DIP Episode 124 - ABIM/Medicine ITE/USMLE Step 3 Review Series 9 (Nephrology)

Okay, welcome. My name is Divine. I am a resident and in today's podcast I will be continuing my series relating to the ABIM, so the American Board of Internal Medicine Exam or like the Medicine in Training, Slash Step 3. I will continue my review. So this will be Series 9 and I'll be focusing on an nephrology today. I'll be focusing on nephrology. So let's jump right into it. Okay, so let's assume you get a question on the exam about, you know, a person that is septic, right? So let's say you have like 55-year-old female, she's septic, a white count is super high, it's like 20,000 and she's been hypotensive and all that stuff. And then they tell you that when she came into the hospital, initial creatinine was like 0.9 and then like two days after admission it's 1.6, right? If you see that, what are you thinking about? I hope you're thinking about an EKI, right? And I could keep me in jury. And what type would you think you're most likely half? A person that has had like hypotension and sepsis and all that stuff. I'll be thinking more about like a prenatal EKI. And again, I'm going to talk about ways you can use to differentiate between those entities, right? So basically EKI right is essentially just an acute, basically, depletion in a person's renal function, right? Is something that happens over like, you know, a couple of hours to a couple of days, right? And I mean, the classic thing you obviously see clinically is that the patient's BUN, right?

And the patient's creatinine will go up. Now, the thing is EKI, I mean, you probably remember some of this from medical, there are three big types, right? There's like the pre renal. And again, the easy way to understand is just to understand the tube in, right? So remember, we have the afraid of tears that feed blood to the kidneys. So if you have problems with that system, now cause a pre renal EKI. And then we have the kidney itself, right? If you have problems with that system, that's an intra-rinol EKI. And then remember, there's tubing that drains the kidneys, right? So like the ureters, the bladder, the urethra. If you have problems with that system, you have a post renal EKI. And the truth is, of all these EKI's, I mean, you may see pre renal quite a bit on exams, but actually the most common one is actually intra-rinol EKI, right? So intra-rinol EKI is actually the most common. The second most common is the pre renal acute kidney injury, right? And then you can jump to the one that's the least common, which is the post renal. And again, try to, because again, right? No renal is classically like, people here in all and they start to shoulder, right? You don't need to shoulder. Renal is a fairly straightforward. Again, you just have to think that's all you need to really do. So the thing is, if a person has, if a person has intra-rinol EKI, right, kind of think about the different components of the kidneys, right?

So remember the kidneys we have like the glomerulus, right? It's the thing that sort of filters stuff in the kidneys. And then the things that either secret or absorb things in the kidneys are the tubules, right? And then remember that there's like renal parenkama that surrounds the kidney tubules. Those are those classic things that refer to as like the interstitium, right? It's almost like the extracellular matrix around the tubules of the kidneys. The reason I'm breaking it down that way is that if you sort of understand, oh, that those are the three parts of the kidneys, then right off the bat, you already know three causes of intra-rinol EKI. You could, I mean, you can have a problem with the glomerulus. I'll talk about that in another podcast. Those are your glomerular low nephrodities, right? So like IJN Fropathy, post-infectious glomerular fritis, stuff like that, right? Alternatively, you can have problems with the kidney tubules themselves, right? That's like an acute tubular necrosis, right? Or alternatively, you can have problems with the extracellular matrix that surrounds the kidneys, the interstitial, that surrounds the kidneys, right? So in that case, you know that you're likely dealing with acute interstitial nephritis. Remember, acute interstitial nephritis? Is that thing we're classically on exams? You see this triad of like, oh, this patient has a fever, they have a rash, they have a elveded synofiosyl and your blood in their urine.

Yeah, on the USML Es, that's usually the presentation you'll find. But on the medicine-entering exam and the medicine boards, they are very unlikely to give you that classic presentation. So there are other things you may want to think about on that those circumstances. So let's, I guess, talk about these different AK Is one by one, right? So let's just go from the beginning to end. So let's talk about like the pre-renol AK Is. So the thing is, in a pre-renol AKI, you're not profusing the kidney appropriately, right? You're not profusing the kidney appropriately. I mean, it could mean that you may be volume down, right? So it's like, oh, you're just not sending a non-blood. So let's say for example, you were a trauma patient, you lost a ton of blood, you have volume down for that reason, or let's say a person has like a very bad like a gastroenteritis and they have a woman in a ton, right? That will also make them volume down, right? They won't profuse the kidneys enough and they can have pre-renol AKI symptoms. Another classic one on exams, right? So if you, again, if you see me see the word exams, I'm referring to these medicine board exams, especially, and step three, because again, you're gonna see the stuff on step three, right? So a person will have, if they're volume down for an ear isn't right, like again, like trauma patient, that lost a ton of blood, or gastroenteritis, a lot of vomiting, right? Those things can all cause problems, right?

But another thing that can also happen is, what if you're not profusing? Like, because the thing is think about you, you may have a non-volume, but that volume may not be going in on their like high pressures to the kidneys, right? They may not be going in on the high pressures to the kidneys, right? So again, that can also cause problems with a renal profusion. And then another thing that may actually cause like a pre-renol AKI, right? So kind of think about like a person that has like an acute CHF exacerbation, for example. If you have an acute CHF exacerbation, right? You may have a ton of volume on board, like you'll see like the peripheral edema and all that crap, but remember that those patients, right? The cardiac output is not great. So if your cardiac output is not great, guess you're essentially not sending enough blood into the other. If you're not sending enough blood into the other, then you will not be profusing the kidneys appropriately, right? So if a person has like a decrease like, almost think of it as I know in in in a in Mexico days to call this effective arterial blood volume. If you have like a decreased effective at your blood volume, right? That can cause a pre-renol AKI, right? And the thing is again, effective at your blood volume means blood volume that is actively profusing your organs, right?

So if a person has CHF, yeah, they have a lot of volume on board, but it's not effectively profusing the organs because the heart's the pump is not working very well. That's one. Think of another person. Let's assume you have a patient with nephrodix syndrome, right? If a person has a nephrodix syndrome, the a pin out a ton of protein, right? That protein helps you maintain on cortic pressures in your in your maintain on cortic pressures in your in your vasculature, right? So if you have like hypopotenemia, right? Then you're not maintaining on cortic pressures. If you're not maintaining on cortic pressures, you also have a peripheral edema, right? So you won't have a decent effective arterial blood volume. Another weird one, if they want to sort of integrate the question with GI, is if a patient has a miniatreous disease, right? Remember, it's like the protein losing gastropathy, where they basically like poop out protein, right? If you have those problems, again, you have a decreased effective arterial blood volume and those things will all cause you to hyper-profess your kidneys and you can get a period of an EKI with that. So the thing is obviously you need to know the labs that go along with a period of EKI. Well, let's talk about the normal situation. Think about it. If you become volume down, right? If you're not profising your kidneys enough, your body is like, okay, you know what? I got to maintain GFR and I got to make sure that my kidneys don't die, right?

So your body is like, okay, you know what? Let me try to raise my GFR. Not necessarily raise GFR, but maintain GFR because think about it, right? If you're not profising the kidneys in the first place, right? Your GFR will go down, right? I mean, it's the amount of blood that's coming in through the afro natural and going into the glomerulus that determines your GFR. So if you're not profising your kidneys adequately, your GFR is low. But the thing is your body likes this whole process of auto-regulation, right? And in auto-regulation, you essentially want to keep your, you essentially want to try to maintain some sort of homeostasis, right? So the way your body maintains homeostasis is to keep your GFR in a constant balance. So if your GFR goes down because you're hypo profising the kidneys, your body will try to get it back up to just again, keep it at a normal level, right? So how does your body accomplish that? And again, let's just again, don't try to memorize anything. Just think about this logically. We know that the glomerulus is a tough, is a capillary tough that you find between the affront material that lets blood arrive at the glomerulus and then leading away from the glomerulus, you have the efferent material that helps blood exit the glomerulus, right? So the thing is, if you want your GFR to be, if you want to like bring your GFR back up to normal, what you try to do is you will try to dilute the pipe that is bringing blood to your glomerulus, right?

And you'll want to try to constrict the pipe that is getting blood out of your glomerulus, right? Because again, by doing those things, you will keep enough pressure of blood in the glomerulus, so your GFR will be maintained. So what is the thing that your body does to help with diluting the afferent material, which is the pipe that sends blood to your glomerulus? It uses Prostaglandins, right? And then what's the thing your body uses to constrict the efferent material so that you have less blood leaving the glomerulus and you keep your GFR up to date. You do that with angiotensin too, right? So again, if you're not producing the kidneys, one, your body makes a ton of Prostaglandin and two, your ring and your tensin out those trunous systems kicked into high gear, right? And remember, your ring and system starts at the level of the afferent material. You have your GG cells, right? So your jocstal glomerulus cells, they make ring in, that ring will convert angiotensin, no gene, to angiotensin one. And then that angiotensin one will go to the lungs, the endothelial cells that make up the long capillaries have angiotensin convertin enzyme. They'll convert that angiotensin one to angiotensin two. That angiotensin two will help you constrict your efferent material so that you stop draining blood away from the glomeruli. But another thing angiotensin two also does is it goes to the hypothalamus, right?

So it goes to the the supraoptic nucleus of the hypothalamus and it helps you make EDH anti-diarradi hormone. As you'll see as I go along with this podcast, you see that anti-diarradi hormone basically has two jobs. It helps you reabsorb water in the nephron and it helps you reabsorb urea in the nephron. And then and that thing angiotensin two also does is it goes to the adrenal cortex, right? So it goes to like your your zona glomerulosa, right? That makes our dosterone, so it increases the production of our dosterone on that of circumstances. So that's the normal way your body should respond, right? So if your volume down, let's say you're dehydrated or whatever, right? Your body will naturally respond by dilating your efferent material by increasing the production of persta glandins and constructing your efferent material by producing more angiotensin two from this fancy shmancy, renean angiotensin, our dosterone system, right? So if you really understand that pathophysial and again, let's kind of think about this, let's maybe stretch this a little further, right? So think about it. If your body is like volume down, right? It will make sense that your body will try to retain some of this volume, right? Retain some of the sodium and all that stuff because if you retain more sodium in your body, you'll be able to retain more volume, right? Because wherever sodium goes, water will follow, right? Sodium is automatically active.

Also the same thing with urea wherever urea goes, water will follow. Although it's if you really think about it on the step one level of detail, it's actually wherever the water goes, urea follows, but that's a different story for step one. And that's not specifically the purpose of this of this podcast. So, right? If you're renean angiotensin, our dosterone system is all revved up, right? You can already see that a person's urine sodium, because remember our dosterone, right? One of the things it does is it increases the reabsorption of sodium in the gut. I mean in the in the nephron, right? Like the distal nephron. So if you have your renean angiotensin, our dosterone system all revved up, your reabsorb most sodium in your nephron, right? So you're urine sodium, the amount of sodium that mixes into the urine that you collect like in a cup or whatever should be really low, right? That's why usually if a person has a pre-reinal AKI, the urinary sodium is usually pretty low. It's usually less than, usually less than 20 on these exams. And then another thing you want to keep at the back of your mind, right? It's like if a person is reabsorb in, because again, remember one of the byproducts of the renean angiotensin, our dosterone system kicking into high gears, EDH, right? If you have high levels of EDH, remember, EDH literally means anti-diuretic hormone. So it prevents you from die recent. So you also reabsorb a lot of water in the distal nephron.

So if you reabsorb an autonomous water in the distal nephron, guess what will happen to your urine or smallality? Your urine will get more concentrated, right? Because it doesn't have as much water in it, right? So your urine will get super, super, super concentrated. So usually if a patient has a pre-reinal AKI on these exams, their urine or smallality is usually greater than like 500, for example, right? And then whenever you're just to kind of make your life easy, your urinary sodium and your fractional excretion of sodium kind of going the same direction. If your urinary sodium is low, what should be true of your fractional excretion of sodium? Your fractional excretion of sodium should also be low, right? So usually on these exams, the phenol, right? The fractional excretion of sodium is usually less than 1%. If a person has a pre-reinal AKI, right? And again, I said, again, EDH goes up, right? As a result of activation of the urine and your tensin-dosterone system. So yes, your urine gets more concentrated, right? But you also begin to pee out less urea because again, EDH increases the reabsorption of urea, right? So your fractional excretion of urea in a person that has a pre-reinal AKI will actually be less than 35%. Okay? So these are numbers you sort of kind of want to keep at the back of your mind, for example.

And I mean, one round about way, your friends that write these tests can try to trick you is instead of showing you that, oh, the urine of smallality is high, so greater than 500 in a pre-reinal AKI. They may just give you the specific gravity of urine, right? They may give you like a specific gravity that's like 1.020, or 1.030, some really high number. Remember, specific gravity is a measure of density, a measure of relative density, right? So if your urine specific gravity is elevated, right? So if it's like a number that's kind of like north of 1.012, right? Like significantly north of 1.012, that tells you that you're dealing with urine that is super concentrated, okay? So you're very likely dealing with a pre-reinal AKI kind of situation. So again, to summarize, your urine of smallality will be high, it'll be greater than 500. Your fractional excretion of sodium will be low, it'll be less than 1%. Your fractional excretion of urea will be low, it'll be less than 35%. Your urine sodium will be low, it'll be less than 20, okay? These are all things you want to keep at the back of your mind. And you may see, okay, divine, it doesn't make any sense. Why am I measuring the fina? I mean, why am I measuring like the fractional excretion of sodium, and also measuring the fractional excretion of urea? So the reason I'm actually mentioning both quantities is that your friends that write this test can actually introduce a small curve ball in the Q step.

So they may describe a person that has pre-reinal AKI, right? And then they tell you that this person is on diuretics, right? If a person is on diuretics, remember diuretics, right? Like your lube diuretics, the block sodium reabsorption, your thazide diuretics, the block sodium reabsorption, right? So the thing is your diuretics actually force the elevate your fractional excretion of sodium, right? So the thing is, under those circumstances, a better surrogate for pre-reinal AKI is actually to measure the fractional excretion of urea, okay? If it's less than 35%, that tells you you're dealing with dealing with a pre-reinal AKI, right? And the thing is, if you sort of step back to the pathophys I described earlier, right? So what are the certain things that can cause pre-reinal AKI, for example, right? Like, think about it. I just said that on the normal circumstances, your body says, you know what? Let me dilute the pipe, dilute the glomerulus. Let me dilute the afrin material. And I say that the thing that makes that happen is your your prestiglandins. So guess what? If a pressing takes an N set, right? And they have volume depleted, can you begin to see how that could potentially cause a trigger or worsening a pre-reinal AKI? Well, I hope you're saying yes to that, right? Because classically, those people will have, because by giving an N set, right? So like ibuprofen, for example, your N sets in hippocycloxiginies.

So if in hippocycloxiginies, your prestiglandin levels will go down. So you will no longer dilute the afrin material. If anything, you would constrict the afrin material and then you get into trouble. Alternatively, if a person is in the hospital, right? And they have volume down, they're super sick. It probably makes sense to maybe stop their ACE inhibitor or their ARB. Because those ACE inhibitors and AR Bs, they basically blond the effects of angiotensin too. So under those circumstances, you will no longer be able to constrict that effrante arterial. If anything, you'll dilute the effrante arterial. So under those circumstances, again, you can trigger or worsen AKI, okay? A pre-reinal AKI. So just sort of keep that at the back of your mind. And then one thing I just want you to remember that goes with pre-reinal AKI is the Biuento creatinine ratio. The Biuento creatinine ratio is usually greater than 20 in patients that have a pre-reinal AKI. The thing is, there are mechanisms behind why the Biuento creatinine is greater than 20. Well, that is a big discussion that is probably more relevant to a person that's taking the USML step one exam. So I'm going to move on. Basically, the Clistino's version is your reabsorbing Biuento faster than your reabsorbing creatinine in the nephron. So, but again, there's a lot of stuff there. I really don't want to spend time going into that now. So I'm just going to keep going. And just right off the bat, so kind of make your life easy.

I think it's kind of like important and helpful to be able to distinguish numbers wise between pre-reinal AKI and intra-reinal AKI. So I said in pre-reinal AKI, your feeder, your fractional description of sodium is less than 1%. In intra-reinal AKI, it's usually greater than 2%. Pre-reinal AKI, I said that the fractional expression of Urea is usually less than 35%. For intra-reinal, that number is like 50 to 60%. Just sort of take a number in the middle like 55%. If it's more than 55%, you're thinking more about an intra-reinal AKI. And then, I said that the urinary sodium rate is usually like less than 20. In a patient that has a pre-reinal AKI, that number you want to think about for an intra-reinal AKI is a number greater than 40. Urinary sodium greater than 40. Think about an intra-reinal AKI. And then, the last value, I guess I can talk about is this whole business with the BU-entocrat-nein ratio. The BU-entocrat-nein ratio is usually greater than 20 in a pre-reinal AKI, but it's usually less than 20 in an intra-reinal AKI. Because you have no ability to re-absorb the Urea nitrogenal AKI. In fact, yeah, yeah. Now I think about it again. It's a big lecture. It's probably like a 10-mini-thx planation to explain why your BU-entocrat-nein. So let me just say this way. If you have any questions on this, like, oh, divine, why is the B-entocrat-nein higher than, or whatever, just let me know, or maybe go back and listen to the Renault podcast half-first step one.

I'm fairly certain I talk about the pathophys behind that there. So I'm just going to keep going. So in an intra-reinal AKI, BU-entocrat-nein is less than 20 in pre-reinal AKI, it's greater than 20. And then, the urinous molality I said greater than 500 for pre-reinal AKI, it's usually less than like 350 in an intra-reinal AKI. Because the thing is, your kidney is an organ that if you're volume down or whatever, right? So if you have some kind of disease, your kidney is like an organ that helps with concentrating your urine. So if your kidney is at dead, like your kidney tubules at dead, right? Like in an intra-reinal AKI kind of situation, you will not really have the ability to concentrate your urine appropriately. Well, guess what? If you cannot concentrate your urine appropriately, your urine osmolality will closely approximate your serimosmolality. And your serimosmolality is really around like 28300, right? So your urine osmolality is usually less than 350. If a person has an intra-reinal AKI. And I mean, if you really do think about it, right? If a person has, I guess if you're kind of like doing your analysis, and I will spend some time talking about like the urinalysis, maybe at the end of this podcast, or maybe like in the next podcast that I'm going to for the medicine board exams. But basically, usually for a person has like a pre-reinal AKI, their urine usually has like high-line casts, right?

So essentially, if you are dehydrated for any cause for like a prolonged period of time, you'll have high-line casts in your urine. It's something that contains, if you remember from step one, that classically described the term horsefall protein, okay? Those are the things that constitute like they're just like ping-gish casts. They're the high-line casts you'll find in the urine in people that are dehydrated. So you potentially find in a person that has a pre-reinal AKI. And then, intra-reinal AKI moody brown casts, right? And again, there are many different terms that they use on these exams to describe moody brown casts. Because if you think about it, how can you make an exam harder than it should be? You can take what a person knows and just put it in different terms. So instead of seeing the moody brown casts, you may see granular casts, right? Like brown granular casts, or the metal you pigmented granular casts. If you see those things, you want to think more about an intra-reinal AKI, right? More specifically, you want to think about an acute tubular necropsis. So I think that's all I want to say about a pre-reinal AKI. So let me sort of jump to the intra-reinala AKI business. The first thing I guess I will start with is really the most common cause of an intra-reinala AKI. Believe it or not, is pre-reinala AKI, okay? Pre-reinala AKI is actually the most common cause of intra-reinala AKI, right?

Because the thing is, as time goes on, your, wait, I hope I'm not mistaken, yeah, I'm pretty sure that's correct. As time goes on, if you're volume down, volume down, volume down. Again, yeah, your kidney can order regularly, tall at once, right? But the thing is, you cannot almost sort of think of it this way, right? Like, oh, if the economy is bad, I'm going to austerity measures. And let's say, oh, you know what, I have only 10,000 in my bank account. Well, guess what? 10,000 can not last forever. At some point, you run out of money. When you run out of money, then you may, I don't know, die of hunger or something weird, right? So that's kind of like the thing that happens. If you have pre-reinala AKI for a long enough period of time, you can then degenerate to having an intra-reinala AKI, right? And I mean, what are the things that can cause, in fact, if you sort of think about it, like many things that cause like a pre-reinala AKI can cause an intra-reinala AKI, right? So say, for example, like contrast nephropathy, many people think, oh, contrast just kills the kidneys. Yeah, it does that, but there's other things that contrast does for the most part. One thing contrast actually has the ability to do is it can actually cause a constriction of your afferent arterial, right? So blood will not arrive at the glomerulus, right? So that's kind of like replicating pre-reinal physiology. And that those are circumstances, right?

So again, many of the things that can cause a pre-reinal AKI can ultimately cause an intra-reinal AKI, right? So what are the big things that can cause the intra-reinal AKI? So basically, I keep a cute tubular necrosis, right? Again, pre-reinal AKI that has gone on treated, right? Over time, your kidney will run out of auto-regulatory measures, right? And your tubules will then die from like a skin, right? Because your GFR is not high enough. Another classic one, right? So they can give you like a person that I don't know, like is like an alcoholic and they pass out for like 18 hours or it can be a person, let's say it's an old, like it is something year old person that falls down and cannot get up and then they're stuck on a floor for a long time. Or let's say you have a person that suffers like a crushing during trauma or a person that just ran like a heavy marathon and let's say maybe they've maybe they didn't train wisely or they've never really run a marathon before, right? And then they tell you that, oh, this person's creatinine is like super high, right? And then they tell you that, oh, you check the blood. You, I mean, you checked the urine and you have like four plus blood in the urine on dipstick, right? But then they tell you like, man, I'm looking under the microscope and only seeing like one or two red blood cells, right? It's like the, what you're seeing on dipstick does not appear to be agrarian with what you see on, on a urine microscopy.

If you see that, you really want to think about a rabdo myolasis, right? Rabdo myolasis. And again, rabdo myolasis, the thing is your friends that write these exams, they love to test many things relating to rabdo, right? So again, I've talked about the classic presentations, but what are some associated things you can see in rabdo on an exam, right? They can give you the electrolyte of normalities, right? So if, for example, they give you like a prolonged QT interval in a person that has rabdo, right? You want to think about hypochalcemia, because those dead muscle cells, they begin to sequester the calcium in fricelularly, right? So you can get EKG antecedents that go with hypochalcemia. Probably the one that's more commonly tested is hyperchalemia, because remember, if you remember from, again, you're studying in med school or whatever, remember that your potassium is an intracellular iron, right? Because of the activity of the sodium, potassium, ETP is pumped, right? So that pump, it gets three sodiums out of cells, so sodium is primarily extracellular, and it dumps two potassiums into cells. So your potassium is primarily intracellular. So if your muscle cells burst open, right? They die, right? All their intracellular will spill out into the circulation, like potassium, right? And that can cause hyperchalemia, so you can see like the topic, T waves, you can see the YQRS, right?

Again, if you're seeing those EKG findings, you probably want to start doing those are fancy schmancy, calcium glucone, insulin with glucose, right? You want to start giving like K-exilate, right? Stuff like that. You want to give like a diuretic and all that crap, right? And again, rabdo, I mean, obviously for rabdo, you're going to hydrate, hydrate, hydrate, right? Like normal ceiling, give a crap ton, a normal ceiling to flush that myoglobin through the, through the, through the, through the, flush that myoglobin through the nephra, right? And I mean, something that I guess is sort of kind of closely related to this whole rabdo business is not exactly a rabdo, but it can present like rabdo at two other things, right? So say for example, they can give you a person that has like a hematologic malignancy, right? And they're undergoing like chemo, right? And then you have a ton of cancer cells dying all at once. Remember, if you remember from again, Met School, the Eureus cycle, right? Happens inside cells, right? So not necessarily the Eureus cycle, I take that back. But you have a ton of DNA, right? Inside cells. And DNA synthesis for the most part happens like in the cell soup, right? So if you spill out, if a, if a lot of cancer cells that I remember, cancer cells reproduce like crazy. So you have a ton of DNA. All that DNA, right? It contains like purines and all that stuff. So you can already see where I'm going with this, right?

The person can have like a ton of eureic acid, so they can have like a ureth nephropathy, right? So hopefully you are thinking like, you know what? Maybe I should have given that person a lupurinol of a big cyst that on like a uricase and a log, right? Like pigloty case or as boricase to prevent that ureth nephropathy. Another one can also be a person that has like really bad, like a really bad himolosis, right? So let's say a person has, I don't know, like let's say they have like a bad himolitic crisis. A lot of red blood cells are dying, right? Remember red blood cells, they release a crap ton of hemoglobin into the circulation. That hemoglobin, you can actually have such a thin as a hemoglobin nephropathy, okay? So just sort of keep that in the back of your mind. But again, the bulk of the question that will give you will give you more clues, right? So like, let me see the elevated LDH, the low-habital globin, you may do a blood smear and see like the the schistocytes, right? Telling you that you are maybe dealing with a hemolitic process, or they may give you something relating to like an indirect hyperbularibinemia, right? Those are all clues that can lead you down those directions. So again, all these things, right, can cause essentially like an intra-inala, an intra-inala, eki. And then, I mean, other things that can cause an intra-inala, eki, right? So you're drugged, right? So like you're amino glycosyth, right?

So like you're gentamysin, you're tuberomycin in a CF patient, right? You're your amicasein, right? They're useful like very bad resistant, gram-negative infections, right? Those things can all cause an eki. And don't forget your, don't forget your, um, infotaryble, right? So if they give you a question about like a diabetic, right? That is like in DK or whatever. And then you're beginning to have like their face like toned dark, right? And they have like severe sinus pain and pressure and tenderness. You may be thinking about like milk or my causes under those circumstances. Remember for those people, you want to debris that ton and then give infotaryble, right? So infotary Sin B, that's a, that thing is super, super-neifer toxic, right? That's why you usually give the liposomal formulation. And then don't forget like if a person is getting like a platmum agent like cisplatin, right? cisplatin, remember cisplatin is a very, very nasty drug. It's super, super, super-neifer toxic, right? And usually, um, hemondoctrists try to give this drug. It's known as an Amyphostin. So AMI, FOS, TIN, to sort of like decrease the incidence of the nephropathy that's associated with taking a cisplatin, right? Remember cisplatin is nephro and auto-toxic. There are three hydro drugs for exams that you want to keep at the back of your mind that are nephro and auto-toxic. Actually, four hydro drugs, I think they're about four hydro drugs.

One is, um, one is cisplatin, cisplatin is nephro and auto-toxic. The next one is vancomycin. Vancomycin is nephro and auto-toxic. The third one are you amino glycosides, right? Like your gentamysin, neo-mysin, amicasein, tobra-mysin. Those drugs are also nephro and auto-toxic. And then the fourth one is a lube diuretic that you give to people that have sofa allergies, ethycrenic acid. Ethycrenic acid is nephro and auto-toxic as well. Okay? So those are four hydro drugs you want to keep at the back of your mind. Amino glycosides, vancomycin, cisplatin, and ethycrenic acid. Remember ethycrenic acid is a lube diuretic. Okay. So those things can all cause um, um, ATN, right? And then also don't forget, right? AIN is an example of intra-inalic acid. So I could get into general for like this. So again, you're used to the fever rush, you're xenophilia, blah, blah, blah, blah, blah, blah. Right? Again, those things, even in the real world, they're found in very few people is like maybe like 20, 30% of people that have AIN end up having that triad of fever rush and elevated eosenophils in their blood and their urine. Although I will tell you that, even if you don't necessarily find it that way in the real world, on USML exams, right? Step one, two CK step three, whatever. That is the classic presentation of AIN. Okay. So those are things you want to keep at the back of your mind, right? So AIN, you'll see that triad, but what are the things that cause AIN, right?

So usually on exams, they're drugs, drugs, drugs, drugs, right? Classic, classic poster child drugs are like your cephalosporins, right? Like, um, or your anti, basically like your beta lat times, those things can cause um, AIN, right? And um, those are the ones where, classically, you'll see like the elevated eosenophils in the blood of the elevated eosenophils in the urine, right? But the thing is, there are actually certain drugs that can cause AIN when you may not necessarily see elevated eosenophils in the blood or in the urine, right? So um, this is one that is probably more attuned to the medicine in training exam or the medicine board exam. And again, this is where you want to pay attention, this is like flurryly high yield. What your end sense, right? Like your ibuprofen, your ketoroelach, or your PPI's, right? Your PPI's, right? So like your meh results and all that stuff that people get like candy in the hospital. Those drugs, they can cause AIN, but it may not necessarily give you the eosenophilia or the eosenophiloria, okay? So those are things you want to keep at the back of your mind. Believe it or not, again, you may see in the vine, it'll be in a little too specific. Again, I promise you, um, I have a lot of experience with these exams. I promise you, those are high yield things you want to keep at the back of your mind, right?

Or they may give you an African-American female that has like shortness of breath and bilateral hyalur lymphadenopathy on a chest x-ray. That's tracoidosis, right? tracoidosis actually has a pretty strong association with AIN. Or they may describe a patient that has like a gritty feeling in their eyes and they have like dry mouth and their secretions like, um, they're having like a pin-full into course, right? Because they're vaginal secretions are very like not, let me just say they're not fluidy enough, right? You're thinking about showgreens. Remember, showgreens has that very strong association, right? Remember, showgreens has a bunch of weird associations on exams. It has the association with AIN, right? That's one. Another thing showgreens has an association with is your type, your type one RTA, right? So like the distal RT As, right? The distal arena of tuberculosis, those have an association with a showgreens syndrome, right? So those are like kind of like weird things you want to keep at the back of your mind with showgreens. And then remember, if a woman is pregnant and she, she, the tell you that oh, she delivers a kid that has like complete hard block, right? Also think about showgreens with that, right? Showgreens, those anti-ro and anti-la antibodies can cross the placenta and destroy the conducting system in the, in the fetus, right? That can cause a third degree or complete hard, complete hard block. Okay.

Um, and I mean, I already kind of talked about how contrast can cause an IKI, right? So the media subscriber person that oh, this person recently got a cardiac calf or whatever, right? Or this person got like image and for PE or whatever. And then the tell you like a day or two later, the creatinine is going up. On that of circumstances, you want to think about a contrast of nephropathy, right? And I mean, obviously for a person to why can, how can you prevent contrast nephropathy? Give a ton of fluids, right? So fluids, fluids, fluids, give a ton of like normal saline before the, they get the contrast and a ton of saline after they get the contrast. Um, throw back to people that if you remember, like the stuff you learned in meds, but about like inner pseudo-system, there's really not good data for inner pseudo-system to be perfectly honest. So usually that is the wrong answer on exams. The best means of preventing contrast nephropathy on any of these tests is to give fluids. If you don't see fluids and none of the other answers make sense, then you can go ahead and pick an inner pseudo-system and usually give a pretty, pretty high dose because I mean, inner pseudo-system is a harmless drug. It doesn't really cause many side effects. So take that for what you want. But usually inner pseudo-system is the wrong answer on exams, right? Um, but one I guess, another thing I want to sort of want to throw you away, right?

So what if a person recently had a cardiac, like recently had like a cardiac calf, right? And then they tell you that, it's like, oh, okay, like four or five days after, they're beginning to notice that the person's like creatins beginning to rise and you're seeing like purple rashes on their low extremities and their tools look necrotic. What are you thinking about? I hope you're thinking about like an embolic cause, basically, of this person's aka, right? So remember after cardiac cath, right? As you're caffeine, the bad coronary artery, you can essentially shoot out embolite. You can shoot out embolite to many parts of the body, right? So those people, they can have like embolic phenomena in the low extremities. So you may see like the classically described a levido reticularis, right? So like purple rashes, net-like appearance in the low extremities, think about levido reticularis. Those people, they may actually have like your synophilia. So the thing that your friends that write these exams try to do is they may try to make you confuse this with acute intestine arthritis. Don't fall for that. People that have AIN, it will usually be like some kind of drug exposure. That sort of triggered that and they would not have like necrotic extremities and they would not have the levido reticularis, okay?

So if you seem like elevated your synophiles in the blood or in the urine and you're seeing like necrotic extremities after like a procedure that may have potentially disengaged like I don't know like cholesterol plaques or something, think about them, think about embolic phenomena. It can cause aniki, I believe it or not. It can cause like people can get strokes, people can get like legischemia, right? From all these things, right? And classically again on labs, you'll find the elevated your synophiles. Another thing you may also find is like low C3 and C4. So your complement proteins may be low, okay? For those people, in general, again this is usually like a heart clinical decision because many of the people that have these problems, they need to be an anti-coagulation. But the thing is for these people, if for example they have no real need for anti-coagulation, it may seem paradoxical but that's actually the right thing to do. You want to go ahead and stop anti-coagulation in patients that have these embolic problems after like cardiac cath. Okay? So it may not be a cardiac cath question, maybe another kind of like vascular, whatever. But if they have no real indication for anti-coagulation, you can go ahead and stop it, okay? Because again, it's kind of paradoxical and again, I don't have the time to explain why that is the case. I mean this podcast is already almost 41 minutes. So that's something to give out the back of your mind.

It's just one of those rare things where it's something that people don't think about. It's actually the right thing to do. And then I guess to kind of round off here. Yeah, I don't know, I feel like this has gone on for a long. You know what? Let me go ahead and stop here. So hopefully with this you feel good about EKI in general. And again, these things are very heavily tested on step three, the medicine training exam, the medicine boards. Okay? And as I do when I end any podcasts, so I do offer one on one tutoring for many exams. So step one, two CS, two CS, two CS, step three. And then like the internal medicine, the training exam and the internal medicine board exams, I've actually treated a ton of people for those for those tests. And then if you're a med student applying to residency, so like an ERAS app or a college student applying to med school, so like an AMCA I do offer like one on one advising and I guess consulting if you may call that for those indications. And again, if you're if you're a college student that you need tutoring like biochemistry, physics, general chemistry, organic chemistry, physiology, histology, all that stuff, I do offer tutoring for those. I have a lot of experience. Just reach out to me and I can give you some more some more details. You can either reach out to me through the website or you can send me an email at the Vine Intervention Podcasts, podcast with an S at the end at gmail.com. So have a wonderful rest of your weekend.

God bless you all seeing the next podcast. Thank you.

Intra-renal AKI.

Glomerulus, tubules (tubules), and interstitium (interstitium).

Fever, rash, and elevated eosinophils in urine/blood.

Low (<20 mEq/L).

FeNa > 2% (or specifically, if it's significantly higher than the pre-renal threshold).

Hyperkalemia.

Aggressive fluid administration (Normal Saline) before and after the procedure.

Greater than 500 mOsm/kg (or elevated, e.g., >1.020).

RAAS activation causes efferent arteriolar constriction and ADH release.

Urinary sediment showing muddy brown granular casts.

Greater than 20:1.

Vancomycin and Ethacrynic acid (or any combination of the four listed).

Association with AIN and Type 1 RTA/Distal RTA.

Elevated eosinophils, low C3 and C4 complement levels.

Greater than 500 mOsm/kg (or elevated, e.g., >1.020).

RAAS activation causes efferent arteriolar constriction and ADH release.

Urinary sediment showing muddy brown granular casts.

Greater than 20:1.

Vancomycin and Ethacrynic acid (or any combination of the four listed).

Association with AIN and Type 1 RTA/Distal RTA.

Elevated eosinophils, low C3 and C4 complement levels.