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Clinical Application of Renal Blood Flow (Part 2)

by Carlo Raj, MD
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    00:02 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.

    00:41 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.

    01:45 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.

    02:55 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.

    03:46 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.

    04:07 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.

    05:45 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.

    06:05 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 my topic.

    06:16 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 material.

    10:36 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 all this together now with RAAS and make sure that you are truly familiar with the entire process of your RAAS system. Lets begin. So here we are. I want you to begin at the kidney. Please begin at the kidney and why would you want to release the renin? Decreased perfusion to the kidney.Okay good. Give me some differentials. I've walked you through renal artery stenosis adequately. What about congestive heart failure? Decreased perfusion to the kidney. In these cases, those juxtaglomerular cells are going to release renin. Hence, take a look, please. Decreased blood pressure is then going to release your renin. Here continue forward. I want you to make sure you clear by this. You are going to be an MD. You are going to be a doctor, but that MD stands for macula densa. Macula densa will decrease blood pressure. Walk me through this. Initially decrease of blood pressure, decreased perfusion, decreased GFR, where is our macula densa? Distal convoluted tubule. What is the name of that sensor? Macula densa. I showed you a picture earlier. What is that macula densa sense? It senses the sodium or chloride right. So therefore now with decreased blood pressure, what is it doing? It's not sensing as much. So all of this is going to help contribute to increasing renin. One last thing, when we have a decrease in blood pressure, can I ask you what branch of the autonomic nervous has to come out? Good. Sympathetic. What kind of receptor on your JGA? Good. Beta-1. Once again get another factor to help you stimulate renin. Here comes out and here is not ogen. Now I would like for you to take a look at this suffix. I would like for you to understand this concept ogen. What does that even mean? Trypsinogen, fibrinogen, angiotensinogen so on and so forth. So the term ogen means weak. Weak precursor right. Most of your proteins come from where? The liver.

    12:56 What is the most abundant protein in our bodies? Albumin. Coming from where? Liver. Here is angiotensin, angiotensinogen coming from the liver. What does that renin do? Cleave off the ogen. There it goes. What do you have? angiotensin I. Where is the angiotensin I headed to? To the lung. What's there? ACE. So here, ACE, angiotensin converting enzyme, will take the I and turn into the infamous angiotensin II. Now lets plug in some pathologies. Are you ready? What if you had a patient that ends up having too much renin? Autonomously. There was no decrease in blood pressure as an in setting event. And imaging study you ended up finding a tumour.

    13:43 Where? In the juxtaglomerular apparatus. Wow! And you ended up finding increased blood pressure.

    13:49 So if you have increase in renin, increase in aldosterone, you have secondary hypertension.

    13:54 Are we clear? What is this called? Reninoma. You understand the physio. You can easy put in the pathology and you see your patient. You can actually see your patient. Next, give me a pathology in which your ACE might be elevated. A pathology. May be something like What if I told you non-caseating granuloma, bilateral hilar lymphadenopathy in an African-American female. You will tell me? Good. Sarcoidosis. And sarcoidosis you could have increased production of ACE. What does this mean? Increased production of angiotensin II Now with all that said lets say that you give an ACE inhbitor. When you have an ACE inhibitor, then you knock it out and you can never form angiotensin II and never release your aldosterone. Stop there for one second.

    14:40 The branch that is important for us, bradykinin. ACE, angiotensin converting enzyme is an enzyme that you must know as being the enzyme responsible for metabolism of bradykinin. Two major effects of bradykinin that you would want to know as being a side effect of what drug? ACE inhibitor.

    15:02 A dry cough, And number 2, angioedema. So bradykinin, increased capillary permeability. And number 2, Might be something like dry cough. And with that dry cough, which is incredibly irritating you change the drug into ARBs. Got it? Lets move on. Angiotensin II vasoconstriction preferentially what part of the arteriole? Efferent. What would it do to your blood vessels in general? It will cause contraction, vasoconstriction. What are you are trying to do? Increased blood pressure. What was in setting event. Take a look, please. The first box, over onto your left is decreased blood pressure. You're trying to increase your blood pressure. There is my efferent arteriole. What does it do? Do not memorize this. Close your eyes. Let me ask you a question. Number one. You have efferent arteriole vasoconstriction. Tell me about renal blood flow when the plasma flow, decreased. Next efferent arteriole vasoconstriction.

    16:05 Tell me about GFR, Increased. Tell me the equation for filtration fraction. GFR/renal plasma flow.

    16:12 Good. You do the math. What do you get for filtration fraction? Increased. Good move on.

    16:20 What else happens? While angiotensin II is going to go where, that's the organ, adrenal.

    16:25 Which part? Cortex. What part of the cortex? and I am going to keep pushing you here. What part of the cortex? Glomerulosa. Angiotensin II is going to work on the glomerulosa to stimulate what's known as aldosterone synthase. Here comes an aldosterone. Close your eyes. You know this from physio already. Aldosterone turns to your collecting duct. Aldosterone works on your principal cells principally. What does it do? It works on your sodium channels everywhere. What do you mean everywhere? Well, principal cell. You picturing that? Where am I? Collecting duct okay fine and it is facing whom? Urine. It is facing the urine. So that is known as the apical membrane. That apical membrane has a sodium channel. Aldosterone could work on that ENAC.

    17:16 It is called Epithelial Sodium Channel. E, epithelium; sodium channel, ENAC. Aldosterone works there to remove the sodium from the urine. You know that already. Next, on the basolateral membrane only, you have your sodium- potassium ATPase pump. So what kind of effect does aldosterone have on your pump Tell me about that pump. Sodium being kicked out. Kicked out into where? Into your blood. Aldosterone will stimulate that pump. We have addressed this. Insertion in principal cells enhances stop there. So you are going to reabsorb sodium. You are going to take out two. What do you mean take out? You are going to literally remove and secrete two substances into urine. First will be potassium, next will be hydrogen. Okay. You can see. We are going to work through a lot of pathologies here, aren’t we? Because you can have issues when you have too much aldosterone, and you can have issues in which you have two little aldosterone. Too much aldosterone. Give me two differentials.Number 1 Conn exclusive aldosterone secreting tumour.

    18:29 Cushing will be both cortisole and aldosterone. Give me one aldosterone deficiency pathology, Addison. Addison's disease. So are these things that we talked about? Of course keep repeating.

    18:44 So when we have aldosterone it will reabsorb sodium. It will kick out the potassium meaning to say urinated out and it gets rid of your hydrogen. So in Conn's syndrome tell me about the pH in that patient with Conn? Take your time. Close your eyes. Reabsorbing too much sodium.

    19:01 Getting rid of too much hydrogen. What happens to your pH? Increases alkalosis in Conn. Confirm it. Why? Because you will find many patients with secondary hypertension and Conn syndrome.

    19:12 Many, not rare. Many.

    19:16 Great favourable sodium gradient and along with sodium what comes out? Fluid. Tell me what is it that contributes to the pitting edema and congestive heart failure? The aldosterone.

    19:28 Why? Because of this entire mechanism, we just went through. Are we done? Not quite yet because a decrease in blood pressure, but there is another hormone that also comes into play, and angiotensin II not only will it be responsible for releasing that aldosterone from adrenal cortex, but angiotensin II also works on the posterior pituitary. Why, why, why, why? Decreased blood pressure is what the kidney is thinking? This angiotensin II is then going to walk on the posterior pituitary and so, therefore, you are going to release ADH. Tell me about ADH, antidiuretic hormone. That works on the, also collecting duct. What does it do? It works through your V2 receptors. How many kidneys do you have? I think one.

    20:12 No no. Who? I think I have two. You have two kidneys. So V2 receptors is what ADH works on. Gotta have fun with this just a little bit huh. So works on V2 receptors and what does it do? It is then going to insert aquaporins. So that you do only what please, antidiuretic hormone. What is another name for ADH? Vasopressin and you are only going to reabsorb water, water, water in the hopes of doing what? In the hopes of restoring osmolarity. In the hopes of restoring some of your blood pressure. Now couple of important things about angiotensin II in addition, is that it does work. Please pay attention. That's its proximal convoluted tubule. Angiotensin II earlier through aldosterone. May I ask you questions? Worked where? Collecting duct. Angiotensin II here is working on proximal tubule. What does it do? It reabsorbs your sodium. Don't memorize this. What are we doing? There was a decrease in blood pressure as being the inciting event right. Now the angiotensin II is going to work on your proximal convoluted tubule so you can try to remove more sodium in exchange for hydrogen. So water reabsorption and then can permit what is known as contraction alkalosis and what that basically means is that you are going to have contraction and along with it you have also hydrogen leaving resulting in alkalosis.

    21:42 Finally, in the hypothalamus, it has thirst. Now all of this is then going to contribute to release of ADH. So ladies and gentleman angiotensin II as you can see here from the origin of it all with that initial event of whatever it may be is causing decreased perfusion to the kidney. Once it gets into the renin realm, now renin along with angiotensin II and aldosterone my goodness gracious right up and down the body has all kinds of incredible effects, and all these pathologies that we're going to put in here including some of our issues with ADH and diabetes insipidus right. Central nephrogenic, we are going to bring all this into play, but if your foundation isn't strong it is going to make it quite difficult for me and you to work together so that we can accomplish our goals effectively.


    About the Lecture

    The lecture Clinical Application of Renal Blood Flow (Part 2) by Carlo Raj, MD is from the course Renal Diagnostics. It contains the following chapters:

    • Changes in Glomerular Dynamics
    • Renin-Angiotensin-Aldosterone-System

    Included Quiz Questions

    1. Increase in hydrostatic pressure in bowmans space.
    2. Increase in hydrostatic pressure in the glomerular capillaries.
    3. Increase in renal plasma flow.
    4. Vasodilation of afferent arteriole.
    5. Increased glomerular filtration rate.
    1. All are contraindicated
    2. ACE inhibitors
    3. Angiotensin receptor blocker
    4. COX2 inhibitors
    5. Beta blockers
    1. Angiotensin II
    2. Renin
    3. Angiotensinogen
    4. Prostaglandin
    5. Aldosterone
    1. NSAIDs – vasoconstriction of afferent arteriole.
    2. Prostaglandins – vasoconstriction of the afferent arteriole.
    3. All are correct.
    4. COX 2 inhibitors – vasodilation of the efferent arteriole.
    5. Angiotensin II – vasodilation of efferent arteriole.
    1. It results in excess cortisol.
    2. It results in excess aldosterone.
    3. It is a tumor of the adrenal gland.
    4. It often presents with patients in alkalotic state.
    5. It often presents with secondary hypertension.
    1. All are correct.
    2. Renin released from juxtaglomerular cells.
    3. Angiotensin I is formed in the blood by renin stimulation.
    4. Angiontensin converting enzyme in the lung forms angiotensin II.
    5. Angiotensinogen formed in the liver.
    1. Metabolism of bradykinin.
    2. Stimulates ADH release from posterior pituitary.
    3. Release of aldosterone from the zona glomerulosa
    4. Stimulation of the hypothalamic thirst center.
    5. Na+/H+ activity in the proximal convoluted tubule.
    1. Addison’s disease,
    2. Reninoma.
    3. Cushing’s disease.
    4. Renal artery stenosis.
    5. Conn’s syndrome.
    1. Sarcoidosis
    2. Addison’s disease
    3. Angioedema.
    4. Renal artery stenosis.
    5. Tumor of the juxtaglomerular apparatus
    1. Decreases water reabsorption in the nephron.
    2. ENac upregulation on the apical membrane in the collecting duct.
    3. Increases sodium absorption overall.
    4. Stimulates the Na/K+ pump on the basolateral membrane stimulating K+ release into the lumen..
    5. Stimulates secretion of hydrogen ions in the collecting duct.

    Author of lecture Clinical Application of Renal Blood Flow (Part 2)

     Carlo Raj, MD

    Carlo Raj, MD


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