Primary hyperaldosteronism in cats: expanding the diagnostic net

Primary hyperaldosteronism or low-renin hyperaldosteronism in cats is characterized by inappropriately high aldosterone secretion from one or both adrenal glands, with systemic arterial hypertension and hypokalemia as leading clinical manifestations. In this thesis, non-tumorous primary hyperaldosteronism is documented, the relationship between primary hyperaldosteronism and chronic kidney disease is investigated, and a new diagnostic test for primary hyperaldosteronism is described. In Chapter 3 eleven cats with primary hyperaldosteronism are reported. Bilateral nodular hyperplasia of the adrenal zona glomerulosa was confirmed histologically in three cats and suspected in the other eight. One cat developed chronic kidney disease and in several others there was progression of chronic kidney disease. Histological examination of the kidneys of two of these cats revealed severe chronic inflammatory changes in the glomeruli, interstitium and arteries. These results suggest an association between low-renin hyperaldosteronism and progressive kidney disease in cats. These findings prompted exploratory investigation of the prevalence of primary hyperaldosteronism in cats with chronic kidney disease, as described in Chapter 4. Seven (14%) of 51 cats with chronic kidney disease had an elevated plasma aldosterone-to-renin ratio (ARR), pointing to inappropriately high aldosterone secretion. This warrants the investigation for primary hyperaldosteronism in cats with chronic kidney disease. The investigation of primary hyperaldosteronism can be rather complicated. The ARR has been widely accepted as a screening test, but is associated with some practical limitations. To circumvent these limitations, measuring aldosterone in urine was explored, as described in Chapter 5. The basal urinary aldosterone-to-creatinine ratio (UACR) was determined in 42 healthy cats and one cat with a confirmed aldosterone-producing adrenocortical carcinoma. The basal UACR in the cat with primary hyperaldosteronism was within the reference range of 46.5x10-9 points to primary hyperaldosteronism; and (3) in cats with a basal UACR between 7.5x10-9 and 46.5x10-9

Primary hyperaldosteronism in cats: expanding the diagnostic net

Primary hyperaldosteronism or low-renin hyperaldosteronism in cats is characterized by inappropriately high aldosterone secretion from one or both adrenal glands, with systemic arterial hypertension and hypokalemia as leading clinical manifestations. In this thesis, non-tumorous primary hyperaldosteronism is documented, the relationship between primary hyperaldosteronism and chronic kidney disease is investigated, and a new diagnostic test for primary hyperaldosteronism is described. In Chapter 3 eleven cats with primary hyperaldosteronism are reported. Bilateral nodular hyperplasia of the adrenal zona glomerulosa was confirmed histologically in three cats and suspected in the other eight. One cat developed chronic kidney disease and in several others there was progression of chronic kidney disease. Histological examination of the kidneys of two of these cats revealed severe chronic inflammatory changes in the glomeruli, interstitium and arteries. These results suggest an association between low-renin hyperaldosteronism and progressive kidney disease in cats. These findings prompted exploratory investigation of the prevalence of primary hyperaldosteronism in cats with chronic kidney disease, as described in Chapter 4. Seven (14%) of 51 cats with chronic kidney disease had an elevated plasma aldosterone-to-renin ratio (ARR), pointing to inappropriately high aldosterone secretion. This warrants the investigation for primary hyperaldosteronism in cats with chronic kidney disease. The investigation of primary hyperaldosteronism can be rather complicated. The ARR has been widely accepted as a screening test, but is associated with some practical limitations. To circumvent these limitations, measuring aldosterone in urine was explored, as described in Chapter 5. The basal urinary aldosterone-to-creatinine ratio (UACR) was determined in 42 healthy cats and one cat with a confirmed aldosterone-producing adrenocortical carcinoma. The basal UACR in the cat with primary hyperaldosteronism was within the reference range of 46.5x10-9 points to primary hyperaldosteronism; and (3) in cats with a basal UACR between 7.5x10-9 and 46.5x10-9

Distichiasis in a ferret (Mustela putorius furo)

A 4-year-old intact male ferret was presented to the Ophthalmology Service of the Department of Clinical Sciences of Companion Animals of Utrecht University with chronic blepharospasm, epiphora, and conjunctivitis of the right eye. Examination of the eye revealed mild conjunctivitis and three hairs protruding from the openings of meibomian glands in the upper eyelid, providing the clinical diagnosis of distichiasis. The distichia were removed by transconjunctival unipolar electrocautery. Recovery was uneventful, but the original signs recurred 10 weeks after surgery. Ophthalmic examination revealed another distichia at a different location in the same eyelid and it was removed by full-thickness wedge excision. Histopathological examination failed to reveal the exact origin of the distichia. To our knowledge, this is the first reported case of distichiasis in a ferret

Evaluation of the oral fludrocortisone suppression test for diagnosing primary hyperaldosteronism in cats

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 9 10 9, the upper limit of the reference range, was found in 3 cats with PHA. All PHA cats had basal UACRs >7.5 9 10 9. In all non-PHA cats with a basal UACR >7.5 9 10 9, fludrocortisone administration induced >50% suppression. In contrast, fludrocortisone administration resulted i