If that was hyperaldosteronism, we will then
move on to hypoaldosteronism.
You do the same thing, quickly tell me.
Serum levels decreased, potassium levels elevated,
hydrogen is increased, thus Ph is decreased.
Can you do it that quickly?
Yes, you can.
Listen to me again, you will get it.
Results in… results from type 4 renal tubular
acidosis or could result in.
What do you mean?
I just told you, if you didn’t have enough
aldosterone, your hydrogen concentration increases
in your plasma, what happens to your Ph?
Oh, renal tubular acidosis.
When you say renal tubular acidosis, what
is that acidosis actually referring to?
Not in the urine, right, it is in the plasma.
Type 4, type 4, type 4.
Remember, RTA, you want to know 1, 2, and
However, the biggest difference between this
type of RTA and any other, if you don’t
have aldosterone, take your time, aldosterone
If you don’t have aldosterone, you are not
getting rid of potassium, you are retaining
it resulting in hyperkalemia.
Hmm, that is dangerous, that hyperkalemia
is dangerous, especially for the heart.
You are then causing, as you remember, depolarization
of your resting membrane potential and that
is not a good thing, is it?
Hypoaldosteronism hyporeninemic, how is this
Common in chronic kidney disease, so if the
kidney starts decreasing in function then
you know that you don’t have enough renin.
If you don’t have enough renin then what
then happens to your aldosterone level?
This is called hyporeninemic hypoaldosteronism.
Say that three times fast.
Language, language, language, apart from may
be a little bit of memorization, but really
understand what this is saying.
Also seen with NSAIDs, cyclosporin and HIV,
you could potentially have hyporeninemic hypoaldosteronism.
Hyperreninemic hypoaldosteronism, how is this
What if you give an ACE inhibitor?
If you give an ACE inhibitor, you have inhibited
the conversion of angiotensin 1 into angiotensin
So, if you don’t even have angiotensin 2,
how in the world are you going to stimulate
that enzyme called aldosterone synthase?
You can’t, resulting in… what is my topic?
Good, hypoaldosteronism, but if you block
that enzyme, all substrates proximally will
You put a block such an… such as an ACE
inhibitor, a pril drug, renin increases, hyperreninemic
Heparin, primary adrenal insufficiency in
In Addison’s disease, how much of your cortex
All of it.
From henceforth, if you want to think of Addison’s
primary adrenal insufficiency, you need to
add hormones to your patient because all hormones
are deficient, that’s Addison’s.
And now, it’s getting really interesting.
Conn syndrome, Cushing, Addison’s, students
get this confused all the time.
Keep replaying this, replaying this, replaying
this so that this is firmly etched in your
You must know the difference between Conn,
Cushing and Addison.
In Addison, a.k.a. primary adrenal insufficiency,
entire cortex is dead, aldosterone is decreased,
what is my feedback for aldosterone?
Renin, I told you clinically, that is what
you are paying attention to, hyperreninemic
Potassium sparing drugs, congenital adrenal
hyperplasia, what is this one?
The most important enzyme deficiency in congenital
isolated hyperplasia 21 beta hydroxylase.
If that is deficient, no mineralocorticoid,
Are we-Are we clear now, hmm?
You should be able to go through each one
of these differentials and understand why
your patient has hypoaldosteronism and what
kind of concentration of renin do you actually
Hypoaldosteronism, transtubular potassium
gradient less than 7 in a hyperkalemic patient
is suggestive of hypoaldosteronism.
If you want to memorize the value, please
do so, but you already know that if you don’t
have aldosterone that your potassium levels
in fact will be elevated.
Urine potassium, this is the actual formula
for what is known as a transtubular potassium
Keep it in mind, clinically becomes important.
After patient upright for 3 hours, check for
plasma renin activity, serum aldosterone and
serum cortisol, after your patient upright
for 3 hours and see as to whether or not you…
what kind of levels do you find of your plasma
renin, what about your aldosterone and so
on and so forth.
PRA and aldosterone will be low in hyperreninemic
Give me an example there, please.
If you are hyperreninemic, it means that maybe
you have chronic kidney injury, no rennin.
Plasma renin activity will be high in adrenal
insufficiency, AI stands for adrenal insufficiency.
That is your Addison’s.
Topic hypoaldosteronism, no aldosterone, plasma
renin activity increased whereas serum aldosterone
and cortisol will be low, right, in Addison’s
insufficiency or adrenal insufficiency.
Tell me about this area in the-in the… in
Addison’s, tell me about this area around
Mineralocorticoid replacement will address
the hyperkalemia, but is not-not advisable
for many patients with hyperreninemic hypoaldosteronism
due to potential for worsening of hypertension
and fluid overload.
Keep that in mind.
So, if you have fluid overload and you are
thinking about giving them mineralocorticoid,
aren’t you making matters worse?
If you have a patient with CHF or if you have
a patient that is in a state of increased
volume and then you give aldosterone, you
are making things worse.
In this setting, low potassium diet and if
needed, a loop or thiazide diuretic would
be much, much, much more advisable to control
Spend a minute here on this paragraph so that
you understand how, what your next step in
management would be, if your patient is suffering
from hyporeninemic hypoaldosteronism.
That is your primary focus in this paragraph.
And your focus here will be more symptoms,
try to get rid of the fluid through proper