Endocrinology: Hyperaldosteronism in a cat with metastasised adrenocortical tumour

Abstract

Laboratory examination revealed hypohalaemia (1.6 mmol/1; reference range 3.4-5.7 mmo1/1) and echocardiographic findings seemed to be compatible with hypertrophic cardiomyopathy. Potassium suppletion, first intravenously and then orally, and treatment with the (13-blocking agent atenolol (Tenormin®, Zeneca;6.25 mg once daily) and acetylsalicylic acid (40 mg twice daily) resulted in good recovery. On 29 June, 3 weeks after stopping potassium suppletion and atenolol, the cat was presented to the owner's veterinarian for weakness in the hind legs. The cat was not lethargic and was eating and drinking normally. The history of cardiomyopathy raised the possibility of complicating thromboembolism. A saddle thrombus at the distal aortic trifurcation was considered unlikely because the femoral pulses were easily palpated and the footpads of the hind legs were warm and pink. The previous treatment was resumed but the dose of acetylsalicylic acid was lowered to twice weekly 25 mg. The cat did well on this regimen but the plasma concentrations of potassium remained low. When potassium gluconate (Tumil Ke, Aesculaap by, Boxtel, NL) was given orally in a dose of 2 mmol four times daily, the plasma potassium concentration remained s 2.2 mmo1/1. On 1 September the cat collapsed again, even though the potassium supplementation had been increased to 2 mmol six times daily for 2 weeks. In addition to muscular weakness, there was mydriasis, restlessness, and panting. Potassium concentrations in plasma ranged from 1.9 to 2.1 mmo1/1. An angiotensin-converting enzyme inhibitor (once daily 1 mg enalapril, Enalfor®, Mycofarm) was added to the treatment. The cat recovered but the plasma potassium concentration remained at the same low level. Hyperadrenocorticism was excluded as the cause of the muscular weakness by the finding that the basal urinary corticoid/creatinine ratio (average on two consecutive days: 24 x 10-6) was below the upper limit of the reference range (37 x 10-6) (11) and the urinary corticoid/creatinine ratio was readily suppressed (to 3.0 x 10-6 ) following three oral doses of 0.5 mg dexamethasone. A possible relation to hyperthyroidism (21) was excluded by the finding of a normal plasma thyroxine concentration (29 nmi51/1).Between the episodes of muscular weakness the cat's condition and behaviour were unremarkable but in search of an explanation for the persistent hypokalaemia the cat was referred to the Utrecht University Clinic for Companion Animals in September 1998. HYPERALDOSTERONISM IN A CAT WITH METASTASISED ADRENOCORTICAL TUMOURA.Rijnberk1,6, G. Voorhout2, H.S. Kooistra1, R.J.M. van der Waarden3, F.J. van Sluijs1, J. Uzer4, P. Boer5, and W.H. Boer5 Vet Quart 2001; 23: 38-43 Accepted for publication: January 10, 2000. SUMMARYIn a 12-year-old male shorthaired cat with attacks of hypokalaemic muscular weakness in spite of oral potassium supplementation, highly elevated plasma aldosterone concentrations in combination with low plasma renin activity pointed to primary hyperaldosteronism. Ultrasonography and ...

Hyperadrenocorticism in Cats

“…In the past 15 years, cats with PHA have been reported more commonly (Flood et al, 1999;MacKay et al, 1999;Maggio et al, 2000;Moore et al, 2000b;Rijnberk et al, 2001;Reimer et al, 2005;Ash et al, 2005;DeClue et al, 2005;Rose et al, 2007;Briscoe et al, 2009;Renschler and Dean, 2009;Djajadiningrat-Laanen et al, 2011;Lo et al, 2014). The incidence of malignant tumors (19 reported cases) exceeds that of solitary benign adenomas (11 reported cases).…”

Treatment of Aldosterone‐Secreting Adrenocortical Tumors in Cats by Unilateral Adrenalectomy: 10 Cases (2002–2012)

“…This disease was considered rare in humans and companion animals for many decades,2, 3, 4, 5 but recently has been found to be more prevalent with improved screening tests and detection in both humans and cats 6, 7. Since the first reported case of primary hyperaldosteronism in a cat in 1983,8 there have been only a few case reports of feline primary hyperaldosteronism (PHA) 9, 10, 11, 12, 13, 14, 15, 16, 17, 18…”

“…In cats, most cases of PHA are attributed to unilateral adrenal adenomas or carcinomas 19. There are only a few reports of unilateral adrenalectomies in cats, and perioperative complications of hemorrhage and death were reported in 8 of 18 surgical cases,11, 12, 16, 17, 19, 22, 23, 24 with 6 of those reported as fatalities.…”

Adrenocortical tumor in a cat secreting more than one type of corticosteroid

“…11 Primary hyperaldosteronism can be caused by unilateral or bilateral nodular hyperplasia, adenoma or adenocarcinoma of the zona glomerulosa. 12–14 Secondary hyperaldosteronism may occur in cardiac or chronic renal disease owing to overactivity of the renin–angiotensin system. 15 Based on normal cardiac and kidney evaluations, secondary hyperaldosteronism was discounted.…”