Hyperaldosteronism

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Primary hyperaldosteronism (Conn's syndrome) is an endocrine renal disease of dogs characterized by hypertension due to excess aldosterone production by the adrenal cortex[1].

The majority of cases of canine primary hyperaldosteronism are a result of adrenal cortical hyperplasia or neoplasia[2] but is rarer than is observed in cats.

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[3].

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[4].

Many cases of idiopathic hypertension in dogs has been recently been shown to be attributed to primary hyperaldosteronism[5].

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[6].

Blood tests frequently reveal metabolic alkalosis, an increased concentration of plasma aldosterone, hypernatremia and hypokalemia refractory to potassium supplementation[7].

A differential diagnosis would include iatrogenic Fanconi's syndrome[8], nephrotic syndrome[9], diabetes mellitus and diabetes insipidus[10].

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.

The use of spironolactone, an aldosterone antagonist[11], is required in cases of idiopathic hyperaldosteronism.

References

  1. Rijnberk A et al (2001) Aldosteronoma in a dog with polyuria as the leading symptom. Domest Anim Endocrinol 20(3):227-240
  2. Johnson KD et al (2006) Primary hyperaldosteronism in a dog with concurrent lymphoma. J Vet Med A Physiol Pathol Clin Med 53(9):467-470
  3. Costello J & Bourke E (1983) Bartter's syndrome - the case for a primary potassium-losing tubulopathy: discussion paper. J R Soc Med 76(1):53-56
  4. Queisser N et al (2011) Aldosterone increases kidney tubule cell oxidants through calcium-mediated activation of NADPH oxidase and nitric oxide synthase. Free Radic Biol Med 51(11):1996-2006
  5. Reusch CE et al (2010) Endocrine hypertension in small animals. Vet Clin North Am Small Anim Pract 40(2):335-352
  6. Breitschwerdt EB et al (1985) Idiopathic hyperaldosteronism in a dog. J Am Vet Med Assoc 187(8):841-845
  7. Donnelly K et al (2012) What is your diagnosis? 12-year-old spayed female Labrador Retriever with a history of polyuria and polydipsia. J Am Vet Med Assoc 240(11):1283-1285
  8. Breitschwerdt EB et al (1983) Multiple endocrine abnormalities in Basenji dogs with renal tubular dysfunction. J Am Vet Med Assoc 182(12):1348-1353
  9. Rondon-Berrios H (2011) New insights into the pathophysiology of oedema in nephrotic syndrome. Nefrologia 31(2):148-154
  10. Shimokawa Miyama T et al (2009) Magnetic resonance imaging and clinical findings in a miniature Schnauzer with hypodipsic hypernatremia. J Vet Med Sci 71(10):1387-1391
  11. Guyonnet J et al (2010) A preclinical pharmacokinetic and pharmacodynamic approach to determine a dose of spironolactone for treatment of congestive heart failure in dog. J Vet Pharmacol Ther 33(3):260-267