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Pathophysiology, Diagnosis, and Treatment of Mineralocorticoid Disorders

Steven B. Magill

10.1002/cphy.c130042

Source: Volume 4, Issue 3, July 2014

Published online: August 2014

Full Article on Wiley Online Library



Abstract

The renin‐angiotensin‐aldosterone system (RAAS) is a major regulator of blood pressure control, fluid, and electrolyte balance in humans. Chronic activation of mineralocorticoid production leads to dysregulation of the cardiovascular system and to hypertension.

The key mineralocorticoid is aldosterone. Hyperaldosteronism causes sodium and fluid retention in the kidney. Combined with the actions of angiotensin II, chronic elevation in aldosterone leads to detrimental effects in the vasculature, heart, and brain. The adverse effects of excess aldosterone are heavily dependent on increased dietary salt intake as has been demonstrated in animal models and in humans.

Hypertension develops due to complex genetic influences combined with environmental factors. In the last two decades, primary aldosteronism has been found to occur in 5% to 13% of subjects with hypertension. In addition, patients with hyperaldosteronism have more end organ manifestations such as left ventricular hypertrophy and have significant cardiovascular complications including higher rates of heart failure and atrial fibrillation compared to similarly matched patients with essential hypertension.

The pathophysiology, diagnosis, and treatment of primary aldosteronism will be extensively reviewed. There are many pitfalls in the diagnosis and confirmation of the disorder that will be discussed. Other rare forms of hyper‐ and hypo‐aldosteronism and unusual disorders of hypertension will also be reviewed in this article. © 2014 American Physiological Society. Compr Physiol 4:1083‐1119, 2014.

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Figure 1. Figure 1. Adrenocortical steroidogenic pathway. Adrenocortical steroidogenic pathways for the production of mineralocorticoids and glucocorticoids. Reprinted with permission (141); From Fig. 1. p 152.
Figure 2. Figure 2. CT imaging of the abdomen in a 39‐year‐old woman revealed a 2.3‐cm left adrenal nodule with HU of ‐13 (arrow). The contralateral adrenal gland appeared normal.
Figure 3. Figure 3. Left adrenal nodule in 55 year old man with primary aldosteronism (arrow). The right adrenal gland was normal.
Figure 4. Figure 4. CT of the abdomen in a 42‐year‐old man with primary aldosteronism. Superior cut of the abdomen. Note the 2‐cm nodule in the body of the left adrenal gland (arrow). The right adrenal gland appeared normal in this section.
Figure 5. Figure 5. CT of the abdomen in a 42‐year‐old man with primary aldosteronism. Lower (more caudal) cut of the abdomen. Note the ∼1 cm nodule in the distal portion of the medial limb of the right adrenal gland (arrow).


Figure 1. Adrenocortical steroidogenic pathway. Adrenocortical steroidogenic pathways for the production of mineralocorticoids and glucocorticoids. Reprinted with permission (141); From Fig. 1. p 152.


Figure 2. CT imaging of the abdomen in a 39‐year‐old woman revealed a 2.3‐cm left adrenal nodule with HU of ‐13 (arrow). The contralateral adrenal gland appeared normal.


Figure 3. Left adrenal nodule in 55 year old man with primary aldosteronism (arrow). The right adrenal gland was normal.


Figure 4. CT of the abdomen in a 42‐year‐old man with primary aldosteronism. Superior cut of the abdomen. Note the 2‐cm nodule in the body of the left adrenal gland (arrow). The right adrenal gland appeared normal in this section.


Figure 5. CT of the abdomen in a 42‐year‐old man with primary aldosteronism. Lower (more caudal) cut of the abdomen. Note the ∼1 cm nodule in the distal portion of the medial limb of the right adrenal gland (arrow).
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Article Title: Pathophysiology, Diagnosis, and Treatment of Mineralocorticoid Disorders
 

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Steven B. Magill. Pathophysiology, Diagnosis, and Treatment of Mineralocorticoid Disorders. Compr Physiol 2014, 4: 1083-1119. doi: 10.1002/cphy.c130042