So, as I said earlier, let's say it's the renal ischemia.
How? Elderly patient male approximately 45
years of age, obese. Without a doubt, you're thinking
what, please? Atherosclerosis. Young female,
37 years of age, not obese, not hyperlipidemia,
lipid profile perfect, but you do a renal
angiogram. What does that mean? You are actually
checking out the renal arteries and in there
you ended up finding a beaded appearance in
a young female 30 years of age. Where am I?
Renal artery. What does that mean in terms
of perfusion to the kidney and the glomerulus?
Decreased, what is this called? Renal ischemia.
What receptor do you have in juxtaglomerular
apparatus, please? Beta-1, good. You have beta-1
receptors, are they stimulated? Yes, they are.
Just like the heart, what does beta-1
mean to you? Catecholamine. Here in the juxtaglomerular
apparatus, the beta-1 receptors have been
stimulated. Why please? Renal ischemia. Why
please? Ask yourself the question why every
single time and you get your answer. Absolutely
you will because you have asked the fundamental
question and at some point you will find the
answer that everyone is satisfied with. Let
it be the patient. Let it be a question. Let
is be an attending. Who may ever it may be.
But now you have renal ischemia due to atherosclerosis
maybe fibromuscular dysplasia. What have you?
You have increase in renin. You continue.
Increase in angiotensin 1 go up into lungs, don't
you? What enzyme do you have there, please?
ACE. What are you going to create? Angiotensin II.
What are you trying to do? We have decreased
perfusion to the kidney specifically. You
increased the angiotension II. Are we done?
No. But what do you know about angiotension II,
please? Angiotension II causes vasoconstriction
everywhere globally. But if it is down in
your glomerulus, where does the angiotensin II
love to act? The efferent arteriole is
its preference. Is that clear? The efferent
arteriole. Are you picturing that? The efferent
arteriole. Remember in physiology, the efferent
arteriole, if it underwent a vasoconstriction,
what then happens to the hydrostatic pressure
over the glomerulus. Good. You increase you
hydrostatic pressure over the glomerulus.
What are you trying to do? You are trying
to restore the GFR, glomerular filtration
rate because it had an initial decrease, why?
Because of renal ischemia. Are you putting
things together? Do you understand this is
not just pathophys, this is medicine? This
is not just pathology. This is not just a
subject. It is the concept of medicine and
you need to bring everything together so you
connect the dots so that you are able to walk
through this particular journey. Now with
angiotensin II may cause direct vasoconstriction
or it may then actually work on the PCT so
that it reabsorbs the sodium. In addition
to that, what else does it do? Angiotensin II works on the
adrenal cortex. Really? Are you picturing that?
Do you know cortex, what are the layers? GFR. How convenient
is that? We have GFR referring to the kidney,
we have GFR in the adrenal cortex. But the
GFR in adrenal cortex stands for glomerulosa
fasciculata reticularis. You learn that from
physio already and in anatomy and every other
subject, which you have already looked at. So here
I want you to focus upon the glomerulosa. Ready?
Your automatic reflex will tell me what hormone?
Aldosterone, good. Guess what is responsible
for releasing or forming your aldosterone.
Angiotensin II. What does aldosterone do? Are
you with me? Where are you now? Aldosterone,
once you go to the collecting duct. What do
we trying to do? With aldosterone, you are going
to reabsorb sodium. My goodness gracious.
You are reabsorbing a lot of sodium. What
is that going to do to your blood pressure?
Secondary hypertension, all because you caused
renal ischemia, why? If it is young female,
what is my diagnosis? Most likely, please.
Good. Fibromuscular dysplasia. If it is an
elderly male, atherosclerosis. Good job. Let
Here it is. You see that arrow right there.
What does that look like? It look like atherosclerosis
to you. My goodness no, that is beaded appearance,
isn't it? It looks like a string of beads
that you may wear around your neck right now.
You see that necklace that you have on your neck. That is
a beaded apperance. Here it is. But where
am I? This is not around your neck it is
your renal artery. It is undergoing dysplasia
in what patient? Young female. What do you
think is happening to the caliber of that
renal artery? Is it decreasing? The renal
artery. What happens to perfusion to kidney?
Decrease. What is that called? Renal ischemia.
What are you going to do JGA? Stimulate. What
is the receptor? Beta-1 receptor. What are you
releasing? Renin. We just talked about all
these. Renin does what, angiotensin I, angiotensin II.
Angiotensin II what does it do? Vasoconstriction.
Take a look at that algorithm we just went
through. Angiotensin II has direct vasoconstricting
activity. It also increases aldosterone, also
reabsorbs sodium, diagnosis number 1. Diagnosis
number 2, atheromatous disease. You think athero.
Please focus upon athero. What does that mean?
Why do I want you to focus on that? Because
I don’t want to get this confused with arterial.
Is that clear? Read my lips. Arterial versus
athero. How important is that? Ridiculously
important. Athero means lipid. As soon as
your athero, it is lipid. Arterio generic. Clear?
You don't know what is causing the constriction
in arterial. It could be lipid granted. It
could be yes, but doesn't have to be. Really,
what else could it be in arterial? Could be
hyalin as we will talk about later called
hyaline arteriolosclerosis or hyperplastic,
but here specifically athero, lipid. What is
going on? Who is your patient most likely?
Male, obese, older, 45, 50. Clear? Renal artery same
story that we just state with fibromuscular
dysplasia. But before we move on a huge point
clinically. Every single license exam is going
to ask you this question and you should be
quite aware. Why is it that you have to avoid
ACE inhibitors? Big time. See that being bolded
right here. It is important. Walk you through
this real quick. Atherosclerosis is taking
place in a renal artery. What happens in perfusion
to the kidney, please? Decreased. What happens
to the GFR, please? Decreased. GFR is decreased.
What does that mean to you? As soon as you
hear GFR decreasing, it means that you
probably going into renal failure. You want
to do everything in your power to make sure
that you restore the GFR. Can you do that
for me? Can you do that with ACE inhibitor?
Are you kidding me? Think about this, please.
You just released angiotensin II. What does
angiotensin II preferred to work? Good. It
prefers to work on the efferent arteriole
so that you can restore your GFR. But what if
you are giving this patient an ACE inhibitor
in the setting of atherosclerosis? You have
just completely inhibited the formation of
your angiotensin II. Why would you want to
do that in this patient when the kidneys are
trying to be protected? So, therefore, it's
contraindicated in this patient, is that clear?
Now give me where an ACE inhibitor would be the
first line of treatment or call it "renal
protective". In diabetes mellitus,
ACE inhibitor is the first thing that you
want to give if your patient comes in with
microalbuminuria. I will repeat this. Don't
worry. I will repeat this so many different
times that it will be part of your unconscious
reflex. That is what I like to call that.
You are sleeping there and guess what, you're going to
and think ACE inhibitor in diabetes.
Good to go. ACE inhibitor and atherosclerosis,
contraindicated, you cannot have it. Where
did you hear that? Right here. Let us go.
Now renal parenchyma disease. What are we
talking about here? Talk about PKD, polycystic
kidney disease. As soon as you hear this, we
will talk about this in nephrology and it
is the fact that you have autosomal dominant
polycystic kidney disease. That is one I want
you to focus upon. You should be able to quickly
tell me the gene, with that remember all we are doing
here is review, but it is also important that
you make sure that you connect the dots very
quickly. Eighty-five percent of your patients
with polycystic kidney disease, autosomal dominant type is PKD1.
Is that clear? As soon as you hear about PKD1,
what might you be thinking about this in patient?
What aneurysm was that up in your head? That
is called a berry aneurysm. What is the other
name for berry please, clinically? Saccular.
Good. So saccular aneurysm is being formed
in PKD, why? It is not because he has cyst
in the circle of Willis, that makes no sense.
The cysts were located down the kidney usually
bilateral. Most likely in an adult. But you
still have to call it autosomal dominant.
Is that clear? Do not call this adult. You'll missed
every single question. You will disappoint
your attenting. You don't want to do that.
Trust me. This is an autosomal dominant. You
have a cyst in the kidney resulting in hypertension.
Do not equate polycystic kidney disease with
renal failure immediatley, is that clear?
They're two different entities. "What did you say
Dr. Raj?" I said do not equate polycystic kidney
disease with the renal failure immediately.
They are two different diagnoses. Could you
go into renal failure with polycystic kidney
disease? Yes, you can. Immediately? No,
,it is insidious. What does that mean? It
takes a long time before we actually go into
renal failure. Is that clear? With that said,
with PKD you have hypertension. What kind?
Secondary may result in berry aneurysm amongst
other things. Diabetes mellitus. Once again
what is that
going to cause? It is called non-enzymatic
glycosylation, NEG. Or some of you might have
heard of it as being advanced glycosylated end
products. What is going to happen to your
blood vessel? Specifically done in your arterial.
It might undergo closure. It might undergo
once again closure in which it may result in
secondary hypertension. Important diagnosis
and differentials under secondary hypertension,
is that clear? And at this point, I will look
at. It is pretty much to kidney. We know vascular