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Right. Hello everyone. Um Thanks for joining today. So we'll just give it maybe another minute or so to see if anyone else joins and then we'll get started. Ok, I reckon as we've got quite a bit of content to cover, we'll just get cracking now and then we exactly, we can um we can shout the recordings and if anyone else wants to join in at a later point, it'll be fine. So, um welcome everyone. So this is our second session in our final series. Um So today's session is gonna be focusing on the kidneys. Er, so Renal today and, er, Doctor Tess Angus has kindly um, volunteered to do the session. Um, so if we just move on to the next slide. So, um this is a series run by Thursday 15 and it's sort of a subgroup of the med teaching, which is the overall organization and basically we're gonna be running um, final focus sessions for the next uh few weeks, um trying to cover all the main areas within the sort of MLA exam as that's what I think most medical schools are going to use um to base their finals. Um curriculums on. Um, so hopefully it should be very relevant and very useful to your upcoming finals. Um, so in terms of how the sessions actually run, er, what we'll tend to do is right at the beginning, just run through 15, um, M CQ questions and you'll get 15 minutes to do these. So I think tests will keep time and make sure you're moving on at the right time and then at the end, we'll go through the answers and sort of the subjects related to the question. Um And yeah, so just keep an eye out for further sessions. We'll be posting details of those um on Instagram, on Facebook. And if you sort of fill in any feedback forms, you'll um get automatically um notified whenever we're running a session. So without further ado I'll let tess take it away. Brilliant. Um So yeah, hi guys. We're gonna cover kidney specifically today. I know the title of the event says Renal and Urology. We're gonna cover urology in a separate session because we thought there was enough in the curriculum to cover just Renal today. Um These are the topics we're gonna cover. So we're gonna look at sort of presenting complaints predominantly and that will cover the um conditions that are on the right. Um The first thing we're gonna do is sort of a 15 minute timed mock if you will, don't worry about getting the answers right, because we're gonna go through sort of explanations for all the topics and we're gonna give you, I think a minute, um, a question. So if you just grab some paper, um, and, and you can just write down your answers. Ok. So if everyone's ready, I'm gonna start the timer now. So don't, well, I'm not starting the timer. Um, so we're gonna go through all the questions, write down all your answers and then we'll go through all the answers afterwards. OK. OK. So we're gonna start now if everyone's ready. OK. We're gonna move on to question two now. Sorry, Tess, I've just got a question in the chat just relevant to the, um, question. So it says here when there is a value in brackets, uh, is that their previous value is the question I'm just like that was me explaining that that's all they need to. Oh OK. Right. So. Oh, apologies, sorry. OK. We're gonna move on to the next one. OK. Question four, question five, question five, question seven, question eight. Yes, question nine, question 10, question 11, question 12, question 13, Western 14 and finally question 15. OK. That was the 15 questions. Well done. Everyone that tried to answer them. Hopefully there was a mixture of easier and hard ones in there. Um, I remember in fifth year I found Renal very hard, um, and just a tip for all these, um, Thursday 15 talks that we give whenever there was a topic last year that I didn't understand from one of the, um, talks or that I knew I wasn't able to answer questions on, I, then that week would go on past med, read up on sort of the past med textbook and answer sort of 10 to 15 questions again on those topics until I was really happy, um, that I sort of consolidated the learning from the, from the talk. So now we're gonna go through each question in turn, look at the answer and then do a quick sort of topic summary. Um After each question, it would really be great if you guys can interact in the chat. So I'll put up each question in turn and just put our answer, you put in the chat, that would be really helpful and then we'll discuss what the correct answer is. So, question one, we've got our 68 year old with pneumonia on antibiotics. Um, and he's not passing urine. I, what did people put for treatment for this patient's reduced urine output? Any answer? It doesn't have to be correct. So we've got, we've got a B, we've got an E any other votes. Another B excellent. OK. Um So for this question, um, it is actually b so we've got to think about what's, what's going on here. So we've got a patient that's got, um, not passing urine. They've got known infection, possibly sort of a sepsis picture. They've got a low BP. And if you look at their creatinine before it was 81. Now it's jumped suddenly up to 230. Ok. So that's an AK is what we're looking at. Um, and the most basic treatment for an AK I is IV fluids. The person that put e was probably thinking, um, well, we'll think of, think about ye is an option later. Um, but basically this patient is not producing much urine. So it's not that there's a problem in the bladder. They're not producing urine. Ok? Um They're not quite sort of super septic if you look at their temperature, um the heart rate and stuff and they've only just been started on the antibiotics. Um Plus the C RPS improved. So I wouldn't change, I wouldn't change the antibiotics right now if the inflammatory markers are improving. Um And we can talk about whether we just sort of hold antibiotics, dialysis or catheter in, in a moment. So, has anyone got any idea what stage of AKI that we're looking at? I think this is a stage 12 or three, two. Ok. Lovely. Ok. So we'll move on to the next slide. Um So an acute kidney injury is a rapid and sustained decline in kidney function causing oliguria, which is a reduction in urine output and a rise in the urea and creatinine. Ok. Um It can be broken into three stages um based on how much the creatinine's increased. Um or by how much urine output they're having. Ok. Um It is a good one to learn. It comes up both in Ay and um like MC Qs. Um and also on Ward rounds, consultants seem to love that question. Um The onset has to be within the last seven days and you usually say you have to see a sustained um rise in your creatinine for 24 to 48 hours, but usually we don't sort of repeat it before we treat it. Um we treat the underlying cause and IV fluids are super important. Ok? Or just increasing the oral hydration, we break down the causes of acute kidney injury into prerenal stuff that happens before getting into the kidney renal. So, intrinsic kidney problems and postrenal. So things in the ureter bladder, et cetera. Can anyone give me examples of any of these like sort of any causes that would fit into these categories? So, any prerenal or renal or post renal causes that anyone can think of. So someone suggested prerenal dehydration, sepsis. Absolutely. So that was probably what was happening in question one, um hypovolemia for prerenal and then um someone suggested obstruction for postrenal. So that's where the catheter would come in real handy. A catheter can also just help us monitor urine output. But it's not gonna, if it's, if it's a prerenal thing like in sepsis, it's not gonna treat, treat the fact that they've got an ak whereas in obstructive, it might help for renal, we've got someone suggesting interstitial nephritis, acute tubular necrosis. Uh and then we've also got prerenal renal artery occlusion. Excellent. Ok. We're gonna move on now. Um So just a brief sort of reminder of what the kidneys look like. So when you zoom down into each nephron, you've got um your efferent efferent arterials, basically the blood supply to each Nephron and that's wound around um your glomerular structure. Um and your um tubules. Ok. So stuff is filtered out of the blood into the, into the whole ne into the Nephron structure of the glomerulus and then can diffuse back to the tiny capillaries from the tubules. Um This is just another image showing that um and water is gonna also travel in both directions. Eventually we get our urine collecting and the collecting duct. OK? Um So, as you guys have said, um you guys got, gave some really good examples of the different causes of AK I um basically prerenal is anything that is gonna decrease blood flow to the glomerulus. OK. That results in decreased filtration. Um because there's a a decreased pressure gradient. So we have a raised urea and creatinine. That's because they're not being filtered out entirely. And also um because urea can then be reabsorbed later on. So it's gonna sort of increase it even more than it is OK. And then overall we get then less urine being produced. OK. So, examples of things that cause blood loss, vasodilatation or any kind of blockage in the arteries leading to the kidneys. Ok. Um renal problems are problems actually in the kidneys. So that can be at the glomerulus like a sort of a glomerulonephritides that's inflammation or you can get acute tubular necrosis in the tubules or acute interstitial nephritis in the surrounding tissue around the nephron. Um ok. Now, a way to tell the difference between prerenal and renal is to look at the urea to creatinine ratio in prerenal. There's nothing wrong with the kidney. So it's, it's normal reabsorption of urea is um is gonna sort of continue working. So you're gonna have a lot more urea staying in the body compared with the amount of creatinine that your body is keeping. Whereas in renal, you've got a problem with the kidneys, the absorption mechanism is not working. So actually, you're getting, you're not gonna reabsorb sort of extra urea II, it's gonna, it's gonna stay the same um as your creatinine sort of filtration rate. Ok. Your postrenal um causes are anything that's causing obstruction. So stops the, the normal sort of relief of urine into the um ureters and bladder. So you've got your Luminal issues, wall um in inside the tubes, you've got your wall issues, mural and you've got your extrinsic things. So things putting pressure on the post renal system. Ok? There's also things like drugs, anticholinergics and sometimes if someone's catheterized, it can be as simple as it being occluded um by clots or something like that. And so it's really good to structure your arms like this in an ay kind of situation. Um Examples of anticholinergics are things like amitriptyline and calcium channel blockers. And we're gonna go more into these r problems in a second. OK. Um Now we're gonna move on to question two. So what answers do people put for? Question two? OK. So we've got a suggestion of D Yeah. One, someone else suggesting B OK. It's OK. Um So in this case, um the answer is acute interstitial nephritis, which we'll talk about in a little bit. Um But I just wanna go through why it's not the other ones. Um So meningococcal septicemia would probably look very similar picture wise. Um But if you look at the inflammatory markers, they're much improved, their heart rate and BP are stable. Um They're only, they've got a mild paraia. Um And the, the rash has developed several days into the sort of treatment period. It would be unlikely for them to suddenly have developed septicemia if they're on the right antibiotics for meningitis anyway. Ok. Antibiotic, allergy. Um, not, not an unreasonable guess the joint pain. Um The fact that they're cardiovascularly stable and the urine output makes it less likely also the timing of the rash. So if you've never had a certain antibiotic before your, your, um, allergic reaction is most likely to happen sort of the second time. Um, you have the antibiotic. If he's been having it, he even has been having it for several days without any problem. It would be unlikely to suddenly develop an allergy, although not completely impossible. Um Eczema is not the right kind of picture for that. Um And um we'll talk about why it's not acute tuber necrosis in a second. So, key things to remember here are, are rash, joint pain. Um And I think eosinophilia as well. Um So if we move on to the next slide, uh causes of um renal AKI. So acute interstitial nephritis, it's as we said, inflammation of the interstitial and it causes this classic triad of rash, eosinophilia and joint pain, which is what we saw in the previous question. Um It's usually caused by drugs. So long term NSAID use, penicillin, acyclovir was in the previous question and diuretics. Um And then I've put some other potential causes on, on the slide as well. It can other symptoms it can cause include hematuria, a fever, um sort of confusion or other mental status changes, nausea and vo uh vomiting, swelling and and also fluid retention that causes weight gain. Ok. Um sa similar condition but slightly different is acute tubular necrosis. So, instead of the interstit the surrounding tissue, this is now the actual tubules and the cells, the tubular cells um die for various reasons and that causes tubal blockage and a reduced pressure gradient at the glomerulus. Ok. Causes can be ischemic. So, confusingly, you can also get this in sepsis and hypovolemia, but it's a different sort of pathophysiology um and any injury to the renal vessels and then also anything that causes nephrotoxicity. So aminoglycosides acyclovir again. So a bit of a red herring in the previous question lead uh contrast for scans and also rhabdomyolysis. Ok. So the things sort of to recognize in a question would be a renal AKI. So you've got that ureter creatinine ratio less than 40. Um And key thing to remember is these muddy brown casts that you see in the urine. So that's sort of debris from the tubular cells. Ok. Well, than that's very high, highly suggestive of acute tubular necrosis. And then the last thing that can cause a renal AKI I is the glome sorry glomerulonephritides. They can cause a here but they actually more usually present as a nephrotic or nephritic syndrome. So we're gonna cover them a little bit later. OK? Um Feel free to pop any questions you have in the chat. Um And if I don't see them Vicky will let me know. OK, so we're gonna move on to question three now. Um So this is asking what intervention is best for this patient as well as catheterizing them. Anyone got any suggestions of answers they might give? Ok. I've got some votes for e thank you guys. OK? Someone suggested D en lovely. OK. Mostly people are going for it looks like. Um So Yes. So, in this question, um, it's ask about interventions. It's very important to, um, sort of, is it asking for investigations or interventions? That's your first sort of thing to look at? I always read the, like I would suggest always reading the last, the actual question before you read all the, the paragraph. Ok. So here we've got an elderly gentleman, he's been treated successfully with antibiotics. Um, and he's, you know, he's quite at risk of delirium with his dementia and his other comorbidities. If you look at his obs, he's stable at present. So I wouldn't be restarting antibiotics and looking at his BP, he doesn't particularly need IV fluids at the moment. Um However, he's not passed any urine for eight hours. Ok. Um, so you guys can look back and, and figure out what ak I stage that was and he's also had a really like sort of pellet like stool recently. Um, so we're already thinking, oh, some seems like an AK I and maybe some constipation going on here and his medications. You see, he's on, um, regular morphine and also breakthrough morphine. Um And on examination, he has suprapubic tenderness and he has, um, he has retention on his bladder scan. So we've got a patient in retention that's causing a post obstructive at and they appear to be constipated. So, we're relieving the obstruction already with the catheter. But what else can we do? And the answer here is prescribing a laxative. Um So he might need, he might need some help with IV fluids, although he's eating and drinking well, at the moment, we need to see his bloods for that. Um Definitely not gonna give him LORazepam at the moment or restart the antibiotics. Cystoscopy can be inappropriate. Um uh investigation for post um renal AKI um but at this point, we've got a more likely cause of constipation. So treating that is more important. OK. And if we go on, so this is question four and then we're gonna go through question three and four together. Has anyone got any answers for? Question four? What medication change would you guys make if you were faced with all of this information, any answers or should I just move on to the next slide? Ok. Um So in this case, uh my recommendation would be to hold Candesartan. Um We're gonna go through that. Why that is in a moment. Um But again, we've got a patient who's got an AKI here, um, the normotensive. So stopping the antihypertensive isn't gonna actually be a problem, but they are on a lot of medications that you need to be careful with in AK and in two sides time, we'll go through why I why this patient only needs to have the Candesartan held? Ok. Um So if we just quickly look at this overview of treating AK I and then we'll talk about the individual drugs. Um So in prerenal, you want to treat the underlying cause. So, antibiotics or transfusion, et cetera, and you wanna increase flow to the glomerulus with increased fluid input, whether that's oral or IV in renal. Um because the sort of atn or a in usually have a, a drug cause you probably want to stop anything that's contributing um or address the cause of ischemia and A TN keep them hydrated and then definitely speak to the renal team. Um, and then postrenal. So we mentioned you might want to do some examinations. Pr exam is the most simple one can identify constipation and BPH, you might send them for a CT or an ultrasound cystoscopy if you're suspecting malignancy or urodynamic testing, um, if they're having problems with the blood, avoiding the most important part of the treatment, if there's an obstruction is to relieve it. And that might involve speaking with urology and then you can stop any contributing medications like your um, anticholinergics and, and make sure catheters are working properly. Ok. So you treat the underlying cause, make sure they're well hydrated but not overloaded. Um And you look at the medications to see if you can make them any better. Does anyone have an acronym for the drugs that you might hold or reduce if renal function is impaired? And there's a, there's a couple of different acronyms. Does anyone have one that they use for r no drugs? Well, things to stop. Someone said damn. Yeah, so stop the damn drugs. Oh, damn. LA. I haven't, I haven't heard of that one. I wonder if that overlaps with my one. Um, so I know there's, yeah, stop the damn drugs is what I've heard before. I, in my med school we got taught one called Diamond, which just has a couple more drugs to consider in it. And that's why I prefer it. Um, so diuretics you'd usually hold them. Although obviously the heart failure, patients present a bit more of a problem. Um That's because they can cause an AK in the elderly by sort of reducing your blood volume. And they can also contribute to acute interstitial nephritis. Iodine contrast can still be given depending on the EGFR, but it needs to be done cautiously and usually a fluid virus is given before and after to sort of flush it out and minimize damage. OK. That's cos it's nephrotoxic um ace inhibitors and ARB s like the Candesartan, we would hold as long as it's safe to do so. Um And that's because they dilate the arterioles that are leaving the glomerulus um which drops the pressure gradient. OK. And then I put under a there's also aminoglycosides that can cause a TN. Now, in the question earlier, Metformin was one of the options but the EGFR if we go back the hall was 74 and we don, we don't need to hold it if it's over 30. So I was like that one was wrong. Um We would hold it if it's less than 30 because there's a risk of lactic acidosis if the renal function is impaired opiates. Um If the EGFR is sort of significantly reduced, we'd switch to oxyCODONE or if it's even more reduced, the palliative team might suggest alfentanyl. Uh That's because opiates are renally excreted and there's a risk of opioid toxicity. Um But that's less. So the case for oxyCODONE and a fentaNYL. Um In our question, the EGFR wasn't so low that we needed to switch the morphine to oxyCODONE. Um And then nsaids, we hold them all because they're nephrotoxic apart from um patients that are on 75 mg, aspirin once a day, that's sort of a cardioprotective dose. And if at all possible, it's, it's best to keep that going. OK. Now, the reason NSAIDS um uh sort of problematic is that they constrict the arterioles that supply the glomerulus, glomerulus. OK. Um And then the last D in diamond is dos so disease modifying drugs, they probably just need closer monitoring um because they have a very narrow therapeutic index and there's a, a big risk of toxicity with them or that they might not work. OK. Um So in, in the question, in that uh that we had um question four, I think it was uh we only actually needed to hold the Candesartan for that patient. OK. OK. So um oh, this is just another other acronym. Um to remember nsaids and ace sort of what's what's being constricted or dilated. Um So prostaglandin dilates the afferent arterioles and then says, work against prostaglandin. So that causes constriction. Um The enzyme ace constricts, the efferent arterioles. Um and therefore the ace inhibitors cause dilatation. Um That's just a nice little acronym to remember it by. Um So if we move on to question five, um, has anyone got any suggestions of how we might treat this patient? So they've got, they're being treated for an infection on antibiotics. Um and they're pretty stable. Um But on their bloods, they've got an EK I obviously these race inflammatory markers and the potassium and, and ph I think hopefully everyone will agree. They're out of range in the exam. Sometimes they give you reference ranges, sometimes they don't. So sort of important things like potassium, I would recommend you learn what's normal and what's not normal. Um Oh, you're welcome, Zane. I'm glad that was helpful. I learned that last year from these talks. So that's good. Um Anyone got any suggestions for question five? Give you a clue. The answer is not just monitor and hope for the best. Someone suggested C and Lara's absolutely on the money. The answer is C. Um So we'll, we'll go through why that is. But the important things here are looking at the ph, the potassium um and the ECG OK, to see if we need to treat them. Now, why have they got this hyperkalemia. It's because they have chronic kidney disease. So chronic and, and both and acute kidney injury, they can both cause hyperkalemia. It's a really important condition to know how to treat because it can cause life threatening arrhythmias. Ok. Um Lovely. Someone's even given an explanation for their answer. See because of the potassium. Yeah, absolutely. So if we go to my next slide, um I like the acronym dread for hyperkalemia. Dread is like a heightened state. So high potassium. Um And that's just the causes of hyperkalemia. So, drugs, it's really, really good to remember them. So you can recognize them in, in exams. Renal failure is obviously what we're talking about here. Um Addison's causes raised potassium. It can sometimes just be sort of lab error. So the sample hemolyzed, we actually had a patient literally yesterday on my ward where we had a potassium that was quite high and we started panicking, we sent another sample and it was absolutely normal. Um So it's just about um thinking about your artifact option and then in DK, it can be raised as well. Um So for the management of hyperkalemia, if I go back, um this patient had a potassium of 6.3 um if it was less than six, we would monitor and think about any causes in reversing them. But as it's above six, in this case, we need to treat and the mainstay of treatment is giving them insulin which drives the potassium into cells. Um and that's given along glucide glucose. So they don't become hypoglycemic. Um You can also consider salbutamol in, in a nebulized form because that helps drive potassium into the cells. Um and calcium resonium which binds potassium and makes you sort of excrete it. If they have E CG changes or really high potassium 6.5 or above, you need to give them um some sort of calcium um calcium compound to protect the heart from arrhythmias as well as giving your insulin glucose and your salbutamol. Um So the calcium can either be in the form of 10% chloride, calcium chloride or 10% calcium gluconate. But you need different milliliters to achieve the same sort of minimal when you're giving that. So it's really important you follow your trust guidelines. Um In my trust, we do 10 mils of calcium chloride. Um But you can also give 30 mils of calcium gluconate. You don't want to sort of underdose or overdose them. OK. This is my trust um sort of algorithm. I appreciate. It's quite small to read, not very pretty. Um But it sort of just tells you what to do. And the fact that the calcium resonium or the sodium xia silicate can sort of remove potassium from the body. OK. Um So my next question for you guys is what ECG changes might you see in hyperkalemia? Yes, there's more than one correct answer. So throw anything out there? Ok. So we've got some to tented T waves. Um, we've got supraventricular tachycardia. Um, someone said a broad cr us some really good answers there. Really good. Ok. Um, so I've stolen some pictures off the internet. Um This one just shows sort of in a very simple form the changes you can get. So as your potassium gets worse and worse, you're gonna get more changes. So you first get your peaked or tall tented T wave. Um And then you could get other changes like a wide pr interval, widening of the QR S. Um then the loss of the P wave and then this sort of sinus sinusoidal wave. Um My next slide sort of shows that in a little bit more detail. Um So the first thing you'll see is your total entity with, then you lose your P waves and you get this wide QR S and eventually you can get ventricular fibrillation. So it's not typically a supraventricular tachycardia. It's, it's, it's ventricular, which is understandably a little a little worse. Um And if you look at that um image on the top, top, right? It just shows how the P waves can sort of become flat, more flattened, wider and then completely disappear. OK? I think that's everything for hyperkalemia. If anyone's got any questions, pop them in the chat, but otherwise we're gonna move on. So, question 60 no, II lied. Mhm We have another high potassium apologies. So this is, I think this is the same patient, but now he's had three rounds of treatment for high potassium. Ok. And the ph people can see is a little bit worse and the potassium is still considerably high. Ok. He's got a low CO2 cause he's probably trying to breathe it off to reduce his acidosis and his ECG now has changes. So what do we think we need to do now Getting lots of these suggestions and I would personally agree. So, d absolutely. Um does anyone know the acronym that we can use to remember why when we would use acute dialysis? Ei ou Yeah, you guys, you guys know all of this? Perfect. So we don't need to cardio about this patient yet because they're not in yeah, a dangerous arrhythmia. They've just got the, the tall 10 to T waves. Uh There's no point repeating the insulin X rays. It's clearly not working. Uh So, and we hope as part of this, they've already had the sub nebulizer. So the treatment is not working. We now have persistent hyperkalemia. OK. So the next thing, the only thing we can do next is the acute dialysis. Um So like you guys suggested it's the EI ou acronym. So, acidosis persistently below 7.15 would be an indication here. We've got 7.14. So they, they meet that um electrolyte abnormalities in like a hyperkalemia that's persistently. Well, either above 6.5 or above seven. Depending on the guidelines, you look at certain drugs, um, poisoning would be an indication for acute dialysis. And if a patient's got refractory pulmonary edema, um or symptomatic uremia, those are also two very important in indications for acute dialysis. Ok. Moving on now, we've got another patient with reduced renal function. Um but a slightly different history now. So patients generally tired, got a bit of back pain, fairly stable and looking at the bloods, there's some changes. So what investigation would be most useful for compounding the diagnosis? Um I'll also accept any suggestions of what the diagnosis might be. So I got a suggestion for C so suggesting myeloma C Yeah. Ok. Looks like people are thinking it's uh a multiple myeloma picture um which is absolutely the case. So we've got tiredness, back pain, hypercalcemia, got anemia and kidney dysfunction. Um and also an uh well, it's not just anemia, sorry, it's pancytopenia. Ok. So we think this is multiple myeloma. Looking at the um other questions repeating the EGFR would be for looking at sort of chronic um kidney function that's not gonna help us right now. Confirming the my myeloma. Um blood film was usually for other types of um blood disorders, serum electrophoresis. Um is an investigation for multiple myeloma that's usually used to rule it out. So it's used as part of a a myeloma screen, but it where you can't actually confirm the diagnosis without a bone marrow biopsy. Um and the CT urogram is entirely inappropriate here because this is not a um obstructive cause of um kidney problem. This is um a picture that's consistent with multiple myeloma. Ok. So in multiple myeloma, you have this over proliferation of the plasma cells and you end up with a large amount of a single type of antibody. It's called multiple just because it affects multiple areas of the body. Um and your main features you get from this are crab. So high calcium renal failure, anemia and bone pain. It's really important when you see that sort of crab um for symptoms or for features that you recognize multiple myeloma because it's quite a common one in exams. Ok? Um Basically, the plasma cells are crow crowding the bone marrow that stops you producing your other cells. You get your pan pancytopenia and then the paraproteins, the immunoglobulins cause damage in the kidneys, active and activation of osteoclasts. That's how you get all your different symptoms. Um the initial bloods um are on the screen. So esr and plasma viscosity in addition to the ones we already had and then you're gonna do serum protein, electrophoresis and urine bent strains, protein test to sort of screen for it. That's looking for those abnormal immu immunoglobulins and then diagnosis with a bone marrow biopsy. Um Plus imaging for bone lesions. Ok? And treatment is with chemotherapy. Um and even and transplant if you're fit enough ok. Other treatments can, can include radiotherapy for bone pain, bisphosphonates to suppress osteoclasts and orthopedic surgery if needed. Ok. Uh So, yeah, so just for everyone to remember, multiple myeloma comes up, I would say, um, my unit came up most years in our osk and it's a really easy M CQ question as well. So if we move on to question eight now, ok. Anyone got any suggestions of what's causing the symptoms? Ok. So we've got a suggestion of E OK, another vote for E Yeah, absolutely. So, um we just need to look at what's going on here. So we've got what sounds like edema, tiredness, shortness of breath, which if you look at the hemoglobin could be due to anemia, uh frothy urine, which is suggestive of protein urea and uh itchy pru pruritis. And then in the history, there's diabetes and sl E which can both um lead to chronic kidney disease. You've got hypertension. Um and if you look at that egfr it, it's not sort of an acute change. It was low before when it was done and it's low. Now, same for the creatinine. So we've got a chronic change in your kidney function and anemia um, and symptoms that are consistent with D. So that's why it's the most likely cause it's less likely to be heart failure because the B MP is normal. Um given the combination of symptoms, a simple lymphedema is less likely, um minimal change disease we'll talk about a bit later, but it's, it's very unlikely in someone of this age. Um, and with the sort of itchy and diabetic and lupus background. Um, and yes, they do seem to have symptomatic anemia, but that doesn't explain the entire picture. So it's better described by the chronic kidney disease. So, chronic kidney disease is a sustained reduction in your kidney function over at least three months. Um, it unfortunately tends to be permanent and progressive. Um, and it's diagnosed by looking at either the egfr over three months or albumin albuminemia over three months. So, if they've had and EGF are less than 60 or their urine album and creatinine ratio of more than three repeated or three months apart and it's sustained low. That's cancers. Chronic kidney disease can then be further classified. Um I think it's the KD go guidelines um into sort of different stages. I've put them up here. Um It's quite small, might be worth learning for your exams, but I would learn the AKI I stages first and the colors here. So the green, yellow, orange, um and red is about your, I think it's about your five year chance of progressing to end stage or something like that or your mortality symptoms. Unfortunately, patients can be symptomatic uh asymptomatic, sorry. Um or they might have these general symptoms that we saw in the, the previous case. Ok. Um, but it's important to have to recognize if you have a patient where their EGFR is declining rapidly, it's called accelerated progression. So that would be if the EGFR drops by a quarter, um, within 12 months or so 25% or, um, it, or by 15, like the absolute value drops by 15 or more within 12 months. Ok. Um, so there are many different things that can cause d um, most sort of commonly you've got your diabetes and your hypertension. Also certain medications, the glom nephritis conditions that we'll talk about in a bit congenital things like polycystic kidney disease and also autoimmune conditions like lupus. So the patient in the question had lupus and diabetes. So it's unsurprising they got d unfortunately will cover these individual causes in a, in a moment. But first, we're gonna talk about um, sort of managing CKD and what complications can arise from KD. Ok. So you're gonna look at the urine and they're using these for your diagnosis. You're gonna investigate causes with a renal biopsy or ultrasound. And then you're gonna look for any complications. Um, by doing various blood tests, we'll talk about that a little bit more in a second management. Lifestyle is super important. So diet exercise, smoking cessation can really improve outcomes. Um, and cardiovascular disease is the number one cause of mortality in patients with CKD. So it's really important to m manage their BP, their diabetes, um, get them sort of generally more well and that will help the kidney disease as well. Um Ace inhibitors and SGLT two inhibitors, specifically Dapagliflozin have shown improved outcomes and their BP target is less than 130 systolic if they've got d um but it's really important to monitor the potassium. If you start them on an ace inhibitor, all patients um with C KD should also be started on atorvastatin. Ok. And eventually the patient might need renal replacement um or even a transplant. Um So now I think, yeah, we've got some questions. Now, I think too about the consequences of COPD or complications. So if we just go through both of them and then I've got a summary slide. OK. So what abnormality is there in, in this patient's bloods? And what would you guys suggest we do about it? OK. We've got a suggestion of C that would be IV iron. See because of the ferritin. OK? Anyone think it's NASI got to vote for B OK? Feel mean cause that was a bit of a trick question. Um The answer is, is C um But ultimately, they are gonna need B after C OK. So this patient has known C KD um which is consistent with their creatinine eg fr and the other abnormality on these bloods is that they have a microcytic anemia with an iron deficiency. Um Now, the treatment for anemia of, of renal disease is the E PR injections. However, you should always correct the ferritin first. So that's why the IV iron infusion is correct. OK. But after that's corrected and they've got a normocytic anemia, then you would go for the erythropoietin. OK. Repeating EGFR is pointless. We already have a diagnosis of D so they're just gonna have their bloods once a year. Um serum electrophoresis would be for a multiple myeloma, which we don't necessarily think this patient has and a renal biopsy would be to look at some of the underlying causes of CKD. But here we're just interested in what do we do about this anemia? Ok. Moving on. Sorry, this is slightly ugly slide. Um Basically, um this patient who has C KD is feeling tired a bit constipated has muscle weakness. Um And the question is, what are the bloods most likely to show? Yeah, in these kinds of questions. Um I figure out the bits I do know um and then narrow it down based on that. So I, if I knew that it was a high or low calcium that would already get rid of two options. If I knew I expected the Vitamin D to be doing that would also narrow it down. Um That can get you closer if you're not sure about the whole answer. OK. In the interest of time, I'm gonna move on. So the answer here is c um we're gonna talk about it um in a second, but basically, this is a patient that has secondary hyperparathyroidism because of their CKD. And we'll talk about why the bloods look like this in a moment. Um So this slide is very busy. It's just a summary of some co common important consequences of KD. Feel free to screenshot it or if you fill in the feedback form at the end, I think you get access to the slides. Anyway. Um That, yeah, basically you've got your hypertension and edema. So you're gonna treat that with antihypertensives and diuretics. Um your cardiovascular disease, which you're gonna do by managing your BP, diabetes and your cholesterol. If they go into metabolic acidosis, they'll need sodium bicarbonate hyperkalemia. We've talked about anemia. Um They aren't, the kidneys produce epo and in chronic kidney disease, they don't produce as much. So, we might have to replace that in order to stimulate um red blood cell production, but iron needs to be replaced first. Um They may get secondary or tertiary hyperparathyroidism. Um And that may sort of lead on to renal bone disease or d mineral bone disease, which is where you get a change in your bone turnover. Um And that can basically be treated by reducing your phosphate intake or binding your phosphate, taking in active forms of Vitamin D because you're unable to activate it normally. Um And then if it's a tertiary hyperparathyroidism, you can consider parathyroidectomy. Um Let me just check if I wanted to say anything else. Um For anemia, it's best to avoid blood transfusions as they can sensitize the immune system and if a patient then goes on to need a transplant, they are at risk of rejection. Um Basically, when you've got hyperparathyroidism, that's gonna stimulate your osteoclasts. And if you don't have enough calcium to keep up with that, you get osteo malacia, then the osteoblasts try and keep up with the osteoclasts and create loads of new bone, but it's not properly mineralized because there's not enough um calcium. So then you get osteosclerosis. Um and then osteoporosis can exist sort of in tandem with renal bone disease, which would need bisphosphonates, but it's not part of the sort of syndrome. Ok. Um The other thing is if you're an in endstage renal disease as well as renal replacement therapy, et cetera, you need special dietary advice, but that's sort of beyond this talk today. Um So if we look very sort of specifically at your parathyroid um hormone, now, this is a topic, I have to relearn every time I look at it drive around the end. But essentially, normally, when you've got low calcium that stimulates your parathyroid hormone to increase levels. And in response to your parathyroid hormone, you get increased burn to ever releasing calcium from the bones. You get increased calcium reabsorption in the kidneys and phosphate excretion. And you get increased absorption of both calcium and phosphate in the gut, which all works to raise your calcium. And when you have raised calcium that um gives negative feedback to the para hormone and reduces the levels. That's when it's all working in primary hyperparathyroidism you have, for some reason, you've got this raised parathyroid hormone. It's usually due to an adenoma. Um, because your sort of systems working that causes raised calcium and low phosphate. Ok. But the, the parathyroid hormone sort of being produced separate to the system, it doesn't listen to feedback in secondary hyperparathyroidism. You've got low calcium. That could be because of your chronic kidney disease. Um or that could be due to just a Vitamin D deficiency. So, Vitamin D helps you absorb calcium and phosphate in the gut as well as reabsorbing it in the kidneys. Um sorry, absorbing calcium. But in chronic kidney disease, you're not a, there's an enzyme sort of missing in the kidneys or not enough of it that activates Vitamin D So you end up with low Vitamin D levels in D but you might also just have it if you live in the UK. So you've got your low calcium because of your other causes. That's gonna raise your parathyroid hormone in response, um which will try and increase your calcium levels, but probably unsuccessfully. Ok. Um And then the phosphate might be high in kidney disease because it, the kidneys can't excrete the phosphate or if it's just a Vitamin D deficiency, it might be low because you're actually able to excrete lots and that's stimulated by um your parathyroid hormone. Ok. Tertiary hyper parathyroidism is when you have your secondary hyperparathyroidism for a long time, usually an end stage renal failure and that causes hyperplasia. So, growth of the parathyroid glands. So now you have raised parathyroid hormone coming from these massive glands and there's actually so much now it's raising the calcium. Um and it's also raising the phosphate because kidneys can't excrete it. Um and it's being absorbed in the gut. Um So if we go back to our question, we've got low calcium because of the CKD stimulating high parathyroid hormone. We've also got low Vitamin D because of the D and high phosphate because it's not being excreted by the kidneys. I hope that made sense. Um This is how I understand it. So I hope it makes sense to everyone else. Um If we move on now, so question 11 is about patient receiving dialysis and sort of what a common side effect might be of dialysis. So all these options are actually possible side effects of dialysis. But it's about what, what are we sort of most likely to see. So we've got an E and we've got an a um someone said in query infected line. Yeah. So in this patient having hemodialysis, um the only option that's sort of not an option here would be Steal syndrome because that's only seen with a v fistulas and this patient has a tunneled line. Um All the other ones are an option so the line can get infected. Um And you can get blood clots because that this patient is on Apixaban. So it's less likely and disc syndrome can happen. But actually, far more commonly patients just feel a bit nauseous the first time they have it. Ok. Um So if we move on to here, so this is just a breakdown quickly of hemodialysis and peritoneal peritoneal dialysis. We use long term dialysis for CKD stage five, end stage renal failure. And we choose the type depending on their comorbidities, lifestyle and what they prefer. Um, hemodialysis involves um a machine in hospital and you have to come several times a week for example, four hours, three times a week. And it's either done via a tunneled lines or a long line or an A V fistula where they do a connection between the artery and, and venous supply in one arm. Ok. It's very important that the patients get anticoagulation due to the risk of clots. Um And there is a, there's always a risk of infection with, with stuff going in and out of the body. Of course, steal syndrome is where there's inadequate blood flow to the rest of the limbs to the rest of the arm distal to the fistula. So in the question, the patient didn't have a fistula, they had a tunneled line. So that was less likely. Um You can also get high output heart failure. Um, if you've got a fistula because basically blood's going very quickly back into the venous system going back to the heart very quickly. Um and increasing its preload, which causes over time hypertrophy of the heart. Ok. Someone else put dis equilibrium syndrome, I think as their answer, which is not, not a bad answer. Um And and can definitely happen in hemodialysis. Basically in hemodialysis, you have rapid removal of urea which is good, we want to get rid of it but it happens can happen slightly too quickly for the body. Um and the body does not like it. You get a shift in the osmotic gradient between the brain and the plasma resulting in cerebral edema, which causes neurological symptoms, like headache, nausea, blurred vision, confusion, usually self limiting, but then can progress to seizures, stupors and stupor and death. Um So it's really important to recognize if a patient is becoming unwell with this. Ok, peritoneal dialysis. On the other hand is where you use the peritoneum as a semi permeable membrane to filter blood. So you add a special dialysis solution that has dex rays usually into the peritoneal cavity um via something called a tens cough catheter. And then you just have diffusion of solutes from sort of across the peritoneum membrane. Ok. This could either be done overnight um by machines or pushing fluid in and out that's called automated dialysis or the patient can change the solution a few times a day, sort of keep it in there for a few hours at a time that's called continuous ambulatory peritoneal dialysis. Um with the peritoneal dialysis, there's a risk of bacterial peritonitis, obviously cause we're introducing stuff into the peritoneal cavity. Um And this can be, these infections can be particularly bad because it's such a sugar rich environment with the dialyte fluid. The most common um bacteria is staphylococcus epidermidis. Rarely. You can get something called encapsulating peritoneal sclerosis, which is a thickening of fibrosis of the peritoneum. Um that it causes encapsulation of the bowel and can lead to obstruction. The whole thing can just fail, unfortunately. Um So stops, stops working as a dialysis um method and then you have to switch to hemodialysis. The catheter can have problems so it can be bent or leaking or not in the right place. And because of all the b um sugar that you're pumping in with this fluid, some of that does go into the body, although it's, it's supposed to cause stuff to flow out. Some of the sugar gets into your blood system that can cause weight gain and erratic blood sugars. And then obviously, there's a psychosocial implications that kind of applies to both of them has quite an impact on your day to day life. Ok. Um So similar um kind of patient, this patient's had a renal transplant because of their endstage renal failure. Um And now he's having low BP, abdominal pain, nausea and vomiting. And the question is which immunosuppressant. So, immunosuppressants are given after transplant is the most likely to have contributed to his Addisonian crisis. So how do we know it's an Addison's crisis? So the symptoms, the BP, the pain, nausea, and vomiting, also the low BP, the low glucose and the hyperkalemia. Those are all clues. Ok. So people are suggesting d is the answer. It's absolutely the case. I probably chose the easier one of the different immunosuppressants. And if we go on to the next slide, so I've just highlighted here all the features of a crisis if we go on here. So I've put the different immunosuppressants on this page and what common side effects they have? Um I would learn this for the MLA. Um It's a very easy um not easy, but like if you learn it, it's gonna be easy to get a point on a question that asks you about immunosuppressant side effects. Um So other, so as well as the immunosuppressants causing side effects like infection and skin cancer, unfortunately, and the specific ones like cardiomyopathy, gum overgrowth, diabetes, Addison's transplant. Um operations themselves can involve infection, bleeding, um urine leak. So if the anastomosis isn't done properly or ureteric stenosis, the transplant can unfortunately be rejected. So if that's, that might be within minutes, hyperacute, if there's an A bo incompatibility, um or it might be within six months. If it's cell mediated autoimmunity or it may be longer, say chronic, more than six months, the transplant can fail as well. So stop working, you can get electrolyte imbalances and renal artery thrombosis. Um So these are just key things to remember. Um Re transplants are indicated in patients who have endstage renal failure. It significantly improves their quality of life. Um And in an osk, they will have a hockey stick scar as you can see in the image there and you'll be able to palpate the kidney in the anterior abdomen. The closer a match is the less likely they are to be rejected. That's not always possible. Um So we're gonna move on to this sort of last bits. Now, apologies. Um I think we're on question 13 now. So that's good. We're gonna move on to causes of CKD. OK. We've mentioned some already, but we're gonna go into a, a few in a bit more detail. Now. Um So I haven't got a question on diabetic nephropathy, but I thought it was important to just briefly go over it. Um So in type two diabetes, um you've got both the high blood sugars causing damage to the kidneys and also hypertension um causing the diabetic nephropathy. Annoyingly KD also leads to hypertension. So then it's a bit of a cycle. The symptoms of um diabetic kidney disease are are no different to the sort of general d symptoms, but obviously in the history, they'll have diabetes as their past medical history. Um, onset and progression of it, of the condition can be slowed by managing the diabetes and hypertension as well as general lifestyle changes like smoking, cessation, healthy eating and exercise. So the most important thing is to treat the diabetes. Um but then going on, um if they are hypertensive, you're gonna add an ace inhibitor or if they have CKD, where the albumin creatinine ratio is is more than three, you're also going to start ace inhibitors in normal population. It, it would just be above 30. Um but if they've got diabetes, you start an ace inhibitor earlier, ok? And then like we said, something like dapagliflozin, an SGLT two inhibitor that will be started. Um In addition to the ace inhibitor, when the albumin creatinine ratio is about 30 diabetics should have their EG fr and urine acr checked once a year. Um And in a question, um in the MLA they might mention the histology changes. So you're gonna have basement membrane thickening mesangial proliferation. And then the key one to remember is Kimmel Kimmel Steel Wilson nodules, which is basically a nodular glomerulosclerosis. OK? I've put some pictures here, but I don't think they'd use that. We what we mean if they use pictures. Um So now I've got a question about other causes of CKD. So what do we think is the most likely cause in this case of this patient's hematuria? So she's got gross hematuria. She's had ongoing flank pain for ages, keeps getting UTI S but doesn't seem to have the symptoms of one. Now, someone suggested B which is polycystic kidney disease. Someone else has suggested iga nephropathy. Um Let me go next. So she's also got a history of kidney stones and hypertension. Her bloods show a picture of d she's got a slightly low hemoglobin cos she's had this hematuria and she also, she knows there's something that runs in her family about kidneys, but she's not sure what it is. Um And in this case, the most likely one is polycystic kidney disease. So PCD is a genetic condition um where you have your healthy kidney tissue being replaced by a fluid filled cyst. The dominant version, the most common one is less severe uh symptoms of chronic flank pain, hypertension. Um If a cyst ruptures, you get hematuria that and that usually sort of self resolves, they can have recurrent uti S and stones and they usually reach endstage renal failure about the age of 50. Um It can also cause things like cerebral aneurysms, cysts elsewhere in the body mitral regurgitation and and colonic diverticula. Um patients might describe a feeling of fullness in their tummy or headaches and you might be able to feel the kidneys cause it's so large. The recessive variant is much rarer and more severe. It can be picked up on antenatal scans often as oligohydramnios which is reduced amniotic fluid. So the baby produces the amniotic fluid. It's basically their, their waste their urine. So if there's less, it's because their kidneys aren't working and this is a common cause. They may be born with respiratory failure because their lungs haven't developed properly. They may have dysmorphic features. Um and they will usually have endstage renal failure before adulthood. Um They might even need hemodialysis within the first few days of life. Diagnosis is with genetic testing and kidney ultrasound. So you'll, you'll see the cysts and you'll check for the genetic changes. Um just briefly, it's managed in various ways. So in the dominant form, you can use a med medication called tolvaptan to slow the development of cysts. Um and then generally pain relief, antihypertensives, antibiotics. If, if needed, they can have symptomatic drainage and then they may need dialysis or transplant. Genetic counseling is super important and they should be a um advised to avoid contact sports due to the risk of cyst rupture as well as nsaids and anticoagulants. Patients with PC KD should be screened for cerebral aneurysms using Mr angiography. Ok. Um So we are on our last few questions. We're gonna do these two together and then got, got an explanation afterwards. So this five year old with swelling seems quite generalized, edematous and funny looking urine with protein urea um and low albumin. What do we a, what do we think this is? And b what do we think the next appropriate step is based on our suspected diagnosis? It's, this is a, a nice common M CQ I think in finals like to it anyway. So someone suggested minimal change disease and that they treat with steroids. Um, and that is absolutely the case. So, we've got a child here with edema proteinuria. Probably the, the funny urine is the frothy or foamy urine. They've got album albuminemia co they're losing all their protein. Um, they've got reduced kidney function. Um We'll talk about why they have high cholesterol later. So, the treatment for minimal change disease, um this proteinuria condition in kids is steroids, antivirals is, is not the right treatment. They don't usually need IV fluids repeating the EGFR would be for diagnosing CKD. It's not useful right now. Um And a kidney biopsy would confirm the condition, but usually we treat these patients and then only do a biopsy if they're not getting better with the steroids. Ok. In question 15. So this is a, a young adult, shall we say? Um with hemoptysis and hematuria. Um the observations are showing hypertension, the urine shows blood and a little bit of proteinuria, the bloods show what looks like an AK. Um So what condition do we think this is? And therefore, what would we expect a renal biopsy to show? Ok. So this person thinks it's good pasta syndrome, um which it is absolutely. Um I think it's a or c fair enough. Any other suggestions, the suggested see? Ok. So um this patient um has sort of some key features of good pasta syndrome, the hemoptysis or pulmonary hemorrhage, you can even get in bad um situations and hematuria. Um Good Pasture syndrome is also known as anti glomerular basement membrane um disease. Um And basically, you've got antibodies attack, attacking the basement membranes in both the glomerulus and the lungs, which is why you get bleeding in both. So, if you ever see bleeding from those two together, um this is a good differential as is sort of a vasculitis picture. They've also got hypertension, um proteinuria and hematuria um which is making us think it's a nephritic condition. Ok. Um And we're gonna talk about the different um different histology you might see here, but in this case, it's, it's the linear IgG deposits along the glomeruli capillaries um for the people that said c so podocyte effacement is something you see in minimal change disease, minimal change disease. The, the one from the previous question um that is mostly seen in Children. If you look at that under a light microscope, you see no change, hence minimal change disease. But if you look at it with an electron microscope, you see this thing called podocyte effacement. So that would be for the other disease. Ok. So I'm on my last slides, I promise. And I'll let you guys go. Um Just a quick overview of nephritic versus nephritic syndrome. Um So, glom glomerular nephritides is a bit of an umbrella term for a group of disorders characterized by intraglomerular inflammation. Um And then the nephritic syndrome has the features of hematuria, oliguria, proteinuria, that's less than 3 g in 24 hours and hypertension caused by fluid retention. Um basically immune in Nephritic Syndrome. Um you have nephritis caused by immune complexes and damage to the basement membrane which disrupts it and allows blood leakage. Nephrotic syndrome is sort of a situation called again, many underlying causes where the basement membrane has become permeable to proteins due to a charge barrier disruption, allowing significant proteinuria. So there's no specific like, oh, I've diagnosed you with Nephritic or nephrotic syndrome. They are sort of clinical pictures that have many underlying causes nephrotic syndrome. You have massive proteinuria. So more than 3 g in 24 hours causing albuminemia. So low albumin in the blood um and peripheral edema, you don't usually get hematuria. Um sorry. Um because they're losing proteins that includes your clotting fractures. So they are at risk of thrombosis, your immunoglobulins. So your risk of infection. Um and you these patients, the liver kind of reacts to the low albumin by starting to synthesize things and it ends up synthesizing more lipids as well. So you can get hyperlipidemia, hypercholesterolemia. Um and the patient also be can become hypertensive, but that's less of a sort of, that's not in the triad of nephrotic syndrome. Whereas for nephritic hypertension is one of the core features. And so if we look at some causes of Nephritic syndrome, the one that has blood um reduced urine output and hypertension as well as smaller proteinuria. Um These are sort of the commonest ones, Iga nephropathy and post streptococcal glo glomeru nephritis. They are both ones that are associated with preceding infection. The way you can tell the difference is that in iga nephropathy, it's a a recent gi or resp infection in the last seven days. Whereas post strep um GN is their infection was, you know, a couple of weeks ago, some people say 2 to 4 weeks ago or 2 to 6 weeks ago. Um usually both, they both occur in of the younger patients and in iga nephropathy, of course, you have IGA deposits um as well as C three deposits. Where is it post strep GN? If you did blood tests to look for um recent strep infection, you'd have your raised anti DNA B and anti streptolysin O. Ok. Um People recover usually fully from post strep glomerulonephritis. Um moving on crescentic glomeris or rapidly progressive GN is a very acute, severe cause of nephrotic syndrome. Um and it's named um Cresentic GN because you see glom glomerular presence on histology and this one also responds well to treatment. Um We've talked a little bit about Good Pasture Syndrome already. It's usually patients in their twenties or sixties. They'll have acute kidney failure and hemoptysis because these antibodies are attacking the basement membranes and you see the linear IgG deposits. Um Yeah, output syndrome is a cause of Nephritic syndrome that um isn't sort of to do with inflammation. It's um a genetic condition um that causes a problem with the collagen in your kidneys. It leads to a triad of poor vision, deafness and nephritic syndrome. It's quite a sad diagnosis. Um And the histology shows something called a basket weave appearance, lupus, nephritis. Um The key points in your question is gonna be the patient has lupus. Um and it, it's gonna cause a diffuse proliferative glom nephritis. So the histology will show sort of high uh extra cells thickened membrane and lots of pro proliferation. Ok. And then finally, um va vasculitic conditions can also cause a Nephritic syndrome. So things like um GPA pe GPA and you look for the specific antibodies um to diagnose them. Overall diagnosis usually requires renal biopsy to actually look at the sort of histology. And then treatment will be guided by the renal team but often is mainly supportive. So, anergic hypertension dialysis if needed. Um and it can involve immunosuppression as well. Um Yeah. And then this is my final slide. You'll be very pleased to hear. So, nephrotic conditions I've highlighted, I've made the really important ones big here. So in Children, the one to know the most common cause of nephrotic syndrome in Children that comes up in exams is minimal change disease. Um So these patients have the key features of nephrotic syndrome, particularly like leg ankle and periorbital edema might have general weight gain and foamy or frothy urine um and it's usually idiopathic, but it can be a like a rare consequence of cancers like hodgkin's lymphoma. Um and under light microscopy, there'll be no change. But under electron microscopy you get podocyte replacement. So basically the the cells um that are lining the glomeruli um that are supposed to sort of stop the big proteins getting through into the tubules are sort of spaced out, there's big gaps so everything can just go through them. Ok. In adults, the most common causes of nephrotic syndrome are membranous nephropathy and focal segmental glomerular sclerosis, um membranous nephropathy, um usually is usually idiopathic and as the name suggests, it has a a thickened basement membrane. Um It can also be secondary to malignancy or certain infections or, or drugs. Um And one key thing to remember for exams is that there, there will be these immune complex deposits that uh for the shape of a spike and dome. Don't ask me what that actually looks like, but that's the sort of terminology they'll use to describe it in exams and then focal segmental glomerosclerosis. Um histology unsurprisingly shows segmental sclerosis. Um and that is linked to um lupus sickle cell disease and HIV um there's a couple more causes less common. Um I popped on this slide. So, membranoproliferative glomerulonephritis or mesangiocapillary glom nephritis. That's your patients under 30 your immune complex deposits and mesangial proliferation. Then you've also got HSP um diabetic nephropathy, which we've gone through earlier that shows mesangial sclerosis and chemos Wilson nodules and then certain infections like HIV can also cause nephrotic syndrome. Um Now I believe, yeah, that is all my sides. So has anyone got any questions? Anything that didn't make sense? Um And please, I beg um please, can you guys fill in the feedback form? Um It will give you guys access to the slides, I believe. And it's, it's really sort of helpful for me and all the other speakers, um, for our portfolios so we can improve these talks as well next time. Oh. Oh, thank you very much. That's very nice feedback. I, yes, I'm glad we made it to the end too. I'm sorry, it was a bit longer than, than I'd like. But as a, a metopic Renal, cool, if anyone's got any questions that I think of later, they can message us on Instagram, Facebook, email tiktok, I think we have as well. Um, and the team can also sort of send the questions to me. But otherwise, um, if you guys are happy to fill out the feedback form, I'm gonna leave you to your evenings. Ok. Awesome. No worries.