Secondary hyperaldosteronism is caused by renin-producing tumors (Bartter's syndrome; hyperplasia of the renin-producing juxtaglomerular apparatus), rarely reported in dogs, which leads to hyperreninaemia and elevated plasma angiotensin II, causing hyperaldosteronism.
Aldosterone is produced by the adrenal zona glomerulosa and plays an intimate supportive role with the renin-angiotensin activating system (RAAS) in blood pressure regulation. Aldosterone acts on the distal tubules and collecting ducts to cause the reabsorption of sodium, excretion of potassium, water retention and increased blood pressure.
Many cases of idiopathic hypertension in dogs has been recently been shown to be attributed to primary hyperaldosteronism.
Clinically affected dogs are usually middle-aged or older and present with signs of mineralocorticoid excess such as hypertension, polyuria and polydipsia.
Urinalysis typically shows low specific-gravity urine with decreased natriuresis and hyperkaluria.
Diagnosis usually requires exclusion of hyperadrenocorticism via an ACTH stimulation test and renal imaging and biopsy.
Treatment consists of identification of underlying disease, frequently neoplastic in origin, by unilateral or bilateral adrenalectomy.
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