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every team, doctor. Much bone. Thank you very much. So Hello, everyone. Thanks for Not for joining me today. Mornings, Alistair. Um, I'm doctor currently working in Bath, which, for people that don't know, it's a quite small town in the southwest of England. Um, Andi, I'm an S h o. Doctors have been a doctor for about six years on I've got interest in nephrology. Understand? You've had a recent talk on a key I and CKD, but I hopefully they'll be kind of some different aspects that will be useful for you that you haven't heard of before. And I try and like into kind of the practical elements so that when your doctors on the ward, when your junior doctors, you'll know what to kind of look out for on do kind of the initial locations, a mountain he wants to be for patients with a guy. And CKD is about 40 minutes for the talk. So try and get through that and then we'll have questions at the end. If people have burning questions. I don't mind people kind of going off newts on. Just interrupt me and asking. That's completely fine on. Also, I'll try and do. I'm not sure how well it always works on Zoom, but I will try and do some interactions a Z well, and ask questions. And for that you can either use the chapped or if you just, um, you yourself and answer a question. It is not working. I can basically congest move onto the next thing if the interaction looks like it's not working very well and say to let that kind of a no overview of the talk eso to start with, we're going to talk about a key. I we're gonna look at what the definition of a guy's and that has changed recently. We're gonna look at pre renal injury know and post renal causes of a K I on D. Look at the indications for patients to have a renal replacement therapy acutely on that's normally done an eye of the intensive care unit or done with emergency on dialysis lie. I'm I'm done on a real unit. Then we'll look at the chronic kidney disease we look at. The different potential causes complicate common complications of CKD is and how those different complications and managed talk very briefly about renal replacement therapy on. Then at the end, we'll see how it goes. But we'll try and have a clinical case to try and consolidate everything that we've spoken about. So achy I first. But often people use so almost computer systems you'll get on estimated glomerular filtration rate. It's which is actually quite poor predictor in a k I. So it's quite useful toe. Use the baseline creatinine in and look at the changing creatinine rather than the change in Egypt. Far, that's a more accurate predictor of somebody who's kidneys are acutely failing. Um, that a. I definition have changed recently on this is the acute kidney injury network criteria. So it's an increase in same crap off 26 or an increase off water in the half times above the baseline within a week, or effectively oliguria persistently for more than six hours. Okay, say ah and I'll see you in grade AKI, depending on what the rise in creatinine is again, it's using creatinine rather than easier. Far so see how severe things are. If patients have a Stage three a k I, then that's when you need to be really looking to make sure they don't have any of those indications for renal replacement therapy on getting the nephrologist involves I'm seeing a rather later. So what, you really want to know what creatinine is kind of a surrogate for is the glomerular filtration rate on which is the amount of blood the flow of blood that goes through the glomerulus within a minute? Um Onda. So it's the volume, the volume of blood that goes through the Mentalist within a minute on all of these different things. Creatinine crowning clearance Your Your Riera's well are different kind of estimations of that, but they all have their own kind of failings, Um, so they need to be looked at in their clinical context. Creatinin is used because it's the best kind of indulge in a substance that your body makes, which is normally not absorbed or I'm excreted into the next nephron. Could be, um, however, it changes from person to person because people who are very high and muscle knots have a high level of creatinine, their blood at baseline, and you see some people with kind of creatinine is of 30. You were really malnourished, and that's not because they have incredible kid need kidneys. It's because they have very little muscle mass, so there needs to very much be taken into the clinical picture of clinical consideration. There's a substance called in urine, which is used just in clinical trials, where they're G F. R is required to be known perfectly, and you can measure the Neurontin, which is injected into the blood. But it is something that's broken down by the stomach so it can't be taken or any. It's injected into the blood, and then you measure it exactly in the urine and in your lung is not excreted. And it is not. A total in the nephron on is not reabsorbed, so that's why it's a perfect measure. So that's what the using reset trials, but in real life or in clinics are in normal clinical practice is not really used. Just this slide is just telling us that when people have very low creatinine, it's a change in creatinine can be very significant in terms of their actual drop in G f er. However, if somebody has got a G f. R of around 15 of really high creatinine, maybe 300 increased from 300 up to 350 is probably not significant at all. So it's just bearing in mind that it's not linear correlation between creatinine and so I cause of achy. I, um, I'm sure you've already been taught this, but this is the most important thing to take away from this lecture today that it can either be split up into a pre renal injury or post reading whenever someone's got an achy I to be able to treat it. You're not coming up street unless you understand what underlying etiology is. What is the underlying cause of this? Um, the most common cause in a hospital is that it's caused by a pre renal course, and that's normally dehydration. But we'll come to that in a second, and we can check for I'll ask for other potential causes. Um, injury. No other kind of conditions that the nephrologist get very excited about and involved with on post renal is the most common cause of that is benign prostatic hypertrophy, but also just generally unwell. Frail only patients quite commonly go into urinary retention, which can then cause back pressure of urine, which then ends up cords, and Katarina Francis andan achy. I so It's an important investigation in any patient, has a new achy I with unknown etiology that you get an ultrasound of their kidney ureter and bladder on. Make sure that there's no evidence of hydron phrases and the dilated, really. So Because the vast majority of you, when you start working in a hospital or the start of your medical careers, you'll be dealing with patients. So it's really important to know what just if you don't know anything about the patient. The most likely cause, initially that your patients A T I Z, is going to be three real. It's going to be related to the perfusion of the kidneys not being good enough. There's a small percentage, which is that with the nephrologist, which is about 15% which are normally quite easy, Terek in rare causes. But you can also get post renal causes, which already spoken about, so start with by all means on default. Adjusts and intensive care only get involved when patients need a renal replacement there. So this is a point where we're going to see how it goes on, like people just a shout out on yourself and shouts out some causes of kind of pre renal hyperbole in years. And what causes you to be intravascularly depleted that then decreases. You're perfusing your kidneys, causing that sepsis. Yeah, double did you get? Um, steps is probably most common cause in hospital. So yeah, that's very good. Anything any of the former shock? So it could be a m. I s So you put her pattering Nose syndrome is well, there is. Well, so they get a couple. Yeah. So, failing heart cardiorenal syndrome and her pattern renal syndrome be a fairly heart failing liver. Any other causes of just being intravascular deplete your quite common excessive sweating? Say that I'm sorry. Excessive sweating, Excessive sweating. Yes. Yes. So it's common in the, uh, countries off tropical regions. Yeah, definitely. So hypothermia and excessive sweating definitely on you that can also coexist with rhabdomyolysis. Eso you normally need to check a ck on these patients on rhabdomyolysis. Interestingly will come into in a second, but that is if rhabdomyolysis is left untreated. Andi, sorry if somebody who is has an a k i because of dehydration because of the heat or because off other cause of rhabdomyolysis, if that's giving fluid aggressively initially, then that can be reversed. But if somebody has prolonged periods of time where they're dehydrated related to that, then it can go into something called acute situation. The crisis, which is a pre real achy I turning into an injury know achy I because of prone, prolonged duration of time of decrease. Perfusion cools anyone else on that night that you consider rap, though as an interim, know cause or a pre renal course really going up So it would technically would be an injury. No cause, because in rhabdomyolysis, it's secondly, to kind of prolonged dehydration. So if you catch it before there's kind of before the significant damage and it's reversible, then that wouldn't be rhabdomyolysis, like, quite felt like like human lysis syndrome. That would also be an injury in a course before treat. Yeah, yeah, that's correct. Very good. So these are kind of the most common cause is like sepsis, dehydration, lot of frail only patients just on drinking so might be confused on then get quite dehydrated hemorrhage and burns. Other other quite common causes on. Also, you're increasing risk off hypovolemia if you already, if you already have CKD, so this is something that, um I think junior doctors in general don't get right very often. Which is what do you do in somebody that has decompensated heart failure so clinically, they're very overloaded so effectively, it's a kind of acute cardiorenal syndrome on. They also have an A k I. And they quite common because exists because the risk factors for CKD and CCF normally quite similar eso. The answer is that you treat their fluid overload despite the fact that they have an A k I. You will give them frusemide or other loop diuretics. It's important that you stop other nephrotoxic So, um on And what you will find is that some patients that take a I will actually improve after you off loaded them on. That's because with decompensated heart failure, you have increased pressure in the effort. Arterial, which then and effectively decreased become big dust, is because of venous Stasis and venous congestion related to the heart failing. So because of that, you decrease the pressure, Grady in between the Afrin and the Afrin arterial, so that then decreases the flow. So when you cough, load these patients with freeze mind then or other loop diuretics, then the difference in pressures increases. And then that means that in some patients that achy I would actually improve in other patients. If you get if you dry them out, it might mean that that gets worse. However, if someone's got quite significant pulmonary edema and then actually go on oxygen requirement you, the most important thing is their lungs. So you will accept a degree off kind of persistent renal impairment by drawing them out. So that's they do know, require oxygen. Eso another one, which is quite complicated, have at a renal syndrome. But actually, I think that's only about 30 to 40% of patients with an A k I with a background of cirrhosis. And actually, you should still be looking for other potential causes on the vast, the most common cause of achy ides in patients with psoriasis. Is that off? Um, dehydration, so fluid resuscitation is normally quite common. Initial treatment on do that is with either course of stress. Crystalloid, because you don't want to give patients with the race is a high salt load because that can cause decompensation or human albumin solution. Um, what I seen in practice quite commonly is that they also empirically treated for a pattern nose syndrome. At the same time, a patent renal syndrome is not a very well understood condition. However, it's thought to be related to inappropriate so kind of aberrant renal artery. They so construction causing dehydration to the nephron big on that kind of all processes kicked off by Splanchnic Vasodilation. But it's still not like said it's still not very well understood. Type one is what you see often in hospital, and type two is nobody seen an outpatient. Be effectively. The treatment is human. Are women solution? Correct any dehydration? I'm on day total oppressing. Some of these patients will get better with telepresence Andrea adoration. Some of them will not on well, potentially going to need reading replacement therapy. It's really important to know that if they get so and well that they require reading replacement therapy, the only way that they are going to get treated is if, because this is all being caused by a process started by the liver, the only way that this is inevitable that this is going to end up being reversible is if they have a hepatic transplant on, then that renal dysfunction will resolve. So as a general rule of thumb patients with renal replacement therapy that require sorry, patients with a battery know syndrome that require renal replacement therapy only do so as a bridge to dialysis, so as a bridge to transplant on. If they're not thought to be transplant candidates, then they will not have the likely futile intervention of renal replacement therapy, say, speaking about pre renal causes about halfway through. So I'm not sure if we'll have time to speak about CKD, but we can talk about diet a bit more detail. She's fine, will speak about intrarenal causes off A I. We're not going to be able to talk about this in gymnastic decell on, because it's a very basically a whole specialty worth off off conditions. However, I'll talk about the most common ones and the one kind of some ms No meds and things that when I was in medical school, I feel work talk very well on things I wish had kind of being imparted to me about these kind of rare conditions so that that was fine apologist. Tell me when your junior doctor, if you recognize if you roll out. Prerenal causes you doing ultrasound scan. Um, without pastry. Was is and do a bladder scan to make sure they're not on your knee retention. Then you know it's gonna be in in treating course on. In that case, well, that's expected of you is to recognize it and refer to a nephrologist. So I'll say a bit about nephrotic into physics and dreams. I say a bit of about good benefits of these patients where she wouldn't grace this on to be below in to see she won't office. So we're not going to have enough time to talk about everything. So these are just some intriguing, of course, is that we know it's covered today. So, firstly, looking at the common causes off problems with achieve use that can cause an acute kidney injury. So just basic anatomy, which probably because you're talking a lot at medical school, you probably are more familiar with that. I am now of a few years after medical school on, but effectively, what you need to know is injury know, causes an achy I. The vast majority of them are either a problem where if the glomerulus, which is the initial place where the blood is filtered into the chewables. Or it's a problem with the tubules, which is where the absorption on the excretion of so use because so today for the first, that we're just going to talk about the cheap yours. And there's two main conditions which can affect the Tribune's that can cause an injury. Know achy I the first one's acute keeping the crisis that we spoke about earlier on that effectively a pre renal, achy I Normally, if it's gonna go so kind of progressed to become acute Children necrosis There is an episode off clearly documented hypertension. But if this hypertension or high profusion is prolonged, then it can cause irreversible damage. And it's like we said before is the mechanism of damage and rubbed minuses. Um, the way that this normally presents is with an A k I, um, if the patient is fluid, replete so they've had their previous lately, I you've given them fluids. They haven't improved, and you're sure that they're still euvolemic. Then the treatment is to continue fluids on to give frusemide as well to try and prevent them from being oliguric on requiring potential renal replacement therapy further down the track. The way to differentiate between Prerenal AKI and Acute um in a crisis is a urinary sodium in previous, like a Are you are Your kidneys are appropriately conserving your sodium to try and conserve fluid in acute cheaper necrosis, your kidneys lose that ability so the urinary sodium is likely to be high because your kidneys have failed. Holding on to the stadium on here is a bit pathology, which I remember. I used to hate us a medical student, but this is the only test on it. E slide that I have. Um, it's effectively just very simple here, looking at the the left side a little cartoon, which is showing the number of nuclear I which have been lost in a in a patient's heart. 80. And if anyone is doing, I'm not sure in the whether you do the British membership of the rule Call it exists physicians examinations. But it's kind of a classic question in these multiple choice questions that they say, What it what would we find on inspection of the urine on like microscopy? And the answer is quite often in 80 and you get is infill urea. So I am moving on to the next condition is there is a condition called cheaper and especially nephritis, which we're gonna come on two now and with this condition you get is in a pill urea just to make that clear. So it's a completely separate condition to acute tumor necrosis, and it's nephritis. So is effectively immune mediated inflammation on. It's normally caused by a known precipitant on it's in T I n, also known as acute interstitial nephritis that you get your is NFL urea. It's because of cheap either infiltration, but off lymphocytes on is enough pills on one thing that kind of takes it apart from what we're gonna come onto in a second. There glomerular Freddy's is that you never get significant protein urea. You might get some protein in the urine, but the vast majority off the protein will stay in the blood. If your gum a list is working well, it's only when you have a leaky gut. Mehlis that a lot of that protein in then go into the cheap use. So if you agree, minutes is working fine. It's a job. You a problem. You won't have significant proteinuria for T i n. The treatment is immune suppressant, so the first time for that is steroid. It's normally diagnosed in a biopsy on you would normally try and look for on underlying cause of it, and you would want to treat that underlying cause so the two things they could be caused by in general are other infections or drugs on the most common kind of well known drug that we know cause Children station arthritis. And what we worry about for patients that have a new kidney injury is NSAID. Also quite commonly, antibiotics can cause it was a patient on the ward that I'm working currently that has two men station arthritis. And that's because of flu cloxacillin that they started on that quite frail. So we haven't done a biopsy to confirm the diagnosis, but we've empirically started them on a low prednisone, say from the cheap. Yours to the gum. A list remain upright. It's I remember it's tour quite fully at medical school. Actually, there are my medical school, anyway, on the fundamentals air. Quite simple, but I think in general yes, not talk very well could be primary or secondary. I think the names kind of make people a bit kind of daunted by it, but actually the names are just different. Specific biopsy findings and Onda. Then the different glomerular fretted. These are named based on histology on. That's because they are treated differently based on what you see on the biopsy. Onda I remember learning at medical Nephrotic syndrome in a frantic syndrome, but not really knowing what they were, What the significance off the MS but effectively different techs in a row. Nephrotic syndrome and AKI or a CKD or hematuria if they're caused by an intravenous cause, are different syndromes or presentations that I a true problem within the kidney is causing on. This is how they're presenting on because you don't get many symptoms in nephrology. The vast majority of conditions can be put down to either hold and presented with a frantic syndrome I came there for. It's more likely to be this. Are they presented with Hematuria? It's more likely to be idea of property, for example. Um, you can actually there's good tables that you can look at to see a lot of these different intrarenal causes what they're likely to present with and some or have a preponderance to be presented in one way rather than another way. But the syndromes are just different ways that the underlying causes off renal disease present on nothing more Senna product syndromes that that's a cause when you have very leaky gram, a less so you leak loads of protein into the into your tribulus, including albumin. So because of that, you don't keep hold of your albumin, you got a demon because of hypoalbuminemia, you get protein urea on the definition of nephrotic range. Proteinuria Proteinuria is more than 3.5 g in 24 hours, but we've kind of moved away from 24 hour urine collection, and then you normally do a protein creatinine ratio. Eso the equivalent protein creatinine ratio would be 350 would be an equivalent of 3.5 350. PCR is not frosted range proteinuria important things specifically for nephrotic syndrome. Yes, it's a marker of they do have some sort of intrinsic renal disease on because it's the front. It's improved, is more likely to be ex wife, said Chlamydia Freitas, which will come on two but also fell on top of that because they've lost that unscrambling proteins in the urine. You need to answer quite late these patients, because they do become pro from about it on. Also, you can use the loop diuretics toe that effectively make some new limit. Eso getting on some kind of nephrotic syndrome hypertension hematuria. And it's also you normally associated with a K I. So it's a triad for a second for ticket. Different triads on day tell you what it's likely to be the underlying Camilla Friday, So this is a table that I'm talking about. You can also have. You could also have a table that have different columns, which would include a K I would include CKD. I would also include visible hematuria minimal change that probably is the most common cause of Nephrotic syndrome. And Children, and actually it's so common in Children on other causes are so rare that these patients, if a kid comes in the Nephrotic syndrome, you treat it with steroids cause you assume that it's minimal change in a property, and it's only if you're having trouble treating them with steroids that you start considering a kidney biopsy on these patients would never present with critics injury on then Adam. Serious common causes membranous nephropathy, but it's just you don't need to learn all of these. Different cause of dramatic price is just the haven't idea that there are lots of different potential causes. Grand a fright it's on. Actually, they present in different ways a lot of them a primary or idiopathic, which is kind of a condition in itself. But also, if somebody comes in with a new the round of writers, you want to make sure that it's not secondary on related to another potential course on these are just a list off know exhaustive. But this is a list off some secondary ends. So ignore that first because that specific to my hospital to talk I did a few weeks ago. Baby Suspected injury. No, AKI. These are sensible investigations that you could do to look for different primary Sorry, different secondary causes off the HPI. So these sensible blood test that you can do, and if you get the answer from some of these, you might potentially be able to avoid a biopsy, which comes with its own complications. But if you don't have an answer, I'm just a specialist for an internal cause. A lot of these patients end up having biopsies, and they're performed by nephrologist and understand. Under ultrasound guided our guidance. They have to be normal, tense it, and you have to stop all anti coagulation on there, not performed if it doesn't look like this patient has an a k I. So if they're on that ultrasound scan, the best way to tell if it's not clear from the history or from previous love creatinin or EDA far results. If it's unsure whether this patient is acutely presented Eliza chronic element to their CK to their kidney failure, then you want to do an open wound scan of their kidneys. And if their kidneys are very small and triple, it's likely that there's a significant amount of scarring on these patients are not biopsied firstly, because the cause is unlikely to be reversible. If they've developed CKD, you've missed the boat effectively. The second causes that the biopsy is very unlikely to fight to show your diagnosis, because you would effectively just get scar tissue in the biopsy, so summary of injury Know if you've ruled out pre and post you want to refer to nephrology. We've covered man, different cities. We've covered a cute you in a crazy It's cheap, you know, Interstitial nephritis on kind of this actually learning what in clinical practice nephrotic syndrome in a frantic syndrome are on how they're useful to apply to different underlying etiologies off renal disease. Speaking about pre on injury, know now we're moving on post renal. I'm like I said before, Know I'm prostatic Hypertrophy is by far the most common cause. Patients will normally have a degree of hydronephrosis if they've got a significant achy I. And most of the complex causes of this are that would by the urologist rather than nephrologist. A bladder scan is a good initial investigation, but any achy I haven't known. Etiology needs an ultrasound scan off their kidney, ureter and bladder. But you can also rule out hard, um, a phrases on a CT scan. If that's easier to get in the center where you're working. Obviously, that comes alongside of radiation days. Um, so you're on your attention is very common in elderly generation. Well, patients. So the treatment for that Custer on That's normally all the treatment that you need in most patients with a post renal okay, was important to know after catheterization of someone with a post renal AKI is that they can have postcatheterization hyper diary cysts in which you need to match their urine output for the next 24 hours to prevent them going into a pre renal achy I because off polyuria So what's, um, common causes off post renal, achy I stones, yet very good and that tumor so they can be bilateral. But that's unusual, the most common, you know, actually, because, you know, actually, hydraface is on. If they are significant enough to cause achy I, you're likely to have other symptoms associated with them. So that would be. Sometimes you can get infection in your partner fright. It's in the kidney that has hydronephrosis clinically. Sometimes you will be able to block to the kidney if they quite significantly dilated on enlarged. And also, obviously, patients have the classic colicky pain and hematuria saying any other quarters proceed. 100 pleasure. Yeah, prostatic hyperplasia, yet very common cause on dyspepsia, we if somebody's acutely unwell. If somebody was had kind of symptoms of prostatism before they came into hospital on, then they've had an infection which is kind of just generally not off their perch. There are a lot more likely to go into urinary retention, fimosis and, like, metals. The nurses will yes, um, inability to pass urine because of, uh, morgue. Kind of desperate problem. Yeah. Yeah. That stuff in the case. Very. I've never seen that. Um Yep. That sounds very plausible. That could definitely cause 100 a phrase it strictures of the ureters. Yeah, And that's quite common, cause you see, um, say if you you said quite a few of these yet you're a tear. It stretches there. And benign prostatic hypertrophy. Definitely. Um, malignancies. Another not common, but something else that you can just have in the back of your mind. So it's important. So, in terms of, in fact, investigations and examinations for a while. Patients with acute kidney injury, usually one in the history. So somebody has come in with kind of obvious infective type symptoms, and they look like they're clinically septic. Then it's very likely to be a pre renal he I or if somebody's got background. Hello, Doctor. Palpable purpuric. Um, so he turned Took two. Um, you actually got cut off while she was speaking. You just come back. No wise or so which which, like I didn't get to It was a slight. You take it in this morning, okay? From the start, that's why. So you're effectively. What I was saying is that it's one of the most you're very like she has with anything in medicine. You're the most likely to get the underlying diagnosis from the history and from the examination of just examining the patient clinically. So if they're very clearly sets it that accept it, they've got kind of chest infection symptoms, cough fever. It is very likely to be sepsis related or if they've got a background of BPH. And, um, you can feel a bladder clinically, you've got your answer. So, on some of the interim oh achy eyes, you could look for rashes related to vasculitis. Or sometimes patients might have at the same time that they're renal vascular. It's is flaring. They might have kind of poor me hemorrhage and popped a cyst. So a lot about the clinical presentation. We'll guide you down one route or another. One thing that's really important in a bug baron of Nephrologists is not to do it, you're in depth before referring them. So it's very rare that previously or post really you know, a G. I will have anything showing up in the urine it apart from blood, potentially in a post real achy I. Whereas if you have quite significant protein urea, which confined literally just by the bedside, then that point you massively down towards Nephrotic syndrome and a glomerular right, it's causing it. If you get the old creatinine to know the significance of the achy I that's really useful and helps with the specific guidelines of achy. I get a bladder scan in the first instance and then optison scan or, uh, CT scan of the kidney doctor and bladder Upside scans will help to look for hygiene a faces, but you also give please to the cause. So, for example, kind of classically in amyloid Reno amyloidosis. You will get very large kidneys and that because of amyloid plaque infiltration into the kidneys, normally bilaterally and that can cause an achy on that. Also, you're looking for the chronicity of the kidney injury. If you have very small, shriveled up kidneys, very likely to be, there's a CKD and you wouldn't be looking to biopsy these patients a lot. The answer, like I said, is clinical. So you want to look at the fluid status in someone just kind of shoutouts? Um, kind of classic things that you look for in the fluid status on examination. Type of the limit? Yes. How How could you tell clinically if somebody's high paper leaving. So we before signed off the addresses of skin Togo Because membranes, um, mucous membranes. Yeah, very good. Mucous membrane, skin, tiger. Anything else? Yeah, BP. That's a very late sign of hypoglycemia. It's very important that somebody is initially and for a long period of time, you will compensate in terms of your BP. But if you're becoming hypotensive related to high privilege Mia, you're very significantly volume depleted. Anything else? You know? Yeah. No, you're not put. And obviously, in this very specific cause, 80 I have any cause can cause oliguria. However, in general, if you're looking for a sign that you know your kidneys are bean perfused well enough if you're not on a uric, that is a reassuring sign. Anything else? Consciousness level. Yep. That's good. Say ah, That normally will come with hypertension in fluid status. So is normally a mean arterial BP less than 65. Is there kind of classic thing that people quote, which, if it's that low than your gang hyperperfusion to your brain? So again, definitely a cause off being dry, but a very late sign of being dry. You want to catch these patients? Well, before then, I wouldn't be too late to check confusion to like the the in the hands. Yep, very good. So one thing that is quite good to document in the notes in somebody who is dry. Not so inception. Normally, people quite warm because they have this kind of days. They get vasodilation and kind of loss of inflammatory markers into their interstitial on into their kind of soft tissue and which makes them quite warm to their hands, normally in sepsis. But in somebody who's dry and hyperbole Nick, normally they're very cold, preferably, and it's quite useful to document how where that the point where they feel warm again is so sometimes if you just write warm to the mid or a cold to the mid four on, that could be really useful, and then if someone's coming back to assess, um, six hours later another warm to just their shoulder and that would make you more concern. So yet just feeling the warmth of they're off their extremities is really useful. Anything else? What about the opposite? What about, like, swelling in the pressure ease swelling? Did you say a Dema? Yeah, yeah, yeah. So your pitting edema? Definitely. So if somebody's hyperbole MC, they're likely to have pitting edema, Which again kind of counter intuitively in either In severe AKI so severe that you can't leave your fluid. You'll get a demon in severe C CF and severe battery. Know all these are in severe real impairment. You can get a Demers well so that that's definitely a clue. And it's something to take into account in there on clinical picture. Anything else? There are low, obviously, those lows of things that you can look for anything else for fluid stays. Could that be like much Humalog tickle genie is How could you tell that clinically Oh, yeah. Things like yes, obviously get clinical signs of anemia. But that wouldn't you can get him in. It's gonna be a witch. Um is associated with the naked eye. But that doesn't help you in terms of fluid status, I would say maybe cyanosis and headaches, eh? So So cyanosis is actually a cause of Sinuses, A clinical manifestation off hypoc CIA. So you obviously you can get hypoxia related to decreased fluid status, but no, not commonly. And because of dehydration thing, other thing that I was thinking off is you could look at someone's JVP on JV piece is an imperfect mark, but but it can be very useful on gets effectively a surrogate marker. There's no valves between your right atrium on. Do your internal jugular vein, so it's effectively a surrogate level off the pressure in your right atrium. And if you're if you're right atrium and left atrium on kind of a left and right side of your heart, you don't have kind of unilateral ventricular failure. That can then be a reason we could surrogate for if somebody's fluid overloaded as long as they don't have any obvious valvular disease. Because patients where the tricuspid regurgitation, we'll have severely elevated JVP even if they've gotten if even if they're completely evil in it, yeah, that was very good. Lots of good things that you could try and find in the history. And so just in terms of perfusion, So again, quite late, start on a pipe of anemia that capillary refill time could be quite useful to look for. Um, so now you need to kind of. So we've got 15 minutes left. I'll just go on So renal replacement therapy quickly and indications for it, because I think that's quite important on then we can have as much everyone's happy. We can have about 10 minutes for questions at the end. Um, so, yeah, examination investigations for a k I. So you want to be looking for the first light here, which is about as you're looking to see, whether it's pretty renal injury or post renal on. Then you want to look for the potential complications of a huge in the injury, and you do that on the venous blood gas toe. Look for acidosis to see whether their patients have severe acid. Eight is you can also look at electrolytes, including calcium, phosphate and potassium, and you could look for signs of uremia. So these include confusion and careful up the or a pleuritic rub or pleuritic pain if patients are awake enough on, not confused enough to tell me that they've got pain on the left side of their chest, especially when they breathe in. Doctor, um, uremia is very rare. Symptomatic uremia Sorry is very rare, with levels of your rear less than 30. So that's kind of a very rough rule of thumb. It's unlikely to be related to their urine. You're if they've only got Humira of 12 15 on. Also, it's always sensible to get a chest X ray was a very late sign of 80 I, especially on uric achy I, where you're not able to on passed any urine, is that you will inevitably develop hyperbole. Mia, um Andi, Then go into on, then go into a pool redeemer. And so the management of all achy I need to stop the nephrotoxic so you want to stop all medications with a renal contraindications. So you pay. Things are really excreted. That don't necessarily cause achy I per se, but that can cause problems of accumulation. If a patient does have kidneys are working very well on ankylosing. Classically metformin can cause a lactic acidosis if given to patients with an achy. I see me to stop that. There's a thing on it. Basically, if you Google renal hum book is a really good PdF, which is free to use, which tells you which medications are safe in renal disease based on their easier far or if the patients on dialysis or if they've had a renal transplant on it's a life saver. So if you're ever unsure, it's better than in the UK We use a book called The British National Formulary The B N F. The renal hum books better than that, So it kind of supersedes that. So I would highly recommend using that I called, so it interrupts. It wasn't a renal handbook. If you let you just Google renal the Reno Hamburg, it will come up, and I'll have all of the most common medications that you normally use that as a matter of pdf, it was like 800 pages. Think it's free? T um, so if you're ever in July, that's a really good piece of advice. Just, uh, you could just look up the medication and just do you control that for command F on your computer and just type in the name of a medication that will see me right to that page on the pdf. And I'll give you all the information that you need. Um, yeah. If they've got a real coarse on your ferritin apology, if they've got a post renal cause which needs treatment, go to urology On Also, the question is, do they need a replacement therapy? Um, so five indications for renal replacement therapy. I'm aware we're kind of quite sure on times I'll just go through it quickly. I'm acidosis is not responding to treatment. So you found that causes are the previous intradural post renal when you're treating it, but they're still getting worse on if you're persistently less than 7.3 that normally need filtration. Hyper cleaner is what you worry about because in an achy I, the most common electrolyte abnormalities hyperkalemic on. Obviously, it's very dangerous, causing cardiac arrhythmias, ventricular tachycardia and ventricular fibrillation. High potassium. So you need to treat that. And if you it's not coming down medically, then that's a direct indication for renal replacement therapy. Some intoxicant could be dialyzed out of the system, including amitriptyline. Um, and you can also have a respect right before fluid overload, which is refractory to diary sis. Um, so in a patient with no renal function that's got fluid on the lungs, we need to take off with humidifier filtration on. Finally, it's symptomatic uremia normally with the real level greater than 30 get So I think that's everything we've got time for in terms of the talk. So I think we've got about 10 minutes to go through any questions that people might have that I will say. I'm not afraid of just myself. I'm a medical training on due to be a registered in a few months. I'm in Reno Medicine, but I'm happy to try and answer any questions that I can if you have about my talk about any specific things that have come up in general. Great. Thank you much for such a formative talk on a K. There were a few questions. Um, the first question waas if you get patient with damage kidneys due to statin drugs, what do you do? Do you stop them immediately? You just starting drugs, did you say? Um, if they already do two now it's already set on statin drugs. Do you stop it immediately or so statins don't directly cause achy I. To my knowledge, however, they can cause rhabdomyolysis. So that's the most common significant side effects from statins. So if the patients come in on, they've got significantly race e k onda kind of muscle pain, then definitely you would stop the statin. But, um, in general, as far as I'm aware, it's not a medication that you would normally stop in patients with a clear unless they come in with rhabdomyolysis. Thank you. Uh, the next question was, if a patient has a very poor G f g f r, but no underlying conditions and is healthy and other aspect such a scrotal mean, what can it be? So if they if they basically got a low, a low gear far but that but otherwise it lowers your far. Could you repeat the question? Sorry, I didn't quite Yes, sure, if a patient has a very poor gee fr but no other underlying condition and it's healthy and other specs that just creatinine, what can it be say if you have a a low G f r. You will. As I said before, Creatinine is an imperfecta marker for glomerular filtration rate. So if you have a low G f r, then you will by definition, have a very be high creatinine, so they won't have a healthy kratom. And that's what something that's possible. Um, and in terms of what can cause is if it's if it's happened acutely, whereby there g f I was great the 90 last week. Then they've gone achy I, and the different thing that can cause it is everything we've spoken about in the last 40 minutes. If it's progressively gotten worse and worse, then by definition, they then got chronic kidney disease. On the most part, I'm not sure about other countries around the world. In the United Kingdom, the most common causes of chronic kidney disease are diabetes and is the most common. But other causes include polycystic kidney disease, hypertension, renal vascular disease. Because of atherosclerosis, disease or remain affected, these are the most common five, so those are kind of your causes of both achy I and see great thank you and you want to. The next question is always good. Um, is angina possible in hyperbole? MC shock is angina, Potter. You're over to angina. By definition, is chest pain associate ID to associated with cardiac ischemia. Right on, due to the extent that you are not causing Sorry. No, I skinnier. Yes. So it's chest pain related to cardiac ischemia, which is not causing infarction and the craziness. So if you were to do a troponin on somebody with an tire in a troponin would be normal. Um, so you have This isn't the quality, but you have a phenomenon where if somebody has obviously, um, iCarly infarction is where somebody has a direct occlusion to one of their coronary arteries, which is causing kind of distal ischemia on. That's what we call a type one. And I You can also get cardiac hypo perfusion, which is related to hypovolemia. Because you're just not getting the blue blood flow to the to the cardiac arteries to the coronary arteries on. That's called a type two. And I so yes, I guess effectively is the answer. If you have a degree off underlying coronary artery disease on, did you become hyperglycemic? You will decrease your perfusion to your cardiac myocyte, which will then cause just pain. So yes is the answer. You can get angina, and you can also get have not just a ski me, and you can have full on infarction related to hypovolemia. And you do see that quite common and click commonly in clinical practice and create Thank you. Next question is there's different formulas to calculate. Dear Far. Which one is the best one? So the right you're right, the writer from Formulas in a different they all have different pros and cons. I don't know there's one which is particularly better than others. The kind of the EEG EFR formula that is normally used in kind of automatically populated in hospitals normally uses the patient's age on do their gender. And that's all that's normally for clinical practice. Everything that we use. But as I said, it's without doing formal kind of testing. That's all we used for clinical practice, just with the knowledge that is an imperfect test. And it needs to be taken into account of the clinical setting. Thank you. I'm Abdulla. You had a question. Could you like to meet yourself and just ask you a question, please? Yeah, Doctor, I just don't regarding how do you balance use needing to use being in a situation where you need to use nephrotoxic drugs we're dealing with like, for example, cardiology who are like stopping the treatment. Um, but your opinion differs. What? How do you work that out? How do you work out? What? How do you balance the treatment outcome versus the risk when it comes to, like, take a CKD things like that. That's a really good question. And that kind of directly points toe one of the kind of challenges of working in kind of multi disciplinary teams in hospitals. And so fundamentally everyone's. You've got to come from the mindset that everyone's view is that they want the best thing for the patient on that. They just have different sets of expertise, which they're seeing seeing the patient's condition through a slightly different lens. So it's quite common that there will be direct discussion between cardiologists and apologists and say it's more helpful if there's a good working relationship between. But the condition has to be a clinical one and there's no kind of right in wrong answer about. I'm kind of continuation off certain drugs or stopping certain drugs depending on different people's condition, and it has to be very tailored to that specific patient, and I know one kind of quite common thing between kind of, say, gastroenterology, So gas andrology is very commonly prescribed, and that result loaded patient to a lot of patients have mild symptoms of gastroesophageal reflux disease, and they'll be on omeprazole nephrologists. No, that was all Control was wanting to be speaking about earlier, cheap, you know, decision or fighters. So it's quite common that the nephrologist will. Then their patients will also got CJD. They'll come in to clinic they don't want. The patient developed is a rare complication of a result, but it is recognized they don't want their patients small renal function to become significantly worse, and they'll stop the omeprazole. But those are, um, those off decisions really hard, where different specialists have different opinions. They're really complicated and involve lots of teamwork, I guess, in a way, that's what makes medicine interesting. Kind of coming to a sensible conclusion with the patient at the center of the decision. That's in their best interest. Thank you, Doctor. Just a follow up question. Really quickly. Sorry. It was just that I've seen, like nothing was just prescribed for, like, non diabetic patients. Sgot two inhibitors. Commonly I've seen it's more recently. Now I don't understand why I like what is the purpose off? They're not diabetic, but they're coming from a nephrology award or something. No, we having this medication. That's, um I'm actually really glad you asked that question, because I've just done some research and quality improvement project in my hospital specifically looking at this. So then what guidelines you're using Ukraine. But in the UK, we use the national IT industry of clinical accidents, which is they're nice guidelines which are based on on the best evidence to give recommendations to clinicians here, um on. But was a big art school which was done. I think it was 2020 in the New England Journal of Medicine, which is called If you want to look up is called dapper ckd d a p um, a ckd on. It's basically a groundbreaking our school, which has shown that in turns off, I quality of life of patients in terms of specific cause, mortality on, in terms off requiring renal replacement therapy, there is an improvement on mortality. Sorry. There is a specific In those three criteria, there is an improvement with SGLT two inhibitors and specifically dapagliflozin in patients who have some K d with significant albumin urea who do not have diabetes. So this is a busy of groundbreaking trials. Are in apologists really excited at the moment in general, about these new medications on actually, So it was kind of sick. So it was a big trial that was done for a lot of diabetic patients to undo was kind of subsets. Cohort analysis for these SGLT two inhibitors with people don't know how it works effectively blocks the reabsorption off glucose in your distal nephron, which they kind of induce is glycosuria two degrees the sugar level in your blood On their found the in subset analysis that patients with CKD were significantly better in terms off these kind of modalities that's big before and also patients with heart failure. So then they were like, Okay, let's see if these changes are significant in patients that don't have diabetes. It was basically completely serendipitous by chance, fighting on getting these big trials on patients with heart failure on also with patients. We have CKD without diabetes on. They found that there is improvement in outcomes for both, so it's kind of now standard of care Patient diabetes. Patients with heart failure without diabetes, on patients with, um, CKD without diabetes on actually, so I'm not sure how much you will know about heart failure, but the way that it's managed is related to what your ejection fraction is, which is a surrogate for your left ventricular systolic function on Diffuse Got a poor left ventricular systolic function is very clear that SGLT two inhibitors work on breathing or outcomes on. This is currently a lot of research going into patients with diastolic failure. You don't have significant left ventricular systolic dysfunction where the SGLT two inhibitors improve outcomes in those patients. But the preliminary results show that they are likely to it, if that's the case, that this will be the first medication with a mortality benefit what's known as diastolic heart failure or also known as kind of half or hot food with preserved ejection fraction. So whoever I don't know which company is that made SGLT two inhibitors, but they are rubbing their hands with a lot of different new uses that they just found by chance for this new medication. Thank you so much, Doctor. I'm definitely gonna looked out. Thank you. Well, thank you so much. Think a couple people ask him. Could you just write the article in the chat, please? Forever. Until a cat, I could put a link in the truck. Yeah, sure. Thank you. Um, okay. Thank you. Um, I just doctor for your time and giving us a today's lecture conscious of time on. Go under the lecture now, starting at seven o'clock. So as soon as the doctors shared link, I'll keep it. One the chapped running for a couple of minutes a couple of about 30 seconds, and then please make a note or the feedback fall on, then rejoined, please. There you go. Yes. New England Journal of Medicine. And it was in the October 2020. Great. Thank you. Thank you very much. Thanks. Everyone from you. Thank you so much. Thank you. Bye. Thanks for my uh hello, my Here, Dan, Could you like, press stop the liquid? That that won't work. Uh, if you have you just look back in. Are you Do you have a button that says to steal the host, right? No, I