbate arterial hypertension.

Conclusions and Clinical Importance

Measuring the UACR before and after 4 days of administering fludrocortisone is a practical method of confirming most cases of PHA in cats, and of substantiating the absence of PHA in cats having an ARR within the reference range.