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No, I think that's wait tools I passed and I, no. Right. Are we live? I will see sharing again. It's visible. Yeah. Yeah. Ok. So we will be getting, um, so, hi, everyone. Um, can everyone hear me first of all and see the screen? I can, um, maybe if someone can just write a quick message on the chat, that would be really helpful. Yeah, it's all good. Ok, brilliant. So, hi, everyone. Um, my name is Maya. And you want to introduce yourself? Yeah, I'm Emma. Um, I'm currently in my fifth year at UCL. Um, so today we're gonna be talking about, um, AK I, we're going to be talking about, um, first of all, defining AK I causes of AKI and then management investigations. Um, so first of all, um, if you haven't been to one of these before, um, we're teaching things and we hold weekly tutorials on at six o'clock every Thursday and where this time we're focusing on sort of core information, um, like interpretation, um, imaging just to give you a base, like a basic idea of the foundations of clinical medicine. And from next time we're going to be focusing on co presentations and how we like go from uh patients history and examination results to um diagnosis. Um We have outside reviewed by doctors and we um will keep you updated regularly about all of the events that we're holding um over the course of the year. So I'm going to be talking today about the causes of AK I um and please feel free to put questions in the chat or just unmute if you feel comfortable. Um We will put up the slides and the recording um after, but um engagement really, really helps. So please do ask if you have any questions. Um Emma's monitoring the chat and you can also just unmute and I'll be have I have a couple of S pa S and a couple of general questions. So do pitch in um throughout cool. So a quick refresher of a little bit of anatomy and physiology because it helps for context. Um Obviously, the kidneys are organs that we find sort of in the lower back. Um They're about 11 by six centimeters on average in size and about 100 and 20 to 100 and 50 g in weight. And they are receive a huge volume of cardiac output about 20 to 25%. Um Let me find that as a pointer in terms of the functional unit of the kidney, we have the Nephron, which basically consists of Aus and our tubule and that forms a function of filtration and we have about a million nephrons per kidney. And also it's important to bear in mind when it comes to examinations that the left kidney is higher than the right kidney because the liver on the right side reduces the level at which the kidney can be placed. So, we've talked about this already. But does anyone want to unmute and summarize the functions of the kidney other than the obvious? Oh, hold on basically. Or is there anything in the chart you put that in as well? Any trouble? Yes. So we have one excretion, excretion. Yes. Fantastic. Anything else? The next one electrolyte balance. Anything else? Yeah. So that's a good place to start. So obviously, the main function of the kidney is filtration of waste products from the blood to form urine and that maintains it removes waste products and also ensures that electrolytes are kept in balance. Um And the kidney is the site of um activation of the renin anti tens and aldosterone system. So it's really, really important for general um generally keeping water, sodium, um potassium, etcetera in balance as well as excreting a variety of other electrolytes through various transporters within the nephrons. And also sometimes um easy to forget but also very, very important when it comes to the presentations of AK I CK of KD. Basically, the kidney has significant endocrine functions. So um the hydroxylation of Vitamin D the last stage of hydroxylation of Vitamin D is performed um in the kidney and the kidney is also responsible for the production of epo. And so, as a result in people who have chronic kidney disease, um due to whichever etiology, you have anemia because you have reduced production of red blood cells due to um a lack of this um signal for blood cell production. So, remember the three essential functions, filtration, acid base regulation, and also endocrine functions. So that's the gross anatomy and basic functions of the kidney. We'll go a little bit into the micro anatomy of the kidney. Um just because it's good context. So when it comes to the functional unit, we said that that's the Nephron and the Nephron basically consists of the glomerulus um which is basically like a coil of red blood cell of um capillaries um from which um fluid uh and electrolytes are displaced um into this epithelial structure called a kidney tubule. Um And obviously, blood enters the sclera from an af arterial and leaves by an ef arterial. And these, the art af arterials come from the um arterial supply to the kidney, the renal artery, the eer arterials joined back up to form the renal vein. So, reminder of F and M which I'm sure no one really wants to do, but it's quick refresher. It's nicer understanding some of the uh functions of the um diuretic drugs. Does someone want to talk? W one step step by step, let's talk through what the actual features of the Nephron are. So does someone want to unmute and say when it comes to filtration through the kidney, where does the blood start? If we look at the diagram on the? Right? So where does the blood start? Kind of mentioned it in the chat or unmute anything job? Uh One thing in the, the glomerulus, the glomerular capillaries? Fantastic. So the glomeru filters the blood and filtration is basically um solutes and water. Basically being pushed through the endothelial and epithelial barrier into the Nephron. That's filtration. So, basically fluid and electrolytes out and into the Nephron. Um where does the urine that's now in the tubule go next. So it goes from the glomeruli into a structure called the B's capsule. Then where does it go? Chat? Next thing in the chat, proximal tubule. Fantastic. The proximal convoluted tubule. And that reabsorbs irons and water um and adjust the ph of the filtrate. Next. Where does it go after the where does the urine flow? Because the fluid in the Nephron is obviously now the urine, where does it go? Next? Next thing the loop of henley. Yeah. So descending and ascending limb and the descending limb reabsorbs water. The ascending limb reabsorbs uh sodium and chloride. And this basically creates a concentration gradient for reabsorption of water. So, filtration is fluid and electrolytes into the Nephron. Reabsorption is uh Nephron into the blood vessels. And we also have um secretion which is basically blood vessels into the Nephron itself. And this is where we have reabsorption of water and solutes. So you're um keeping in the water and salts and body. Um and you're making concentrated urine and then after the loop finally ready to go urine, I mean, the next one, DCT DCT. Fantastic. So we have the distal tubule which secretes certain rons of excretes them into the Nephron and reabsorbs others. And then after that, we have the collecting duct which reabsorbs which kind of fine tunes the concentration of urine very good. So now you know the um broad functions of the kidney, the gross anatomy of the kidney and the functional units of the kidney. So that takes us to what an AK is. So we can understand an AKI as anything that you on an acute basis causes kidney function line and obviously declining kidney function means that you aren't filtering as much water and solutes and you are excreting as much as you usually would and that also causes electrolyte abnormalities. Um It means that you can't excrete the waste products that you usually would excrete. And also you don't produce as much urine when it comes to specific diagnostic criteria. Um bear in mind, you can never diagnose an AKI without a previous um blood result just based on creatinine. So if someone gives you blood results for a patient currently, and they seem to have high serum creatinine, you can't tell from that on, on its own, whether um it's an acute kidney injury or if they have high serum creatinine for other reasons. So to use creatinine to make a diagnosis of an AKI, you have to um you have to have previous blood results. And so if your serum creatinine rises by 26 or more micro mol per liter within 48 hours, that meets the diagnostic criteria for an AK or if you have had a 50% or rate to rise in serum creatinine within the past seven days, that's also considered um an AK. And if your urine output falls to below a certain level for more than six hours, that's also um diagnostic of an AK. So you have an acute decline in kidney function which you can detect um by a change in serum creatinine or increase in serum creatinine compared to baseline or compared to previous results um or due to a foreign urine output. So, can anyone tell me brainstorm a couple of reasons why somewhat of signs and symptoms for an AK? Do you have any? I would have put this in a pole but you can't, it doesn't have three options. Did that just randomly? Sorry, I think mine. So our first thing in the chat is dysuria, dysuria, another one. This is and what, what the other one is, hematuria, hematuria. Hm. So I see what you guys are getting at, but there's kind of like I we'll go through this, you might get hematuria, you might also get dysuria, pain and urination. But it's, we're thinking more broadly if you think about an ak of any cause, what do you think the general findings might be? So, any others, we have another one, oliguria, oliguria, reduced urination. Yeah. Anything else? Not yet. If anyone wants to put something in the chart. Ok. So let's go through them all good ideas. Um So when you think about the signs and symptoms, early condition, it's useful to link it back to what, what's happening in the condition, what are, what's the physiology basically? So we know that in an AK I, we have damage to the kidney and as a result of that, um we obviously have reduced urine output. So all of a, like you said, um because we don't have as much filtration, we also have a number of different causes for an AK. So if you um think about the different causes, you might have the signs and symptoms of those. So you might have pain if um the person has an infection. Um or if it's malignancy related dysuria might be a symptom, hematuria might also be a symptom depending on what the actual cause of the AK is. And then we think about the functions of the kidney and we think that the kidney function is impaired. Obviously, we won't be excreting. So we might get signs of fluid overload, um such as edema, pulmonary and peripheral edema, which is often why you in um SBS, you have people who have puffy eyes, peri edema and also peripheral peripheral edema. Um Also, if we think about how the kidneys are supposed to regulate fluid, um regulate um electrolyte balance, um you think about urea building up and as a result in severe um ak where you weren't um excreting any urea, you will see the symptoms and signs of um urea build up such as fatigue and nausea, pruritus. Um And in severe cases, pericarditis, encephalopathy. And also it's really important to bear in mind that AKI might be completely asymptomatic and might just be purely based on blood results. Um So there's a whole spectrum of symptoms. So when you're thinking about signs and symptoms of the condition, think about um the underlying causes and how those might have their own signs and symptoms also think about how the physiological system is being deranged and what the consequences of that might be. So overall, the signs and symptoms could be related to the cause or they could be related to the consequence, which is the kidney isn't functioning or how does the kidney normally function? What would happen if it didn't function? Um I won't go through this in detail, but you do need to remember uh specific um criteria for the different AKI stages, but this is something to memorize. Um But now we're on to the meat of the topic. First of all. Does anyone have any questions on anything we talked through so far? Anything that isn't clear and flu shot? Nothing in the chat? No. Ok. Brilliant. Um I team everything is clear and go on to my next question for you guys, which is brainstorm. Sorry, sorry, sorry, we do have one question in the chat. Um Do we need to memorize the stages criteria? I would say yes you do. It does come up in F ba it's a bit annoying but you do have to know it. Um So we'll go on any other questions, just put them in the chat and I'll Emma will let me know. Um Does anyone know any potential causes of an AKI just brainstorm them or tell me if anyone knows any ways of categorizing them. Uh One question, will we get the slides? Yes, the slides will be sent out. Yeah. Um in terms of causes of AK, we have some messages. So we have uh medications causes, for example, paracetamol, maybe um-hum. Um we then have someone who sent prerenal renal and postrenal. Fantastic. Uh Someone else said, obstruction, um dehydration, glomerulonephritis. Brilliant. Oh my goodness, infection, uti renal stones, tumors. Wonderful. Just get the tutorial. Fantastic. So those are all great. So the summary of what can cause an AK is anything that affects the kidney can potentially cause an AK just like um yeah, basically anything that can affect the kidney can cause an AK an acute decline in renal function. And the way we categorize, the causes of an AKI are prerenal, renal and postrenal so well done for that. So, prerenal concerns perfusion of the kidney. If you aren't perfusing the kidney, then it can't perform its functions. And also you aren't um it's losing blood supply and that will also impair its function um and cause damage basically. And also if you aren't, you, you kidney, then you aren't able to filter any of the waste products or uh perform the function of excretion. Um Renal causes of api basically involve anything to do with the structure and function of the kidney itself. So this is, we're talking about disease of the kidney itself. Post renal causes of AKI concern, anything that's downstream of the kidney. So anything that can affect the drainage of urine. Um and that might be anatomical or related to the surrounding anatomy, um that will basically prevent urine from draining. And we'll kind of go through how, what the etiology of all of these different types of AK I um are any questions so far? Ok. So that brings us on to our first SBA. So Emma, could you start the poll, please? The 75 year old man. Never mind that. How do I delete a slide? Could you start the poll, please? 75 year old man, wait, I I'll start the poll. Can everyone see the poll? 75 year old man. I'll just stop sharing my screen for a second. Ok. Do you have answers in? I'll just start you on this. Uh, not yet, but there's a lot to read. So maybe we'll give it a bit of time but it's visible. I can see this. Ok. I'm just gonna sit with my answer. Sure. Um, and uh was this starting to come through? Very nice. We have 10 responses. I wonder how many people do you have 20 people? So, wait a couple more. Yeah. What's the difference between acute necrosis and should be renal tubular acidosis, renal tubular? Oh, it's renal tubular acidosis and acute tubular necrosis. We'll go through that in. I'll go through that towards the editorial. It's OK. I was about to type and cross as well. Uh How many responses do we have? I think we have a good um 1313 responses. Um It looks like very split results. Yeah. Very interesting. So, um let's talk through this. So, what we have here is, and I'm going to reveal the answer. So sorry about spoiler. The answer is dehydration. So, what do we have here? We have a 75 year old man who's presented to A&E following a fall. So, first of all, naturally, you're thinking fall and he was found on the floor in the morning. So we're thinking, oh, he's had a long life and that's kind of reminiscent of lots of s pa question that you might see on pad. Um And so a lot of you guys might jump to a certain answer because of that. We also know he's got a past medical history of left sided heart failure. Hm. Interesting. And he takes other medications, some of which might be considered nephrotoxic. Um His blood and urine results are shown here. So he has sort of within normal ranges, sodium and potassium. His creatinine looks quite high. Obviously, we can't diagnose an AKI on the basis of this alone because we need blood results very high serum urea because normal urea is sort of between two and seven minimal per liter, urine sodium is low and urine osmolality is very, very high and you get normal ranges in the exam, I just haven't put them here. So when it comes to the thing that most likely cause this presentation, let's talk through this. So the important learning point here is using results to decide using blood results um and urine uh results to identify an history in combination to identify what the cause of an AKI is. So when you see a patient, um you have to consider first of all their history and then their examination and then their investigation results to kind of identify what the cause of um their presentation might be. And obviously, we know that an ati might be prerenal renal or postrenal in um its course. And it's really important for us to identify that so that we can actually get to the bottom of the course and treat the appropriate course. Um Because if we do so incorrectly, then we won't actually be able to restore kidney function. Um So when we think about this, let's talk through the options. So, acute heart failure, it is actually a potential explanation for his um for his presentation. Um because if you have acute heart failure, then you're likely to um you have a lack of perfusion of the kidney and that can lead to a decline in kidney function. So that is valid, but we don't actually have any evidence of um fluid overload or any other signs or symptoms of heart failure. So, acute tubular necrosis, um people consider this as well. So acute tubular necrosis is basically damage to the kidney tubule itself and that can happen when you have a long lie. Um and rhabdomyolysis. So basically, if someone's after a fall and lying on in one place for a really long time, muscle starts to break down and um it basically releases a lot of myoglobin and damage to the kidney tubule occurs and that causes um like secretion of muddy brown casts in the urine. Um You basically have like a high creatine kinase. So it's ex and so that's kind of another potential explanation for why he's having an AKI because if you have a rhabdomyolysis that can cause an AKI um but the blood results paint a slightly different picture and we'll talk through this renal tubular otosis is kind of just an option I put there, but there's no evidence of that being the case. Um that's basically caused by um uh the transporters in the kidney not working properly. Um It's quite complex and I can't, I don't really have a slide on it, but there is, there are youtube videos which I would recommend um dehydration. Um So, dehydration can cause a prerenal AKI. Um because obviously, if you have dehydration, you have reduced circulating volume and that will reduce perfusion of the kidney. Um And actually our blood results point to that and I'll talk through that in a minute. Um And again, we've talked about why it's not rhabdomyolysis because actually the blood results you otherwise. So I've been going on and on about how these blood results um point to dehydration being the cause of his presentation. So let me talk through what happens. So we said that a prerenal AKI is basically an AKI where you have reduced perfusion of the kidney. Um and that reduces uh the filtration of waste products and the excretion of waste products. So, what are the potential reasons for um perfusion of the kidney dropping? So, the first is renal vasoconstriction and this can be because of ace inhibitors or um angiotensin receptor blockers. So, some patients when started on these medications, um they develop um AKI s because um because of them causing this uh renal vasoconstriction. So, whenever patients are started on ace inhibitors and um you will see a slight drop in their kidney function uh when you look at blood salts. So you might have a slight rise in serum creatinine, um slight rise. You shouldn't really have a rise in serum uria, but sometimes you do have a slight rise in serum creatinine. The thing is sometimes it's quite confusing because actually ace inhibitors and Arbs in the long term, they improve kidney function. But in an AK they're supposed to, you're supposed to stop them. And the reason for that is that when someone has, for example, diabetic nephropathy or um kidney disease of various other causes, if you give them an ace inhibitor because of this, um because they constrict the AP and arterial, they reduce the burden on the kidney and the amount that it has to filter. So if you long term give a patient, this medication, you're reducing the burden on their kidneys and you're reducing the work that their kidneys have to do. It's just that when someone's acutely unwell or is having or for some reason, they've had an AK precipitator for another reason, reducing the blood flow to the kidney tubule is actually just going to worsen kidney function. So you need to stop the stop ace inhibitors and Arbs if someone is having an AK. So it's just important to remember that ace inhibitors and Arbs, they are good for kidney function in the long term. But if the kidney is acutely damaged, then you have to stop these medications because they're going to reduce blood flow to the kidney. So it's kind of like the reason they're good long term is the reason they're bad, long, short term. Does that make sense? So anyone not want, doesn't want me to repeat that or explanatory? Ok. No, nothing on the chart. No, nothing on the chart. Um So another cause of prerenal AKI is renal artery stenosis. Obviously, sorry. We have a message, please. Could you repeat that? So what I basically sometimes you'll see that patients, for example, with diabetic nephropathy um have been prescribed ace inhibitors and that might be a bit confusing because you might think hang on. Aren't you supposed to stop an ace inhibitor when someone has impaired kidney function acutely? But the key thing is ace inhibitors and arbs, they improve the function of the kidney long term. But in the short term, because they reduce perfusion of the kidney, they can worsen an AK I. So they're not as such nephrotoxic, they actually help to improve kidney function. It's just that when someone is has acute kidney damage, you can worsen that by giving them an ace inhibitor because you, you're reducing blood flow to the kidney. So if someone has an intrinsic renal pathology, you might prescribe them an ace inhibitor to reduce the burden on their kidney. But if they have a short term reduction in kidney function or an AK I, you stop their ace inhibitor so that you maximize perfusion of the kidney and minimize any damage to it. Is that better? Any response at all? No response so far in the chat. But it might take a while. I will, I can explain it again at the end if you want anything so far. Ok. Ok. Someone said helpful. Ok, thank you. No worries. Um Other, let's recall. Prerenal AKI I is a lack of perfusion of the kidney that can happen because of renal artery stenosis, narrowing of the kidney will reduce blood flow through the kidney and reduce the blood to reaching the glomeruli, reduce filtration, reduce excretion. Um A really, really important cause especially in older patients and hospital patients is poor oral intake or increased losses if you just have reduced circulating volume because of dehydration or patients not eating properly older, um especially older patients. Oh, you have diarrhea and vomiting. You have reduced circulating volume and reduced perfusion of the kidney. And for the same reason, imperative systemic circulation, either due to hemorrhage, septic shock, massive va vasodilatation and reduced circulating volume. Um or heart failure, you basically have again, less blood reaching the kidney, less perfusion of the kidney, less blood filtering and um the kidney doesn't excrete as much as it should be. Um Does that make sense for the cause of the prerenal AKI? So just think to yourself, anything that impairs the circulation, anything that reduces circulating volume can cause a prerenal AKI i because less blood is reaching the kidney and it's not filtering as much any questions. We have a question on the chart. Um So does that mean that renal artery stenosis would also be protective for the kidney in the long term? Or is it more complex than that? I mean, it probably wouldn't be protective for the kidney in the long term because you have less blood reaching the kidney as a whole. Um in general blood reaching the kidney isn't a bad thing. But if someone has another form of kidney pathology, um like a type of uh glomerular nephritis, um then that their kidneys overburden, the kidney is meant to work for life, right. So, and the blood it's receiving is supposed to be receiving cos it's supposed to be filtering renal artery stenosis that blood isn't reaching the kidney and the kidney will lack the fusion and undergo ischemia and damage. So, obviously, that's not good for the kidney. The reason ace inhibitors are good for the kidneys because they constrict specifically the afer arterial. So it's the same amount of blood reaching the kidney as a whole. It's just that each individual nephron gets a bit less. Um So the renal artery stenosis is not to go to the kidney long term because you need blood to reach to the kidney so that its tissues have enough oxygen. Um ace inhibitors in certain other types of um about non individual nephrons, see the amount that each individual nephron has to filter. Does that make sense? The other thing to mention with renal artery stenosis is because most people have two kidneys and kidney function is kind of a sum of both kidneys functions. Typically renal artery stenosis is only on one side. Occasionally, it might be on both sides but typically on one side. And so it it, it's something to consider in terms of it might not impact overall kidney function that much because often the other kidney is then also able to step in. So that's um in terms of renal artery stenosis, just something to add. Um I think that makes sense. Oh, sorry, sorry. I think your, your wifi has been cutting in and out a little bit just I hope it, I'll keep talking. Please let me know if it stops again. Did, did the answer to the question make sense? And are there any other questions? Um Currently no other questions? OK, brilliant. So I'm getting to the answer for why the SBA was the answer. So I'm trying to explain the answer to the F ba. So let's think about prerenal AK I, so we know that central to a prerenal AKI I is a reduction in renal perfusion. And that can be because of reduced cardiac output due to, for example, heart failure, which reduces BP and obviously reduces flow to the kidneys. We know it can also be because of renal vaso constriction. Because of certain medications, we can be because of renal artery narrowing. Ok. Renal artery stenosis. What happens when you have reduced renal perfusion is basically a compensatory mechanism. And that compensation is mediated by um the ras system which basically thinks, oh, the kidney's not receiving enough blood, we need to maintain, we need to keep as many um electrolytes and as much water in as possible. So the R system gets activated, you also have release of um A DH and you also activate the sympathetic nervous system. And so what happens when the R system gets activated? And aldosterone is released as a result of that, you have increased sodium, water and watery absorption by the kidney. So it seems like there's less circulating volume. And so the kidney thinks, oh, we need to conserve, we need to conserve, let's conserve sodium and water. Um as a result of the activation of these hormones secondary to increased sodium and water absorption, you have increased absorption of urea. And I think that's because the sodium and urea reabsorption are coupled in the kidney. So what you have is the kidney holding on to as much sodium and water as possible and holding onto urea as a result. And because you're absorbing more sodium and water, your urine concentration drops. So you're reabsorbing sodium and you're reabsorbing water, but you're reabsorbing more water than sodium. So you're keeping more water in and you're also keeping more sodium in. But overall because you're reabsorbing more water, your urine ends are more concentrated. And that results in the investigation, findings that we saw with the previous patient because the urine is more concentrated, you have an increase in urine osmolality. Um because you're absorbing more urea um your serum urea to creatinine ratio increases. So you're reabsorbing more urea compared to creatinine. Um And also if you look at the plasma in the urine, your, you have more urea in the plasma compared to the urine because you're increasing reabsorption of urea. And as we know, because you're reabsorbing more sodium, you'll have less in the urine. And so your urine sodium drops and your fractional sodium excretion drops. So as a result of a prerenal ak you basically hold on to more sodium, more water and more urea. So you have a rise in um serum urea and serum urea to creatinine. You have an increase in urine osmolality and you have a drop in urine sodium and obviously secondary to sorry, just going back to the previous slide. Um I think you've stopped sharing your screen. Have I stopped sharing my screen? I'm so sorry. Did I don't understand how this keeps happening. I mean, talk through all of that again. So for most of the, when you were explaining it, it literally just cut out as I was going to talk. Um we can see um when you're sharing the screen, we can also see the little tab at the bottom. I will hide that. Um If that's OK. Yes, thank you. Does any, were there any other questions in the meantime, other than no other questions so far, if anyone has any questions, please put them in the chart. Oh, we have one. How would you differentiate between urine concentrated because of dehydration and urine concentrated because of renal, for example, renal vasoconstriction. So it will probably be history and then also one second. So history and then also other investigation findings. So dehydration might lead to concentrated urine, but then that won't necessarily be an AK I unless you have the creatinine increase um compared to baseline and then you said the urine. Yeah, I think the only way you can really tell is history. So if someone's got like family history of renal artery stenosis, um and also if, for example, someone is, for example, likely to be dehydrated because they have oral intake, oral intake or um they've just been unwell and not um not eating or drinking if they're an older person, not eating or drinking. Um So those are all that might point to dehydration and then renal vaso constriction if they've recently started an ace inhibitor. Um If they have, for example, a family history of renal artery stenosis, that might also, that might point to renal artery stenosis or renal vasoconstriction being a course. Does that make sense? Because I understand they're both pre renal AKI causes, they'll have similar investigation findings really, the way you can tell is via the history and that will be really, really important. That should be, that should tell you a lot. Basically here. It is a bit more confusing with that SBA now. So, so we have a question which is um so the, the from the SBA, the was the point that the on, let me read this again. So from the SBA was the point that the only prerenal cause was dehydration. So there could be a variety of prerenal causes. In this case, they could be, it could be the acute heart failure. It could be the fact that he's on Ramipril. Um but there are a variety but actually, like if you think about his results and also his other history, it's likely to be dehydration because if we think about the other causes acute tubular necrosis, renal tubular acidosis and rhabdo, those are all intrarenal causes. And we need to differentiate that this is a prerenal ak I from the blood results. Once we've identified it's a prerenal AKI, we think it's either acute heart failure or dehydration. It's not likely to be acute heart failure because he doesn't have other signs and symptoms. But we know he's been lying on the floor for a while and he probably hasn't been eating or drinking. And he's also, he might, he seems like he's got otherwise a complicated medical history. He might be an older person who's not eating or drinking. And so that leads you to think of dehydration. So there are two kind of steps to this. The first step is, is it prerenal? We've got a variety of potential causes. They could be intrarenal, they could be prerenal, postrenal. Then we look at his blood results and we think, oh, this is a pre renal AKI, we look at our list of options and we think to ourselves, what's prerenal, what's intrarenal and what's postrenal? Then we've identified the prerenal causes dehydration or acute heart failure. We go back to the history and think, oh, what makes most sense of the history? And then we kind of conclude dehydration because of him being on the floor in the morning, probably a bit of a stretch. If he, it's unlikely that not drinking or eating for a day is going to do make, make much difference. But then in the context of the rest of his history and the fact that he hasn't actually been eating or drinking, and we don't actually think it's acute heart failure, we can rule that out. Does that make sense? Um We'll wait for any answers. But in the meantime, we also have another question. Do ace inhibitors affect the renal arteries? They affect the afer arterial. So I'm not sure about them affecting the renal artery, but they do affect the small vessels. So this, I don't think they, they don't affect the sort of main artery to the kidney. If that makes sense, that would be a very drastic. They affect this part basically. And if this constricts, you have less blood going in here. Um Does everything make sense so far? Are there other questions? No other questions in the chart? Ok. So to summarize, we know that there are anything that affects, cause a kidney function to decline acutely will cause an AK we can classify things that cause the kidneys function to decline decline. As prerenal AK A relating to renal perfusion, intrarenal AK relating to the kidneys, um anatomy and physiology itself and then postrenal relating to the filtration and drainage of urine. The prerenal causes of AK I um basically uh can be summarized as reduced blood going to the kidney because of a systemic cause or because of renal artery stenosis or constriction of the small vessels in the kidney. When you have a prerenal AK I, what happens is that the kidney tries to compensate via activation of the ras system, um release of a DH. And as a result, you absorb more sodium and water and you reabsorb more urea that basically causes your serum urea to creatinine ratio to rise and your urine sodium to drop and also your urine to become more concentrated. And because the kidney's function overall is being reduced, you see a rise in creatinine a drop in urine deranged electrolytes and acid base imbalance. Oh, does that make sense? We have another question in the chat. Um What does, what do ace inhibitors do to the afferent arterial, they constrict it. So they reduce the blood entering the glomerulus. Does that make sense? And he does the kind of pathophysiology but prerenal ak I make sense to everyone. Yes, thank you. OK, brilliant. Um So and the SBA so the reason this is so murky is because I deliberately made it. So because there could be, if we look at his history, there could be any range of causes for his um slightly aberrant kidney function. And obviously, we can't say it's AKI for sure, cos we don't have previous results, but we have a quite high serum creatinine, high serum urea, it's making us suspect an ai um So we kind of need to tease out from his history. What are the potential causes? And the investigation results do they point to prerenal AK I or an intrarenal AKI and they point to a prerenal AKI because of his um high serum urea, pointing to increased urea reabsorption and his low urine sodium, meaning that more sodium is being reabsorbed, high urine oal. So really, these are the three key results that shows that it's a prerenal AKI. I. Then when we distinguished prerenal from other causes intrarenal causes like acute tubular necrosis, renal tubular acidosis and rhabdo when we've identified it as prerenal AK I, we go back to the history and we think what's it likely to be acute heart failure. We don't have signs or symptoms of that dehydration. Hm. He has been lying down for a bit. He has been sort of in his kitchen on his own for a bit. He might be dehydrated and that would fit with, um, kind of a, more a prerenal ak I any questions, sir. I just wanted to let you know in the interest of time. It's currently quarter to seven and I think the tutorial is scheduled to end at seven. quite a lot to get through. So we might run to 730 but I'll quickly go through um intrarenal and postrenal. And I've got a lot of slides on nephrotic versus nephritic. But actually, that's more of a reference, that's more of a reference point view. And so I'll quickly go through intrarenal and postrenal. But thing with intrarenal is that it's anything wrong with the kidney itself. So that can be damaged. If we think about the structure of the kidney, it could be damage to the glomerulus, it could be damage to the kidney, damage to the tubules themselves or damage to the vasculature. And that will basically the functions of the, of the kidney. So you don't have as much filtration of fluid and solute. You don't have as much secretion. Basically, you don't have as many solutes that are going into the kidney tubule from the blood. You also have as much reabsorption of fluid or so, and as a result, you get a with any, you have a build up of creatinine. You have a reduction in urine output to electrolytes and acid base imbalance. Because these are all of the functions that the kidney is usually supposed to perform. Get rid of creatinine, get rid of urine, keep electrolytes and acid base in balance. If you have an AK I, you don't have any of these. So basically, this is the consequence and these are the kind of clinical manifestations of any AK I when it comes to the intrarenal care, there's a variety of places. So I've talked through them and you guys can go back to the slide. Um And I probably won't have time to go through various A I causes, but there are lots of slides on them. Um And you guys can let me know any questions on how an intrarenal AK I quote on intrarenal AK. Um So I found nothing in the chart. OK. So you've been through a prerenal Leki, intrarenal AKI now a postrenal AKI. So postrenal AKI is related to urinary outflow obstruction. So, anything that's downstream of the kidneys, so that can be the ureters, uh the bladder. Um Anything that stops urine from flowing out of the kidney causes urine to be backed up into the kidney. And obviously, um the urea the electrolytes that are being excreted um because they're backed up into the kidney, they impair the kidney itself. And as a result, you have all of the manifestations of the AEA that we've talked about. Creatinine cos you can't filter it out. Increases, you have less urine because obviously blocked from leaving and electrolytes and acid base can't be kept in balance in terms of what can cause urinary outflow obstruction. It can be because the lumen is obstructed. So there could be something stuck in the actual path of the urine and that could be cause that could be a renal stone or a clot. You can also have thickening of the walls of the ureters of the bladder, um of the kidney. And that could be because of malignancy or because of strictures, which basically just narrow. Um The ureters, you can also have something that's physically obstructing the urine from flowing out such as um prostatic hypertrophy, which will obviously narrow the kind of space um for the urine to flow out. You might also have retroperitoneal fibrosis, which might also obstruct outflow um infection. That's um for example, uti that's in a uti that descended and also malignancy in the pelvis because that will also put pressure on um the ureters, the bladder and stop urine from being excreted. Does that make sense? We have no more questions in the chat? Brilliant. Um So I'll quickly go through these two slides, but sometimes it's hard to bring all of renal together. But the way I understand it is that when it comes to diseases of the kidney, basically an AK and D can be caused by, sorry, we have a, we have a quick question on the last box. So if you go back to the previous slide, the last box, can you elaborate on that, please? The last box urinary outflow. So basically, if you think about um the abdomen, um and all of the structures that are close to the bladder, the ureters and the kidney. If there is hypertrophy of the, of the prostate, you obviously have um the urethra flowing through, moving through the prostate. If that's, if the prostate gland is enlarged, then it will stop urine from flowing through the urethra. If you have fibrosis or malignancy, then that will put pressure on the ureters or the bladder or the kidney and stop and like close up the usual part of the urine. And as a result, it will be backed up into the kidney. Um and ascending infection. Um For example, if you have like inflammation and infection of the urethra and then that ascends to the bladder or to the ureters, you obviously have inflammation and you won't have the, basically the the outflow of the urine will be obstructed because of all of this inflammation. Um and the kind of like process of resolving the infection basically, does that make sense? So anything that presses on the like, anything that presses on your, the ureter, the kidney, the bladder, the urethra might close up the outflow tract for the urine and as a result, it will get back up into the kidney. Does that make sense? It says, uh it says the infection doesn't, the infection doesn't make sense. So basically, if hm I can't really explain this one either. I think if you have, if you have a uti that then ascends to then become like pyonephritis, the general information will probably, unlike potentially in the ureters will probably reduce the space for urine to flow. That's what I think. But I can also look at it and get back to you. Sorry, I can't give you a better answer. I just think if the tissues themselves are inflamed and um there are bacteria within the tract, it's likely that otherwise that because of the inflammation and narrowing, they wouldn't be urinary outflow would be reduced. Yeah, I think that makes sense now. Thank you. Brilliant. Fantastic. Um So prerenal is reduced renal perfusion, which can be because of reduced circulation. And um also because of narrowing of the renal artery and also certain medications. Intrarenal is anything wrong with the kidney. Postrenal is anything stopping urine from leaving the kidney. Sometimes it can be really confusing when it comes to renal to bring everything together because you have AK you have CKD and you have all of these random conditions affecting the kidney. But the way I like to think about it is um we've been through the courses of an AKI that can be related to the kidney or they can be related to factors outside the kidney relating to circulation or other um like uh urinary system structures. Um T KD relates to the kidney itself, but if we were to zoom in on the kidney itself, and we were to think about all the things that could go wrong, we could have damage to the plumulus, damage to the tubules, damage to the interstit or damage to the vasculature. And if you have damage to any of these parts of the kidney in the acute setting, you could cause an AK. But long term, if you have damage to any of these or these um features of the kidney, you'll develop D and sometimes people who have CKD can develop an AK I because their kidney function drops um acutely for any reason. Um and an AK I won't cause KD. But if someone cause of an AK I is damage to their kidney, they might later develop C KD if that makes sense. So the way you can think about it is anything that damages the kidney can cause an AK I or D. Um and sometimes people who have D can develop an AK I basically, and if you have an AK I because of renal damage that can, that renal damage can develop into D. Does that make sense? We have no comments. Uh Yeah, it does make sense. Yeah, it does make sense. Brilliant. And when it comes to nephrotic and nephrotic syndrome, there's syndromes. So syndromes are like um sets of symptoms or sets of investigation results that you get associated with particular diseases. So, nephrotic and Nephritic syndromes are not like diseases themselves, they're manifestations of a variety of diseases. So, if you have damage to the kidney for whichever reason, it can cause you to develop nephrotic syndrome, but it can cause you to develop nephritic syndrome, either one um or both or like a mixture of both. So you can think they're all separate things, but just bear in mind that when you have damage to the kidney, you can develop an AK or C KD. And when you have damage to the kidney, you can develop a nephrotic syndrome or nephrotic syndrome as like a series of potential symptoms. And I'll finish on this one. You guys can go through the rest. Um and email me if you have questions. But nephrotic syndrome is just protein in the urine because of damage to the podocytes and basically excretion of protein into the urine. Whereas Nephritic syndrome is blood in the urine because the endothelium is damaged and blood in the urine um is often accompanied by hypertension. So, nephrotic syndrome is protein in the urine. Nephritic syndrome is blood in the urine and kidney d various kidney diseases can cause nephrotic or nephritic or both. And the way you can remember which, which is, which is that if it ends in itis, it causes nephritis and the ones that are named after people. The eponymous conditions are also nephritic. Um So the rest of my slides basically go through nephrotic nephritic and like common S pa presentations and things. So you guys can go through those. Um And let me know if you have questions, but in the interest of time, um I will go to em S slides because you know, generally what causes an AK I and the rest are just details about how the kidney, what, how renal pathology works. And that's something you kind of just memorize and recognize for SBS. It's really more important to understand what the causes of an AKI are generally and how you identify them, how you, and then how you investigate and how you manage. So I will start on that stage and would you like me to share and then you continue to, yeah, I think that, yeah, if you just present that, then I can let you know when to move the slide. Um OK. So starting off with a quick question on AK I assuming previous um, results were, you know, previous things were normal. Um What is considered to be AK I for a 70 kg adult? Um I'll just start the poll. There we go. Ok. And if you want to, um, put your answers in. OK. OK. I'll wait for a few more. Uh, wait, hang on. How many people are still here? Yeah, I'll wait for a few more. Few more um responses. Wait, um a few, a few moments longer. No. OK. Last answers and then we'll move on. Uh No, the slides are not frozen. We're just waiting um for the phone and then I'll move on to the answer. So, um if you want to go to the next slide, please, OK. So the correct answer is d um so less than 35 mL per hour for more than six hours, which most of you got right. Um The explanation is what is considered to be AK which may mentioned earlier is less than naught 0.5 mL per kilo per hour for more than six hours. Um The calculation would then be naught 0.5 mL per kilo times 70 kg for the 70 kg adult, um, which makes 35 mL. Um And again, please note this isn't diagnostic. So this is just one factor to consider in diagnosing AK I um, apparently the slides aren't moving this one. I think this is interesting. It's frozen for you guys. I think I can see it moving. Um Can you see that I can see this? Um, we've got a lot of messages that the slides are frozen. Yeah, we're going to stop showing start again. This is visible for me. Yes, I can see one of this. Um, I don't know if anyone else can. Yeah, I think it's working again. Ok. Ok. Um, so in terms of investigations, um, I've broken it down into different types of investigations for AK I. Um again, all of this is in the context of an acute change. And the other thing is as all of medicine, no single result should be determining your management. So all of this is in the context of the clinical picture. Um Is there an explanation for what's going on? Is the patient acutely unwell potentially in an AK they might be asymptomatic. But um you know, in, in medicine, it should never be determined by one singular result. Um So as I mentioned, the urine, a reduced urine output for more than six hours um is considered AK as well as um at a urine dipstick. Um while a urine dipstick won't necessarily diagnose an AKI, it can help um answer any questions regarding the underlying cause. Um So, as mentioned in terms of protein, blood nephrotic nephritic syndrome, um having nitrites um indicates a uti having glucose, indicates having diabetes. Um If there is evidence of a uti or dip sick or if the patient is symptomatic, you might also consider sending um the urine sample off for culture to see whether there's any growth of organisms. And you might also consider um checking the protein creatinine ratio if you're considering glome glomerulonephritis. Ok. Next slide please. So, OK, our next, our next S VA um is which of these is not used to investigate an AK I IE all other ones are used, but which one isn't used. Mhm. Yes. This might include looking at um, underlying causes of AK. Ok. Ok. Mhm. Just let me know. Ok, I think results are still coming in. I'll wait until we're at 15 and then we'll move on. So two more, two more responses. Yeah. Yes. Ok. Should we, should we move to the next slide? I'll close the pool. Um. Ok. So the correct answer is actually EGFR which might be a bit surprising, a bit confusing. Um So I'll talk you through it. Um In terms of serum creatinine, as we've discussed plenty of times tonight, um serum creatinine is absolutely used in investigating AKI S. Um And then looking at FBC CRP and bone profiles actually helps you understand potentially about underlying causes of AKI. So the only one that we don't actually use in terms of investigating the actual AKI is Egfr and that's because Egfr is fantastic for long term trends and that's why in chronic kidney disease we absolutely all the time use EGFR. But in acute changes, it's actually quite unreliable and often shows zero when perhaps Egfr isn't going to be at zero. And because it's so unreliable, we just don't use it in an acute setting. Ok. So in terms of the, the bloods that we use using these are the mainstay. Um So particularly looking at electrolyte abnormalities, especially potassium. Um I'm sure you guys are aware of um how potentially dangerous hyperkalemia can be. Um We also look at urea creatinine um to monitor the AK as I mentioned before. So FBC CRP and bone profile are, are looking at potential underlying causes. Um So FBC, you might be looking at infection markers. Um You might be looking at um whether there is any anemia going on indicating a prerenal cause. Um Again, CRP would indicate any infective causes. Um as well as bone profile, you might be looking at um calcium abnormalities. Um So bone profile is there are multiple different um different markers that we look at in bone profile. And one of them is calcium and then looking at the calcium, you might look at um underlying causes of the calcium abnormalities. If you can't find any underlying cause for the AK I, um you might consider any of the following um blood tests. Um for example, creatinine kinase, if you're thinking about um rhabdomyolysis or a muscle um problem, you might be looking at any antibodies, anti GBM, um complement levels, infections like HIV or hepatitis B or C can also cause AK OK. Next slide, please. So then um our next, our next SBA I will just make it live. There we go. OK. OK. OK. No. Yes. And we'll wait till there's about 10 responses in. OK. Um Yeah. Do you want to go to the next slide, please? So looking at the answers um in terms of which is the most appropriate we would use an ultrasound um to look at the kidneys. So, Ku stands for kidneys, urethra and bladder. Um hang on your, your screen isn't showing at the moment. Ok. So, um in terms of an abdominal X ray, you, it's very difficult to see the kidneys. If II don't think it's possible to see the kidneys on an abdominal X ray. Um potentially you might be able to see some kidney stones, but it's very inaccurate. Um So we don't use abdominal x-ray for kidney problems. Generally. Um An M CG assesses the flow of urine and in an um in an AK generally, we're not particularly interested in the flow through the urethra. It's not something that we would do on a regular basis. It's more to look at um urological problems. A CT contrast contains nephrotoxic contrast. On the one hand, on the other hand, it's not going to give us as much information as quickly as an ultrasound. So therefore, again, it's not routinely used immediately. Um And again, MRI, very expensive, very, usually long waiting times um compared to how easy and um how much information we can get from an ultrasound. An MRI is just not used. Um So yeah, if you would like to go to the next slide, please. Um As I said, we, we use ultrasound kub. Um In fact, they're used for most cases of most new cases of AKI to have a look at any underlying structural abnormalities. Um They're also used if there's no identifiable cause. Um, if you can't find a cause on blood tests or on other, um, urine tests, then every patient should be having an ultrasound and if there is a suspected post renal cause, um, they should be having an ultrasound within 24 hours to see whether there's any obstruction anywhere. Um, things you might find on an ultrasound is, um, a small size of the kidneys, although that would be more in line with longstanding CKD. Um but as Maya mentioned before, um there's often an overlap with patients with CKD being more prone to having an AK. Um You might also see different differences in kidney architecture if there's potentially um been a renal infarct somewhere. Um You might also be able to see um decreased renal blood flow on ultrasound Doppler and you might be able to see hydronephrosis if there's a blockage and obstruction. Um further down, you might be able to see a hydronephrosis which might indicate a post renal AKI. The other thing that we use is a biopsy. Uh Now, a biopsy would only really be used if um we're suspecting an intrarenal course and if it is going to change management, um simply because getting a biopsy is quite an invasive procedure, you have to physically get some tissue from the kidney. Um And therefore, there's the risk of thrombosis or bleeding um from the actual procedure itself. Um And therefore, only if we're really suspecting that um that, that firstly, there's an intrarenal course. And secondly, if that uh getting the biopsy is going to determine our management, then we would consider getting a renal biopsy. Ok. Um I've mentioned again the diagnostic criteria of the AK I which I mentioned before. Um So this is according to nice again, I would recommend lining this um for exams because they, they, it is possible that they will ask this. Um OK, next slide please. And again, the KD go classification of AK I um I just wanted to highlight the reason why it's important to have a classification system, um which is that it may indicate the prognosis. So in stage three AKI so very severe AKI um there's actually a 30% mortality which is quite high. Um And therefore we we use a classification system. Ok. Neck slow, please can behind here. Um preventing a I exactly, I think, I think everyone can see that. Um So before we move on, does anyone have any questions at this stage? Um again, I've, I've kind of flown over it just in the interest of time. Um Mhm. I can't see anything on the chart. Ok, brilliant. So I'll move on to preventing a care and management. Um So one of the big things that we do is monitoring, um as I said, we can use all of the investigations that I mentioned if we know that patients are at risk of developing AKI, for example, if they've got known CKD and they're potentially dehydrated, we'll be monitoring them much more carefully. Um, also consider using IV fluids. For example, if you're, um, using an investigation, requiring contrast or an MRI or a CT scan, um, potentially for a different reason. Um, but if you know that the patient has um, potentially worsened kidney function, you might consider using IV fluids to kind of dilute that contrast a bit more and to, um, kind of flush it out of their kidneys faster, um, to prevent the, the contrast from causing more damage. And the other one is avoiding nephrotoxic medications, which I think somebody has already sort of touched upon, um, with ace inhibitors and Arbs. These are medications that I strongly recommend you learning. Um, so some medications you can prescribe with caution. Um, these include Metformin, lithium and digoxin. They're quite well lithium and digoxin are relatively specialist drugs. Um, but Metformin, certainly in diabetes management, consider if their kidney function is, is not great, consider the risk of risk benefit. Um, of them being on Metformin, things that the medications that definitely should be stopped if a patient is developing an AK has developed an AKI nsaids. So, um, Ibuprofen Naproxen, anything, any NSAID should be stopped, um, because they're highly nephrotoxic and you'll notice, um, that often patients with impair kidney function. So also CKD will not be taking nsaids or will be taking alternatives. Um I think we had a comment earlier about paracetamol. So paracetamol is actually um not particularly toxic to the kidney. So generally it's a good alternative for pain relief. Um if patients need pain relief but have poor kidney function. Um And as I mentioned, the ace inhibitors and Arbs should absolutely be stopped in an AK. Um this is a common exam question. They like to kind of throw it in. So it's definitely something worth remembering. Um, also diuretics and aminoglycosides. Um is again, it's something worth just remembering noting for um the exams that you should be stopping these um in AK OK, next side, please. Yeah, I just wanted to highlight that. Um OK, in terms of the management, how do we manage AK I generally, it's supportive. Um So as I mentioned before, we monitor very carefully and we look at the fluid balance, looking at how much the patient is taking in how much they're excreting. Um we'll do careful fluid examination, flu fluid status examinations, um looking at how hydrated the patient appears. Um and we want to make sure that we're um prescribing fluids adequately. Um So don't make, make sure that your patient isn't um neither dehydrated nor are they fluid overloaded. Um As we mentioned before, we want to stop nephrotoxic drugs in AK and we want to look at um managing the underlying cause. So in a pre this this will be different depending on the underlying cause. So, in a prerenal AKI, um if there is, for example, hypovolemia. We will want to give the patient potentially fluid bolus a blood transfusion depending on what the underlying cause is. Um they might need circulatory support. Um further circulatory support if it's a potentially more cardiac problem. Um Sorry, your slide is not showing again. There we go. So, if it's an intrarenal course, um as we mentioned before, we might consider a biopsy, um and this will fall under the, the um work of a nephrologist. Um So this will be generally quite specialist management. They might involve rheumatology. If um the cause is a rheumatological cause, they might involve other specialties. But um this is generally, um as I said, very specialist management and a post renal cause will be managed either by relieving the obstruction with a catheter or again, specialist urological management. Um The other thing to mention is that some patients in an AKI will have so poor kidney function that they'll need to be placed on renal replacement therapy. Um So these are patients who aren't responding to the supportive treatment that we're able to give them or patients who are at high risk of complications, developing complications from the AK they will be some of them placed on only temporary renal replacement therapy and gen generally, this is called hemofiltration. Um Some patients will be put on potentially long term renal replacement therapy if that kidney function doesn't improve. Ok, next side, please see that. Uh Yes. So as I mentioned, complications of AKI these are quite important to be aware of. Um So we mentioned before that patients with CKD are more likely to develop an AK, this also works in the other opposite direction. So having an AK having um kidneys acutely damaged is more likely to develop uh is more likely to lead to long term kidney damage. Um If you've got an infarct, for example, in your kidney, yes, you might have an acute um injury of your kidney, but potentially long term your kidney function isn't going to pick up to what it was before. Um I think your slide isn't showing again. I think it might be your wifi. Yeah. Yeah. Ok. We also mentioned fluid overload again. It's because the kidneys um are potentially not able to filter out everything that and sort of perform their usual functions um that might lead to high output cardiac heart failure and pulmonary edema. So you might have um fluid overload, which again is an important reason for carefully monitoring patients, fluid balance. Um patients might develop metabolic acidosis and uremia, which we mentioned already can um in severe cases lead to encephalopathy and pericarditis, which again are pretty severe complications which we want to avoid in patients as much as possible. And the other complication to be aware of is hyperkalemia. Um So hyperkalaemia, it can be life threatening. Absolutely. Um and that's why it's important I would suggest to memorize the management of hyperkalaemia. It's a very commonly asked question. Um And as a junior doctor, you will need to know the acute management of hyperkalaemia. Um There are kind of three levels to the management of hyperkalemia. I've just included them here. Um So sort of the absolute immediate management of high potassium is stabilizing the um heart's membrane with IV calcium gluconate. Um that's just to prevent any acute arrhythmias. Um but it doesn't actually deal with the underlying problem of having high potassium. Um So in the short term, we use um usually a combined insulin dextrose infusion or nebulized salbutamol or a combination of the two um to shift the potassium from inside the cells, hang on from outside of the cells to inside of the cells. Um and that temporarily reduces the risk of arrhythmias um or risk of the other risks of having high potassium. However, you've still got the potassium in your body. Um The hope is with most patients that they're able to metabolize this and it will resolve itself. However, in more longstanding hyperkalemia, um there are other options to reduce uh to remove the potassium from the body. Um That includes calcium resonium, you might consider using loop diuretics or even dialysis in severe cases. Um ok. And just a quick note on recovering from an AK. Um So generally renal function improves over 1 to 3 weeks, as I mentioned before. It's possible that your renal function isn't back to the same baseline level as it was before. Um again, it depends on the patient, it depends on the underlying cause of the situation. Um And generally, you'll notice that the GFR recovers faster than the capacity of the tubules to reabsorb and that for a few days will lead to volume diuresis. Again, another reason why it's so important to monitor the fluid balance in patients with AK. Um ok, thank you. I think that's hopefully not too or not run too much. Um Please, please, could you fill out the feedback form? It would be um fantastic to see your feedback um so that we can improve things for next time. Um Yeah, thank you for for coming. Thank you for watching. Hopefully you've learned something today. And are there any other questions? We had some questions that we wanted to come back to from the pre renal AKI? Um Hang on. Should I send the feedback form? I think I've just sent the feedback form. There we go. Can you please explain volume diuretics again? I'm not sure what you mean. I'm not sure what you mean. Uh My, yeah, we can get the slides. Are we um we should put, we will put them up after the session. Um If you can re type your question about diuretics, not quite sure I understand. In the meantime, I can um we can go back to the questions um from earlier that we weren't able to cover just in the interest of time. Um I'm just trying to find them now. So the very last slide, here we go. So, do you wanna answer that first? I get the very last line. Yes. Um Do you want to shower again? Thank you. See this. Yeah. Yeah. OK. So the reason I included the graph um is just to visualize it a bit better. Um So the G fr is the sort of light blue, pale blue line and the tubular resorptive resorptive capacity is um the less the darker blue line. And that's just to indicate. So, the glomerular filtration rate is how, how much um volume the glomerulus can filter out the tubular absorb capacity is how much the tubule can reabsorb. So for a few days, you will be filtering out more than you can reabsorb. And that means overall, you've got a net diuresis net fluid loss. Um Again, this only lasts for a few days. Um So that's why it's acute um fluid balance monitoring is so important. Um It will resolve itself or should resolve itself over time. Does that make sense? Can we go through the questions I think is that the sbs that you had the S PA S that I had? Um Yeah, we can go through them quickly. Um So I'll just open the first one and there was another question about the slides. Um The slides, I think we have a Google Drive. I'm not sure if we, or, or we'll link them under the event. Um Either one. Yeah, so they, I think we can link them here with the recording and or there will be a Google Drive link and we can get that sent out to you uh The questions that we missed. So I will share this. So a 45 year old woman. So can you go see the pole if I even? Yeah, we can. Yeah, cool. Um Let me just see what's coming through on the pole. Mhm OK. Three. I don't know how many people are. We still have a couple of people. So I'll wait for a few more responses. I'll go through it. I'm just gonna stop sharing actually. OK. So we've got seven responses and I don't remember if he put me out. So 19 0 I'll wait for a couple more responses. OK? So you've got two more and then I'll go through. Yeah, cool. We will do that. Thank you. Yeah, thank you. OK. So we've got a mixture of answers. So I'll share my screen again and we'll go through this SBA. So what we have here is a sort of we would still consider this woman a young adult who has protein in her urine and evidence of fluid overload. So very nice evidence of some edema basically. So what we have here is protein in the urine, a little bit of blood in the urine, no other urine dipstick abnormalities. What is the single most likely cause So the answer to this is focal segmental sclerosis. So let's see what she has. So she has protein urea and she has some fluid overload and periorbital edema. And basically what we're kind of getting up with this question is that she has nephrotic syndrome. And this is about differentiating the causes of nephrotic and nephrotic syndrome. And also identifying um what the most likely cause of nephrotic syndrome is. We said before, when it comes to kidney pathologies, they can cause you to either bleed, have blood in the urine because there's inflammation and damage to the endothelium or there's damage to the filtration barrier, which means that you have protein secreted into your urine, um or excreted into the tubule when you shouldn't do um when you have damage to the endothelium, you get, they get protein in the urine and when you have protein in the urine, um or you have reduced protein in the blood, you basically um lose fluid from the blood and that causes periorbital edema and swollen legs. So you have less oncotic pressure in your um plasma. And as a result, you lose fluid and it escapes from inside the vessels and out of the tissue. So you get swollen legs and puffy eyes. So we know that she's got a nephrotic syndrome and then we have to identify what's nephrotic and what's so based on the pneumonic that I told you um remember not, number three is out, it's a nephritic syndrome. Um number five is out nephritic syndrome and also you don't have any like in evidence of um in the stem of like infection or anything like that. Um So that makes and also syndrome is a cause of nephrotic syndrome. So that's also out, that means that it's either number two or number 41 of the causes of nephrotic syndrome. And in young adults, the most common cause of nephrotic syndrome is FSG S or focal segmental Marlos sclerosis. So generally, so when you have this SBA, you think she was, she's got nephrotic syndrome, she doesn't seem to have any signs or symptoms consistent with. Um and when you look at like she doesn't have any signs or symptoms consistent with any other presentation and then you think she's a youngish woman. Um and the most common cause of nephrotic syndrome in someone of her age would be FSGS. Does that make sense? I can't hear anything? Did that come through? Don't even have that. I was able to hear a 28. Um I think it might be your wifi but are there any questions on that? I pa Yeah. Ok. Ok. Brilliant. So the answer to that was FSGS. So basically, she has a nephrotic syndrome um because she's got prudent when it comes to looking at these five causes. We remember that to differentiate between nephritic and nephrotic syndrome, you can remember it as anything that ends in itis is glomer is a nephritic syndrome and the ones with names are also um cause of glomerulonephritis. So we think to ourselves good pastures is a glomerular nephritis. So it can't be that. Remember. Her nephritis is a neph nephrotic syndrome. And post streptococcal is also a cause of nephritic syndrome. She has nephrotic syndrome, which means we're thinking either number two or number four. Ok. And if we think about her age and the fact that she doesn't have any other symptoms, um or hi other than the Puffy ice swd and eggs and the protein in her urine. And she's a youngish adult. We think the most common cause of nephrotic syndrome in someone of her age is F SS GS focal segmental Felos sclerosis. And that's basically um caused by like sclerosis of again, the glomeru is becoming sclerosed and as a result, um there's damage to the epithelial filtration. So you have protein being secreted into the urine and as a result of protein being se Exced into the urine, you get hypoalbuminemia. So you have less albumin in the blood as a result, fluid moves out of the blood and into the tissues. So you get puffy eyes and snacks. Does that make sense? Um I'm just sorry. Sure. So I can see. Ok, brilliant. Um We'll do the final SB one. She has blood in her urine. So it wasn't, it's kind of like she doesn't have that much blood in her urine. So it's more nephrotic than nephrotic. So she has protein in her urine and also she um it's only a little bit of blood and actually, when it comes to like the different glomerular diseases, they can cause like a spectrum from nephrotic through to nephritic. So some things are way more nephrotic than nephrotic. Um like for example, FSG S membranous nephropathy and will change, they're more on the nephrotic side of things. You'll get more protein in your urine than blood. Some conditions, nephrotic. So they only cause blood in the urine, but don't actually affect the filtration barrier at all. So kind of from this, we can get that she's got high protein in her urine and also her puffy eyes and swollen and legs point to the fact that she's got hypoalbuminemia. So less albumin in her um blood and as a result, she'll probably be losing fluid. Um and that points to it more nephrotic than nephrotic? And so we're thinking this is more of a cause of nephrotic syndrome. And so that's why we, it points to membranous nephropathy and all membranes from nephropathy. And then S GS is more common, more likely to be the case because she's a younger adult and me nephropathy in SBA S is often associated with malignancy. Um So that's why we're thinking more nephrotic than nephrotic. Does that answer your question? In the meantime, I'll just pull start the last. But OK, no problem. Let me start this last question. And we will start holding. So can everyone see this? Mm. Wait for a couple a few more responses. It or you can just go through it for of time. I'll just go through it and I actually to get more influences. But uh oh no, you suddenly had a big jump. Ok. So I'll just talk through this. So we have um sort of young adult man um who has developed what looks like nephrotic syndrome. And if we think about the causes of nephrotic syndrome, um we can kind of rule in um number one and number three, number four and number five, the only one we ruled out FSGS because that caused syndrome. He's also got a cold and flu like symptoms that's kind of pointing to a post infectious cause of g and the timing really does help us to differentiate iga nephropathy called glomerular nephritis. So most you are right because you have develops a or usually to post infection. Um He's post infectious and it's very his the infectious symptoms. And so he's got opathy. Do you are cutting out a lot? I don't know why my wifi is. So it should be good in this room. Sorry about this. I don't know, what can you feel better now? I think it, it's cutting in and out. I've, well, me personally, I understood everything that you said, but I don't know if um everyone else also understood it. Maybe I should, I don't think the strong. My, and we're about to finish. I think it, I'll just, it's not post to how long the call. Yes. Yes. Basically we're thinking nephritic syndrome, which means the one we're ruling out is number two, it's either four or five and it's five because it's only been a day. If it were 1 to 2 weeks, then we might think five. And there would be other, um, we'd have like antistreptolysin o titer would be high. There would be other um information in the stem with regards to investigation findings. So it's iga nephropathy because it's only a day post infection and he's got Nephro syndrome. Was that audible? Thank you, Katrina. The other thing to mention in terms of post streptococcal is um generally, they'll sort of give some kind of indication as to um the fact that it was a streptococcal disease specifically and generally streptococcus doesn't present with um a sort of flu like symptoms and a cough. Um Yeah, take it with a pinch of salt but um generally they give a bit more information for that, just a note on um and the diseases they are very annoying. Um but there's certain and they're not testable at um like it's really, really important to know how to manage an AK I and how to manage CKD because it's obviously very, very common. And um it's really important as a junior doctor to be aware of um fluid balance in patients. I IG nephropathy um because it's post infectious and it's a day after infection and it's a nephritic syndrome. That's why does that make sense? So, if someone has like blood in their urine and they just had an infection, you think it might be IJ nephropathy, um because it's very shortly after their infection and that's a cause of, um, that's called a nephritic syndrome. Ok. Brilliant. Um So basically, it's really important to know how you manage fluid balance in patients, how you identify an ak the necessity of considering the things that affect kidney function. Um That's really, really important to know as a junior doctor throughout our careers when it comes to glomerular diseases, uh like intrinsic renal pathology, it's kind of niche. Um you really need to know it for SBA and that's why when it comes to learning it, I would just recommend learning like little um like you need to kind of look for the hook in the, that will help you remember things um as opposed to it being like really, and the reason that's acceptable is because you aren't actually you don't need to have a depth in depth understanding of it because you will just refer to renal. So there are certain like little bits that help you to remember. So for example, if someone's got, you think to yourself, I need to identify between nephrotic and nephritic, nephrotic is protein, nephritic is blood. If I have a nephrotic syndrome, then I'm thinking to myself. If it's a child, it's minimal change. If it's a young adult, it's FSG S. If it's an older adult with cancer, it's probably membranous nephropathy. And this is a shout out to my um GP partner in fourth year for reminding me of this for basically telling us this is helping us to remember it. And I've got these little speech bubbles on the slide, which I won't go through now because it will take too long. These speech bubbles on the slide are the. Um Yeah, so that, that's kind of how you categorize nephrotic syndrome. Nephritic syndrome is anything that ends in itis. And um there's such an like SBA hooks for different, the different causes of glomerular nephritis as well. So just try and categorize it in your head in a way that makes sense. I'll try, I'll say it again. So kids, minimal change adults is um FSG S yeah. And older adults with cancer membranous nephropathy, it's a bit annoy. Most of these are treated with steroids um or immunosuppressants. So the treatment isn't that different between people and then for sbs, you kind of have to have a, a bit of an understanding of like what the pathology looks like. Um You don't need to understand it, you just need to know what it is. Um And there are some weird ways of remembering when it comes to the nephrotic syndromes. Um Nephrotic syndromes good pastures is generally just like a young adult male coughing up blood and with renal impairment. Um, so I'm just gonna put these in the chart so that you guys can see them. And also it's on the slides. They're all types of nephrotic syndrome. They're all um causes of nephrotic syndrome ones above, of course, of nephrotic syndrome. The other thing I was going to mention in terms of nephritic syndrome and um, blood in the urine is um how you can kind of remember the itis conditions being nephritic ie blood. Um is that if you've got inflammation, you're more likely to eat blood, like in my mind, sort of the inflammation itself is more likely to make blood appear in the urine rather than protein. It, it doesn't quite make sense why protein would be in the urine. But if you think like the inflammation, it's more likely to make your blood vessels and just everything is a bit inflamed. And then that's where you find blood in the urine. There's kind of a way to remember which way around it is. Yeah. So yeah, that's, that's like a nice way of keeping in mind how like it's, if you understand it, it makes sense and it helps you remember it. Um But I've included the details in these little boxes on the slides which will be the how to identify it from an SBA. But I will don't through will take really long. So uh we will put those up. Um And you guys can um email um if you have questions but are there any other questions? I'm sorry. It was cutting out a lot I think is just a bit funny. Uh To be honest, I think it's been fine for most of it. It's just individual moments where I decided to cut out any other questions or we finish and then please do fill out the this um I think in order to get your certificate of attendance, um, we have to fill in the feedback form, but also feedback is generally really helpful for us. Thank you. Time any other questions before we finish? Because I think I don't have anything else to add unless you do them. No, no, I think we've covered it pretty much all. Yeah. So we'll see about putting up the slides and putting up the recording and if you have questions when you see the slides or just afterwards, you can let us know. Ok, in that case, I'll stop recording now, um, then am I able to stop recording? Uh.