Renovascular Hypertension

by Carlo Raj, MD

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    00:00 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.

    00:47 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.

    01:21 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.

    02:11 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.

    03:35 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 us continue.

    04:02 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.

    04:36 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.

    04:45 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.

    05:06 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.

    06:42 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.

    07:35 You are sleeping there and guess what, you're going to and think ACE inhibitor in diabetes.

    07:40 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.

    08:31 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.

    08:46 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.

    09:11 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 hypertension, secondary.

    About the Lecture

    The lecture Renovascular Hypertension by Carlo Raj, MD is from the course Hypertension.

    Included Quiz Questions

    1. Beta-1 adrenergic receptor
    2. Beta-2 adrenergic receptor
    3. Beta-3 adrenergic receptor
    4. Alpha-1 adrenergic receptor
    5. Alpha-2 adrenergic receptor
    1. Renin
    2. Angiotensinogen
    3. Angiotensin II
    4. Epinephrine
    5. Aldosterone
    1. Efferent arteriole
    2. Afferent arteriole
    3. Macula densa
    4. Granular cells
    5. Mesangial cells
    1. Fibromuscular dysplasia and renal angiography
    2. Atheromatous disease and renal angiography
    3. Fibromyalgia and renal angiography
    4. Diabetes mellitus and renal ultrasound
    5. Fibromuscular dysplasia and renal ultrasound
    1. Enalapril
    2. Metoprolol
    3. Nifedipine
    4. Hydrochlorothiazide
    5. Aliskiren

    Author of lecture Renovascular Hypertension

     Carlo Raj, MD

    Carlo Raj, MD

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    Too good
    By hao t. on 03. December 2020 for Renovascular Hypertension

    Make me understand this so well. Thanks you Dr. Carlo Raj

    Great Lecture!
    By Pharlin N. on 03. August 2020 for Renovascular Hypertension

    excellent short, precise and informative lecture on 2ndary HTN. thanks so much Dr Raj!

    makes so much sense now
    By Fiona L. on 13. May 2019 for Renovascular Hypertension

    linking the dots for you between normal physiology and pathology. Great!

    By Zoraida F. on 29. September 2018 for Renovascular Hypertension

    One of the greatest lecturers I even had the pleasure of listening to. I love listening to this guy.