Continuing our discussion of, clinical
application of renal blood flow. We are going
to take that information that we have seen
prior, with that table and make sure that you
then associate it with that picture where for
example we looked at Bowman's space hydrostatic
pressure being increased with obstruction
such as BPH may be a renal stone or there
is increase in oncotic pressure in the
Bowman's space in those dealing with
something like minimal change disease,
the most common cause of nephrotic syndrome
in a child. Continuing our discussion and
putting in a
little bit more detail, but just enough where
you are able to create a story for yourself.
Lets take a look at this picture. Now in
the very beginning, we talked about the anatomy
of renal blood flow. We began by looking at
the renal artery headed towards where the
hilum of that kidney. Next, the interlobar and
you had your interlobular. In other words,
that would be your, well, arcuate gives rise to
your corticoradiate. This then gives rise
to your afferent arteriole. You tell me as to what
normally keeps the afferent arteriole open?
Prostaglandin. Keep that in mind.
Whereas on the efferent side, we continue
the blood flow. There is a very important
hormone known as angiotensin-II, which then
causes preferentially vasoconstriction at
the efferent arteriole. There is a balance
that is taking place constantly between the
afferent and efferent known as autoregulation
in which you will then have blood flow well depending,
as the range of blood pressure, maybe approximately
from 40 to 140 where that blood flow will
remain the same so that's your proper GFR.
Now on the efferent side, we are moving beyond
the arteriole, now what's really
interesting about this, is the fact the
afferent, what is that? That is an arteriole
is going to form a tuft of capillaries.
Now usually if it's most any other part of
the body, you go from arteriole, capillary
and you go to venule. Anatomically that is
not what is happening here, is it? It is afferent
arteriole, a tuft of capillaries, efferent
arteriolar. Okay. Now you go down and you travel
around the nephron. It's called peritubular
capillaries. This is the second set of capillary.
What's another name for this? Welcome to
vasa recta. Now, vasa recta eventually will give rise
to inter.. go backwards now, interlobular veins, interlobar
veins out through renal vein really important
that you know about your renal vein especially
the left side. Tell me about its course.
Renal vein, renal vein, renal vein, renal
vein. What's up with it? Oh look at that, that's my friend.
Who? Left gonadal vein and
you move towards what please? Inferior vena cava
is that going to come in handy. Oh yeah we'll see.
Okay now lets add some clinical correlations.
There is a prostaglandin. What is it doing?
It is causing vasodilation. You take me through
this, please. If there is vasodilation, then
what happens to renal blood flow or renal
plasma flow? Obviously increased. When you
increase the amount of blood passing through
afferent arteriole, please tell me what happens
to hydrostatic pressure. What does P mean?
Hydrostatic pressure. What is GC mean? Glomerular
capillaries. How important is it for you to
pay attention to those abbreviations? It will
tell you between where you are. Is the capillary
or is it the Bowman space. Here we're at the glomerular
capillary. What are you doing? You can use that P for
pushing pressure. What's your pushing pressure? Hydrostatic.
It's increased. What then happens to GFR? Increased.
Very good. Now we have afferent arteriolar
dilation. You tell me once more what may then
remove the prostaglandin. What about that
patient who had arthritis? For 10 or 15 years
was taking what? NSAIDs. Anti-inflammatory.
And therefore removed or inhibite the COX a
cyclooxygenase and therefore resulted in decreased
prostaglandin. That decrease in prostaglandin then
causes what, please? A decrease in the diameter
of the afferent arteriole. What then happens
to renal blood flow? It decreases. It hit
the constricted afferent arteriole. What happens
to hydrostatic pressure? Decrease. Pay attention
to P and GC. What is P? The pushing hydrostatic
pressure, pushing up the fluid out of your
GC into the Bowman space. That obviously has
been decreased in the setting of NSAIDs. What
happens to GFR? Decreased. Now you tell me. Hmm.
If this continues and that the patient is not paying
attention and family medicine doctor is not
paying attention, the primary care would
have you? What is this patient prone to? Renal
failure. Okay, lets move on. Let us now switch
over to the efferent arteriole shall we? Efferent
arteriole. Here we are going to bring in angiotensin II
This angiotensin II works in the efferent
arteriole preferentially to do what? Now let
me give you the setting. I am always going to do
this to you. Because otherwise you are just going
to sit here and memorize. We cannot have that.
So, we have a patient that has renal arterial
stenosis. Yet once again. We will take as
if 52-year-old male who has renal bruits and
has secondary hypertension. We talked about
this patient already. So renal artery stenosis.
Why was it that the angiotensin-II and the
renin system was activated to begin with?
That RAAS system. Renin, angiotensin II and aldosterone
system was stimulated so that it can then
restore some of this blood flow to the kidney
because if the GFR dies, as does the kidney.
So now in the setting of renal artery stenosis,
you are going to release renin. Here comes
my angiotensin II, what it is going to do?
Constrict the efferent arteriole. That is
Now close your eyes. May I ask you question
by question? You tell me. Ready? If you are
going to have efferent vasoconstriction, what is
it going to have renal blood flow? It is then
going to decrease. If you are going to have
efferent vasoconstriction, what happens to
hydrostatic pressure? Stop! Wait for me to
finish. What happens to the hydrostatic pressure
in your glomerular capillaries. It increases.
Why did I have you stopped? Because on your
exams, you want to make sure that you understand
where exactly are they asking you about that
hydrostatic pressure. Was it in the glomerular
capillary or was it in the Bowman space? It
was my question to you. Where was the hydrostatic
pressure increased? Here in the glomerular capillaries
obviously. When that is increased, what then
happens to your GFR? It is increased. Now
we go one step further. Early we talked about
filtration fraction. What is that equal to?
It is equal to GFR/RPF. In the setting of
angiotensin II, where vasoconstriction of
efferent arteriole, what happens to GFR? It
increases. What happens to renal plasma flow?
It decreases. What happens to filtration fraction,
please? Good, it increases. Excellent! Move on. How
might you move that angiotensin II and this
will be contraindicated in a patient with
renal artery stenosis. Why? This angiotensin II
was put here by the body, hormonally,
so that it can restore some of that GFR, wasn't
it? Why? Because the renal artery stenosis
in that patient was causing decreased perfusion.
Are you following me? So that angiotensin II
was there to protect the kidney. And you. Not you.
But a negligent doctor did what? Not that he or
she was going to take care of the blood pressure
by giving an ACE inhibitor. By giving an ACE
inhibitor gone is the angiotensin II, bye bye
goes the patient. What happened? Remove the
angiotensin II. Aren't you going to exacerbate
that renal failure? Yes, you are. ACE inhibitors
are absolutely contraindicated and definitely in
bilateral renal arterial stenosis, but clinically
also with unilateral. Keep that in mind. Lets
take a look at this. There is ACE inhibitor
and what does it do? Removes the effective
angiotensin II. What happen to efferent arteriole?
Vasodilation. I just walked you through
all this. I am going to walk you through something
that could be a little tricky. Watch this.
Renal blood flow, efferent arteriolar vasodilation
increased. Okay. Here's your question. Next
what then happens to hydrostatic pressure?
Efferent arteriolar vasodilation. Hydrostatic
pressure is going to decrease in the glomerular
capillary. Dr. Raj you said that it is increased
renal blood flow with vasodilation. How could
it be decreased hydrostatic pressure? Because
look where the vasodilation is. Way past the
glomerulus and when i said way, it is beyond the
glomerulus in the efferent arteriole. So you might have
increased renal blood flow, I am not arguing
that point, but because of vasodilation is not the
afferent, you will have a decrease in hydrostatic
pressure of your glomerular capillary. What
then will happen to your GFR? It will decrease.
When would this be contraindicated? One more
time, bilateral renal arterial stenosis and
as I said clinically even with unilateral
you don't get this. You just don't. Okay.
Beta-blocker, maybe that might not even be a good idea
because in that setting don't you need that
angiotensin II? What kind of beta receptor
is on your juxtaglomerular apparatus? Good. Beta-1.
So therefore by giving a beta-blocker, you
might also inhibit the release of renin. So
Dr. Raj what am I going to use? Maybe calcium
channel blocker. You have other options,
you definitely do. Might be a good time for
you to take a look at antihypertensive drugs.
So all that pathology is just a combination
of many things like tentacles, like an octopus
and all of it has different arms and branches
and it is all different points in which there
may be if you are weak in a particular area,
you go back and take a review of relevant
Come back though and we will continue our discussion,
until we hit another wall. We build and
build and build this information
until you are confident. We are going to put