Hyperaldosteronism refers to an endocrine disorder where the adrenal gland produces
above normal levels of the hormone aldosterone.
Now, there are two adrenal glands, one above each kidney, and each one has an inner layer
called the medulla and an outer layer called the cortex which is subdivided into three
more layers, the zona glomerulosa, zona fasciculata, and the zona reticularis.
The outermost layer is the zona glomerulosa, and it’s full of cells that make the hormone
aldosterone.
Aldosterone is part of a hormone family or axis which work together and are called the
renin-angiotensin-aldosterone system.
Together these hormones decrease potassium levels, increase sodium levels, and increase
blood volume and blood pressure.
Aldosterone is secreted in response to elevated levels of renin, and it’s role is to bind
to receptors on two types of cells along the distal convoluted tubule of the nephron.
First it stimulates the sodium/potassium ion pumps of the principal cells to work even
harder.
These pumps drive potassium from the blood into the cells and from there it flows down
its concentration gradient into the tubule to be excreted as urine.
At the same time, the pumps drive sodium in the opposite direction from the cell into
the blood, which allows more sodium to flow from the tubule to the cell down its concentration
gradient.
Since water often flows with sodium through a process of osmosis, water also moves into
the blood, which increases blood volume and therefore blood pressure.
The other function of aldosterone is to stimulate the ATPase pumps in alpha-intercalated cells
which causes more protons to get excreted into the urine.
Meanwhile, ion exchangers on the basal surface of the cell move the negatively charged bicarbonate
ion into the extracellular space, causing an increase in pH.
Hyperaldosteronism can happen due to primary causes which is where the adrenal gland itself
is responsible for the excess production of aldosterone.
The most common primary cause is called idiopathic hyperaldosteronism, because the zona glomerulosa
has an increase in the number of cells secreting aldosterone, but it’s not really clear why
this happens.
The second most common cause is called Conn syndrome and this is where an adenoma or tumor
in the glandular epithelial cells secretes too much hormone.
A third cause is familial hyperaldosteronism, and this is a genetic condition that runs
in families, and it’s when the zona glomerulosa cells inappropriately make aldosterone in
response to adrenocorticotropic hormone which is secreted by the pituitary gland, and this
is in addition to responding to renin as normal.
Hyperaldosteronism can also be due to secondary causes where the pathology lies outside of
the adrenal gland.
Secondary causes of hyperaldosteronism are usually due to excess aldosterone production
in response to high levels of renin.
This might happen when there’s a chronic decrease in blood pressure like in congestive
heart failure or cirrhosis.
Hyperaldosteronism leads to hypokalemia, which is low potassium levels in the blood, as well
as hypernatremia—high sodium levels in the blood.
With more sodium around in the blood, water moves into the blood vessels, which results
in a high blood volume and high blood pressure, or hypertension.
Finally, the loss of protons also results in an alkalosis, and more specifically a metabolic
alkalosis, since it’s caused by the kidneys.
Individuals with hyperaldosteronism typically develop hypertension related symptoms like
headaches and facial flushing, as well as hypokalemia related symptoms like constipation,
weakness, and potentially changes in their heart rhythm.
The diagnosis of hyperaldosteronism is mainly done by measuring levels of renin and aldosterone.
In primary hyperaldosteronism, the main problem is that zona glomerulosa cells secrete high
levels of aldosterone, and that aldosterone has a negative feedback effect on renin, and
so it actually inhibits renin production.
So in this case aldosterone levels are high and renin levels are low in.
In secondary hyperaldosteronism, on the other hand, the main problem is that there is too
much renin produced by the juxtaglomerular cells of the kidneys, so even though aldosterone’s
inhibiting renin secretion, renin production’s still being stimulated by those cells, and
this means that there’s both high levels of aldosterone and high levels of renin.
Treatment of hyperaldosteronism is usually with potassium-sparing diuretics, especially
spironolactone, which competitively binds to aldosterone receptors on the principal
and alpha-intercalated cells.
With these medications around, aldosterone can’t exert its effects.
Additionally, treating the underlying cause can be helpful.
For example, in Conn syndrome surgical removal of the tumor can help, and also managing heart
failure and cirrhosis.
All right, as a quick recap, hyperaldosteronism is the chronic, excess secretion of aldosterone
from the zona glomerulosa of the adrenal gland, and these high aldosterone levels can lead
to hypokalemia, hypernatremia, hypertension, and a metabolic alkalosis.
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