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Review
. 2022 May 3;9(1):6.
doi: 10.1186/s40575-022-00119-4.

Diagnosis of canine spontaneous hypoadrenocorticism

Pedro J Guzmán Ramos  1 , Michael Bennaim  2 , Robert E Shiel  3 , Carmel T Mooney  3
Affiliations
Review

Diagnosis of canine spontaneous hypoadrenocorticism

Pedro J Guzmán Ramos et al. Canine Med Genet. .

Abstract

Hypoadrenocorticism is characterized by a reduction in mineralocorticoid and/or glucocorticoid production by the adrenal glands. Several subtypes have been described with different clinical and clinicopathological consequences. Most affected dogs have vague and non-specific signs that precede an eventual life-threatening crisis. This review aims to appraise classification, the available data on epidemiology and the clinical and laboratory features of naturally occurring canine hypoadrenocorticism.

Keywords: Addison´s; Adrenals; Aldosterone; Cortisol; Endocrinology.

Plain language summary

Canine hypoadrenocorticism is a relatively uncommon endocrine disease that can present with a wide variety of clinical signs resulting from cortisol or aldosterone deficiency or both. Hypoadrenocorticism should be considered in all dogs with severe illness and typical electrolyte abnormalities but also in those with waxing and waning clinical signs. Multiple clinical and laboratory features are suggestive of the disease and should prompt evaluation of adrenal function. The ACTH stimulation test is the best test for diagnosing hypoadrenocorticism but, in those cases without the typical presentation, evaluation of aldosterone secretory capacity and endogenous ACTH concentrations should be performed to distinguish primary from secondary disease. In this review we discuss the pathophysiology of the disease, the clinical signs and laboratory features that should raise suspicion of hypoadrenocorticism and the performance of the different diagnostic tests.

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Conflict of interest statement

The authors declare that they have no competing interests.

Figures

Fig. 1
Fig. 1
Normal feedback regulation of cortisol and aldosterone secretion. A Hypothalamic–pituitary–adrenal axis. Adrenocorticotropic hormone (ACTH) is secreted from the anterior pituitary under the influence of corticotropin releasing hormone (CRH) although other factors such as stress and arginine vasopressin (AVP) may also play a role. Secretion of CRH and ACTH is inhibited by cortisol, highlighting the importance of negative feedback control. B Renin–angiotensin–aldosterone system (RAAS). Renin is secreted by the juxtaglomerular cells in the kidney dependent on renal arteriolar blood pressure. Renin converts angiotensinogen to angiotensin I, which is converted in the lungs by angiotensin converting enzyme (ACE) into angiotensin II. Decreasing extracellular fraction of potassium (K+) has an important direct inhibitory effect on aldosterone secretion. Reproduced and modified with permission from Newell Price and Auchus, 2020 [2]
Fig. 2
Fig. 2
Expected electrolyte and hormonal abnormalities in dogs with hypoadrenocorticism. Apparent isolated glucocorticoid deficiency (with reference interval electrolyte concentrations) can occur with sufficient, insufficient and deficient aldosterone production. Reproduced with permission of UK-Vet Companion Animal [24]
See this image and copyright information in PMC

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