Students always ask me to talk about renal blood flow. I always think of this as being anatomy
and then physio. But then how do you actually apply this into what’s going on in the clinical realm.
Well, let’s find out. Renal blood flow, to begin with, just simple, simple facts,
20% of your cardiac output, kidney. Does that mean that the kidney is that demanding? No.
It means that the kidney requires plasma so that it can properly do what? Conduct GFR. That’s it.
It’s main job in its life is to filter plasma. Now, at each renal hilum, where are you?
You see where it says renal artery. Renal artery is coming in to the hilum of the kidney,
whereas if it was a lung then you would call that the hilum of the lung. Now, all of these are
important things and important anatomical landmarks. But let’s continue forward
through the renal artery, shall we? Now, as you branch your renal artery, you then get into your
interlobar and then you form your arcuate. See where is this arcuate. Arcuate is exactly that.
It’s an arc. Now, before I move any further, I want to make sure that you’re completely familiar
with just the normal organization of the kidney or really just any organ. The medulla will be
the inner aspect, the pulp of the kidney or the organ. The cortex will be the outer aspect.
Are we clear about that? Okay, do not ever, ever confuse those two. Anyway, you won't.
So, the medulla has interesting structures in it that you also want to pay attention to,
the medulla, the inner aspect. The medulla contains the pelvis. It has the calyces.
These are things that you know from anatomy. If you don't, make sure that you take a look at them.
And it has something that we will take a look at called the papilla. Now, before I repeat any of what
I just mentioned here, we then go into the arc. Look at the arc. The arc is the arch over the pyramid.
It gives rise to your cortical radiate arteries. You see those? The cortical radiate arteries,
well, technically called interlobular. Now, ultimately, all of this is going to give rise to afferent arterioles.
You stop there for one second. Why? Because afferent arterioles as you know in physiology
is incredibly important. The afferent arteriole is about to arrive to whom? A, afferent is about to A,
arrive at which organ? The glomerulus. What is it? An afferent arteriole, you pay attention to that term,
versus renal artery. Why? Because as we move forward and we start getting to renal vascular diseases,
we are going to plug in pathologies into the renal artery. We already have, for example,
atherosclerosis, fibromuscular dysplasia. And we’re going to put in certain physiologic changes
both in pharmacology and as a reflex in the afferent arteriole and we’ll bring in
our juxtaglomerular apparatus. That’s a lot of stuff going on at the afferent arteriole
that you're familiar with. I'm not overwhelming you. I’m just telling you things that you've seen before
or heard before. All we’re going to do is keep repeating it. Okay. Now, pay attention here.
Diabetes and hypertension, how common is that? Really common. Now, I'm going to be technical.
So we'll go ahead and call this diabetes mellitus because we’re in the realm of the kidney.
Obviously, there’s another diabetes differential. It’s called diabetes insipidus.
So now, osteomyelitis and hypertension, they're macrovascular diseases. What do we mean by that?
Resulting in progressive loss of these vessels. Meaning what? The afferent arterioles.
We then call this nephrosclerosis. So when we get to that point when we start talking about
kidney diseases in greater detail, I will start asking you questions such as, well, where did we have
issues first with diabetes? And it’s a fact that you have blood vessel issues.
We call this hyaline arteriosclerosis as you shall see. What kind? Hyaline arteriolosclerosis.
Once again, everything that we’re doing here is not just so that you can memorize this stuff.
It’s so that you can take this information and give a clinical application. Isn't that why you and I
are here right now? Now, pathologically, this change that you’re going to find, you then refer to this
as your granular surface of the cortex. What does that mean? Granular, what does that mean?
Rough. So, because of the nephrosclerosis that might be taking place secondary to diabetes
or hypertension, the cortex of the kidney, which is what, the superficial and that’s why I stated this
from the get-go that the surface, that cortex is undergoing granular changes. When the time is right,
I'll show you pictures of this as well. If there's anything else that you're required to know here
in terms of anatomy, go ahead and take a look. But I’ve given you the important information
that you need to take out of this for proper clinical application. Let’s go into the medulla.
What’s going on in the medulla as we passed from the renal artery? Well, with the medulla,
there might be certain issues. What kind of issues? I want you to go ahead and think about the nephron.
With the nephron, I want you to move down the proximal convoluted tubule. Are you moving down?
Come on, are you there? Are you with me? I want you to produce your urine. As you produce your urine,
what are you doing as you’re going down your PCT? You are, especially the descending limb,
you're removing more and more and more of what? Water, right? Water permeable,
remember that from physio? Good. As you move down into the nephron and medulla,
what then happens? It means that you have hypertonic fluid. What’s hypertonic mean?
It means that you have increased concentrate on solute, in the medulla. That's exactly what you have.
So now, as you move that thick ascending limb, there’s an interesting pump there, isn’t there?
It’s called the sodium potassium two chloride. Do you remember that from physio?
Well, these are very, very highly metabolically active, you see the phrase, metabolically active.
So, say that you did have some type of ischemic event taking place. Once you have some type of
ischemic injury as stated here, then what do you think? Which part of the kidney
is most susceptible to damage because of the increased metabolic activity in the medulla
such as the sodium potassium two chloride symport and the fact that you have to go in deep.
in the medulla. Those are areas that are highly, highly susceptible to ischemic injury. Do not forget that.
Let’s move on. Now, the blood supply, the blood supplied to the tubulointerstitial tissue. Where is that?
What does that even mean? Well, in order for you to create a tubule, what’s a tubule?
The nephron. In order for you to go from the renal artery, and we just walked through the arcuate,
and talked about the afferent arteriole giving rise to your tuft of capillaries, where am I, glomerulus,
and you're going to filter. Filter what? Plasma. What's the structure that filters plasma?
I believe it’s called what? Good, the glomerulus. So, correct me if I’m wrong.
Do you first have to go through the glomerulus and then go into the tubule or vice versa?
You have to go through the glomerulus first, then the tubule. What does that mean? Read this,
the glomerulus, which then expresses the pathophysiologic changes of tubular interstitial fibrosis,
so when we get into actual pathologies of the glomerulus and tubular interstitial nephritis,
your first issue is going to be with the glomerulus. Then you get into tubular interstitial diseases.
Keep that in mind when you get such questions because by the time you get into such pathology,
I can almost guarantee you that you probably already had damage to the glomerulus.
Let's move on.