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Um, so we'll get started. People might trickle in, um, tonight. Um, we're gonna be covering renal medicine. It'll be myself and doctor Kelly. Um, one of my colleagues from work, um, Cash will also be here answering any messages in the chat. So please do ask anything that you're not sure about. Um, we're happy to answer as we go along. I've got quite a few questions this week. Um, I haven't managed to get the poll set up. So if you just answer, answer the questions by putting the letter in the chat that will help us be nice and interactive. Um, so we've based what we're covering on what's in the MLA curriculum. You can see we're covering quite a lot of different differentials and conditions and we'll try and get through that in a timely manner, but please interrupt if you have any questions. So without further ado, we've got our first question. So this is a 68 year old man being treated for pneumonia with antibiotics. He's got a past medical history of COPD osteoarthritis, hypertension and a hernia and the nurses are worried because he's not passing urine. You can see his observations and bloods on the um on the slide. What treatments do we think should be started to try and improve his urine output? Yes. Give you all a chance to read the numbers and then just go for your best test. Ok. Have we got any answers from anyone? Mm No, no, that's ok. So just to sort of highlight the key things in the question for people. So someone suggested e lovely. Yeah. So a catheter, we've also got B IV fluids, both good suggestions. Um So if I go to the next slide, so the important things here, the patients not passing urine, they've got a raised creatinine above what their baseline is. OK, which is A N AK and the BP is also a bit low and generally the pictures they are being treated for infection. So it's reasonable to assume this patient's a little bit dehydrated from their BP and IV fluids is what's gonna help improve that. AK I there's no real point in changing or holding the antibiotics cos if you look at the inflammatory markers, they're trending downwards, the treatment's working and we'll talk a bit more about dialysis later. Catheters. Um probably not going to solve the problem. Um Depend if it's related to the infection and the dehydration, but it can be really helpful for monitoring. Um So treatment wise, probably the IV fluids, but II would also consider catheterization for this patient. Oh, hopefully not, not everyone read that. Um looking at this question, can anyone suggest what stage of ak I we've got in this question? Yeah, the options are 12 or three, got any suggestions. So stage three, that's a great answer. So if you, there's different ways of looking at your um staging of the acute kidney injury, um you can either look at the creatinine and look at how much it's increased from the baseline. So has it increased by 50%? Has it doubled? Um or is it even tripled? Um And then also the urine output? So this patient hasn't been um we haven't got the urine output. I don't think we just said reduced urine output um or an urea for 12 plus hours. Um So that comes into the stage three, if you look there on the graph, it's anuric no urine output for 12 or more hours. So when we've got an acute kidney injury, what does that actually mean? It means we've got a rapid, so coming on with a L within the last seven days and sustained. So lasting for 24 to 48 hours or more decline in your kidney function causing a reduced urine output and a rise in your urea and creatinine. It can be caused by something before the level of the kidney. So, prerenal, it can be a renal cause actual problem with the kidney itself or it can be a post renal cause something sort of ureter bladder downwards. Can anyone give me any examples of prerenal renal or post renal causes of AK I dehydration? Absolutely. So that was the case for this patient. That would be one of your prerenal horses medications. Yeah, that can be actually that can come into all three categories and we'll talk about that later. Um, prosthetic, um like hyperplasia. Absolutely. That would be a post renal cause. Anything that decreases, perfusion is going to cause a prerenal um problem. Or it can also cause ischemia which then becomes a renal sort of intrinsic problem. Lovely. So basically, you figure out the cause, try and treat the underlying cause and then give them IV fluids if they need it. OK. So a little overview of the kidney structure, just to remind ourselves, you've got the flow in um from the arterioles filtration into the glomerulus and then like reabsorption and sort of balancing out of your electrolytes in the tubules um and the loop of henley and then you collect the urine and the collecting duct. Um If we take away the blood flow on this picture, this just sort of summarizes nicely for you and you will get the slides of what happens in each segment. OK. So in your prerenal causes you have decreased blood flow to the glomerulus and that results in decreased filtration because of a reduced pressure gradient. That means you end up with um sort of not filtering out your urea and your creatinine and because the kidney is still functioning and urea is often reabsorbed. You end up with quite a lot of urea in the blood and you don't make much urine. So your urea creatinine ratio is going to be really high. Um and both values will be raised. Ok. In your renal problems, there's a problem with the actual kidney itself. It's not doing what it should do. Ok. So here it's not, it's um not sort of filtering out any urine creatinine but sort of on an equal basis. So the ratio is much lower. That's how you can kind of tell is the problem prerenal or renal when you're looking at the bloods. Ok? I've summarized some examples of prerenal and renal problems here. Um So it can be things like blood loss, systemic vasodilation in sepsis or renal artery stenosis. That's all gonna decrease your blood flow. When you've got a renal problem, we'll go on to talk about that, but it could be inflammation or it could be um sort of death of the cells. Ok? And then post renal, we have some really good examples in the chat. There can be a problem with the sort of internal um lumen of the ureter like stones. There can be something in the wall, something pressing on the urinary system and certain drugs can also impact your bladder function and always think about whether or not a catheter could be occluded. Ok? Um Examples of anticholinergics. So the drugs that can cause post renal problems include things like amitriptyline and calcium channel blockers. But we'll talk a little bit more about um renal and post renal problems in a second. So, moving on to question two. So we now have a younger patient. They're being treated for meningitis with ceftrixone and acyclovir. Um They have a history of asthma and anxiety and two days into the treatment, he develops a rash and joint pain. I've got the observations and the bloods on the screen. Do we wanna think about what the most likely cause of the rash is? Given this picture? If we up any thoughts, someone's uh two people have suggested d um which is absolutely the right answer. Um So the key things to see here is that the patient is being treated with Acyclovir, which is um a known sort of cause of um A I and the, the rash has developed a couple of days into the treatment. So it's unlikely to be an allergy. The patient doesn't have any history of eczema sepsis is unlikely now because the patients, you know, doing much better, the white cells have come significantly down. So we're left with a bit of an achy eye and eosinophilia and reduced output alongside a rash um and joint pain. So, the most likely thing here is acute interstitial nephritis. Um A I and A TN are the most common causes of renal AKI. You can also um have an AKI with a g glomerulonephritis um cause but that's usually more a nephrotic or nephritic syndrome picture. So the main ones are A I and ATM, I've summarized here how we can tell the difference. Basically in acute interstitial nephritis, we have inflammation um of the interstit widespread throughout the body. So you get all your immune cells migrating to the incision causing this typical rash that I showed on the screen earlier. So if we just go back, this is a typical a rash, um eosinophilia and joint pain, the patient might also have an achy eye fever. Um They can have hematuria, nausea or vomiting, mental status changes, swelling and weight gain due to fluid retention. But this triad is the key thing to look out for an exam, especially in the context of an AKI eye. It's usually caused by medications. So uh long term NSAID use acyclovir in this case, penicillin, et cetera, but can also be caused by other things that I've listed on the screen. So, infection and autoimmune conditions and allergies as well. Acute tubular necrosis is more specific to the kidney. It involves the death of the tubular cells within the Nephron which blocks the tubules, um reduces your pressure gradient at the glomerulus. So then you're not filtering properly. Ok. And there's different things that can cause the the cell death ischemia. So almost the prerenal causes can lead to ADN which is why it's important to look at that urea creatinine ratio to figure out where the problem is. Um and also anything nephrotoxic. So certain medications including Acyclovir, but we had the symptoms, the triad of the A I, that's how we knew it was the other one. and also things like contrast and rhabdomyolysis. So the bloods will show a renal AKI and there'll be sediment in the urine which on microscopy will be shown to be muddy brown casts. So if they mention muddy brown casts in your exam, sort of in the A KT that's like um A that's very suggestive of a TN. Ok. Um aminoglycosides. So the antibiotics that can cause cause um atn include things like gentamicin, Amikacin and Streptomycin. Ok. We'll talk a little bit more about pro nephritides later on. So, question three, you guys are doing really well. So far, this is an 84 year old man recovering from pneumonia just waiting for a social care package. Um He's got vascular dementia arthritis, hypertension diabetes and af um his hobs are on the screen. He's eating and drinking well, but his last urine output was eight hours ago and yesterday had quite AAA solid type two. These are the medications he's on and he's got some suprapubic tenderness and confusion. So the question here is as well as giving this man a catheter, what single intervention is gonna be most appropriate for him? This, it's quite commonly seen on the, the Jerry's ward. Ok. I'll move on in the interest of time. So this gentleman is, is constipated and that's causing bladder um retention, urinary retention. So, the most effective thing here is going to be to prescribe a laxative alongside the catheter that's going to resolve the underlying cause. Um should improve any achy eye that he experiences. Um And probably looking at his morphine is going to be necessary. Ok. So there's question four and then we'll go on to the treatment of AK. So this one's looking at um, a lady um, who's being treated for dehydration and she started on IV fluids. So that's the first part of treating your AK. Um, and she's on all these medications. Um, her creatinine has jumped massively. So we've got an achy eye. What medication change would you guys make if any? Ok. So we've got a suggestion of stopping Metformin. Someone else has said hold candles are on all the options are like valid depending on the circumstances, but there's one that's particularly needed in this question. Got a couple more CS. So, yeah, absolutely. So if we go on to treating a KS, now, I will talk about the medications on the next slide. So basically managing an AK I involves treating the underlying cause giving them fluids and a medication review which I'll talk about for prerenal that might be antibiotics or blood transfusion, vascular intervention if they've got a stenosis. But generally you just want to increase blood flow to the glomerulus. However, that is gonna happen. It's a renal cause, stop anything that's causing the problem, um and speak to the renal team for these patients. Ok. Post renal. Um unless it's an obvious cause you might need to um investigate a little bit further. Any, any like patient that's in retention and confused and elderly, you're going to need APR exam. Unfortunately. Um Then you might want to do things like looking for stones with a CT KB or looking for other kind of strictures or masses with the CT urogram or an ultrasound cystoscopy, if you're worried about malignancy, et cetera and then treatment is just relieving the obstruction, stopping any medications. Um, and then considering things like laxatives or tamsulosin depending on the cause and always check your catheter. Ok. So does anyone know an acronym that might help them? Remember which drugs to amend or hold during an AK doesn't have to be in my acronym? Just any acronym that people use? Damn. Nice. I suspect my letters fit into that as well. Does everyone use Ryan's one or has anyone got any different ones? Ok. So the one I use is Diamond. So similar letters overlap. Oh D yeah. Nice. Nice. Agreed Eric. That seems like some very good ones to think about. Um, so shorter ones are gonna be easy to remember for the exam. Um, but I found Diamond quite useful because it had a couple more, um, sort of explanations of what to do. When. So some of them, you need to hold some of them, you just need to amend the dose or use with caution. So, diuretics, they can cause um acute interstitial nephritis and they can also cause AKI if they reduce the blood volume in elderly patients. So ideally, you'd hold ok, iodine contrast, the radiologist is gonna get super um nervous if with an EGFR less than 30 but you can use them with caution if needed. So speak to um the renal team if you really need a scan with contrast and then give a fluid bolus before and after to sort of flush out the contrast because it is nephrotoxic. Um your ace inhibitors or A RBS should ideally be held. Um They dilate the arterioles that leave the glomerulus so that drops the pressure gradient and then you get less um filtering. Um aminoglycosides doesn't quite fit into Macron, but I've added it here. You'd also hold that due to the risk of um acute tubular necrosis. Metformin. Um So if we go back to the question before Metformin was one of the options here, but if you look, the EGFR was 74 and Metformin only needs to be held if the EGFR is less than 30 because that's when you have your risk of lactic acidosis. So this patient could continue that Metformin if they need it for their diabetes opioids. Um I'm not sure Ryan, if you remember the cut off values but below a certain eg fr you'd switch your morphine to oxyCODONE. And if it goes really low, you'd switch to a fentaNYL. But that would probably be with the help of palliative care. That's because it's really excreted. So it's gonna build up if it's, if the kidneys aren't working and then you've got a risk of opioid toxicity. NSAIDS, you're going to hold the majority apart from your cardioprotective aspirin. That's because it's a nephrotoxic effect long, long term. And also because um nsaids constrict, the arterioles entering the glomerulus, which again reduces that pressure gradient. And then finally, all your disease modifying drugs, anything with a narrow, narrow therapeutic index. Um that's gonna, that's renally cleared, et cetera and needs much closer monitoring and you might need to adapt to the doses. Ok. Um Just a little way to remember what nsaids and um ace inhibitors do. So it's the sort of a, is it an acronym? I don't know PDA is a. So the hormone prostaglandin dilates your afferent art arterial and then says act against prostaglandin. So they constrict the afferent, the ace enzyme constricts your efferent arterioles. So ace inhibitors dilate it. So it's just a remember way of remembering afferent versus efferent. Ok. If no one's got any questions on that, I'll go to the next slide. So now we have a 50 year old man being treated for cellulitis. He's been started on IV. Antibiotics has a history of hypertension, chronic kidney disease and alcohol excess. Um, his observations are there and his bloods, including ABG are on the screen, his ECG is normal at the moment. What treatment would you want to give this gentleman? And if you're not sure what you'd want to do, then just tell me what's, what's the problem that you've seen for this patient? Thanks. Fun. What do we think of the bloods? Anyone concerned about them or we happy he's acidotic. Absolutely. Anything else going on with the bloods? Obviously, his CRP and white cells are up, but that's because he's being treated for cellulitis. We know we know what the cause is and we're treating that. Is there anything else on there that we're worried about before hyperkalemia? Absolutely. So we've got an acidosis and a hyperkalaemia. Does anyone have any ideas what they'd like to do to get rid of that? Ok. Um In real life, the answer would be I'd speak to the med reg, but unfortunately, we don't have that in the exam. So anyone got any idea ABCD or e what would be the best thing for this patient? Ok. I've got t anyone else. This is a bit of a trick question because depending on the level of the hyperkalemia, we've got various, these are all kind of valid options, but let's move on to the actual answer. So, for this patient, um they've got an AKI um on top of their D and that is causing a hyperkalemia and acidosis based on the level of the um potassium and the fact that the ECG is fine, we'd do medical management first for this patient. Um And we'll talk a bit later on about when we would do dialysis and when we wouldn't. Ok. So, as Ryan has beautifully said, um, we'd give um insulin to drive the potassium into the cells and then dextrose alongside that to make sure they don't become really hyperglycemic. Ok. So um potassium is co transported with insulin into the cells. So that's why it works. And the dextrose is just to balance them out. Ok. So causes of hyperkalemia, they can be remembered with the acronym dread. And so you've got a height and state. It's dread. D for drugs. I've listed some here. Um It's impossible to remember all the drugs that cause hyperkalemia. But these ones um sort of some common ones that I thought might come up in exams, renal failure, which is what we've got going on in this patient. Endocrine causes like Addison's big one to not forget is artifact. So, humilis samples, I had a patient today. Um they rang me up because on the patient knows Best App, it said that potassium was 5.4 and the, the top of the range is 5.3. But actually it said that sample it hemolyzed and that's why it was raised. So just repeat it if that's what you think is the case. Um And if you're not sure, always go with the lab value, don't go with the, um, sort of the blood gas machine because the, the lab value is much more reliable. OK. And then DKA can also cause it, um, which is important to think about in your diabetics. Ok. So management depends on how high the potassium is and whether or not there are ECG changes. If it's sort of mildly elevated, we monitor and we try and reverse any underlying causes, stop any causative drugs, treat the DK A et cetera. But if it's six or more, we're gonna need to treat you. Ok. And that would be with an insulin glucose IV infusion. And you can also um consider nebulized salbutamol, which helps drive it back into the cells and calcium resonium, which is a potassium binder, but that works a bit slow more slowly. No. Um That's what we would do for this patient. However, if their potassium is 6.5 or above or they've got any ECG changes, we need to consider the risk of arrhythmias um and sort of life threatening arrhythmias. And that's when we give our calcium salts. So that can be calcium chloride or calcium gluconate, depending on what your sort of local guidelines say. Let's give IV every five minutes. It's really important that you know which one you're giving. Um because um you want to give 6.8 millimoles of calcium and that can either be 10 milli 10 mL of 10% calcium chloride or 30 mL of 10% calcium gluconate. You don't wanna be giving sort of three times the dose or a third of the dose. It's important you follow your, your local guidelines and make sure you give the correct dose. That's what to protect the heart from your arrhythmias to stabilize the the cardiac membranes. And then you're gonna also give you insulin glucose infusion and your salbutamol nebs to try and bring down that level of the potassium. You can also consider lokelma, which is sodium zirconium cyclosilicate. Uh that's gonna um reduce um your potassium over a longer period of time. OK. So this is just my trust guideline. It sort of summarizes what I've said depending on if the um hyperkalemia is mild, moderate or severe, you do different steps and if there are any ECG changes, then you do need to give calcium salts. Ok. So um can anyone suggest to me what E CG changes you might expect to see in hyperkalaemia to T waves from two people? Lovely, three people. We're all in agreement. We like that. Mhm Lovely. And a wide QR S nice. So that's something I learned sort of actually, I think in f one rather than final years. So your level of um hyperkalemia determines how much your ECG changes. Initially, you're going to get that tall tender t wave that people talk about. But later on, you can get much more significant changes and essentially the whole ECG becomes sort of stretched out. Your P waves, um become flatter and flatter and your pr interval gets wider, your QR s um duration gets wider and eventually you lose your P wave and you get a sinusoidal wave. OK. I've also included on here. What can happen with low potassium. So you can get a, a depressed ST segment and a sort of biphasic T wave. OK. This is just some more pictures that shows as you increase the potassium. It gets free here and free here and you can end up with a sinusoidal pattern or even VF or Asystole. Um So it's important to be treating these patients early on to prevent getting anywhere near this on your ECG S and these patients should all be on telemetry if they've got a raised, if they've got a raised um, potassium, just hook them up to a monitor. They should be in a AU or CCU anywhere that has a monitored bed. OK. Cash is very helpfully just popped in the chat about the cut offs for changing your morphine to oxyCODONE if you have a um I if you have a, a eye, OK. And then in the top right hand corner here it shows the progression of those P waves. So they get sort of flattened, the PR gets longer and then the P waves just disappear as things get worse. OK. So moving on to question six, I got a 50. Oh, this is the same gentleman. Apologies, the same gentleman, but we've now treated him three times um with the insulin dextrose and his V VG shows is shown on the screen. Um, he also now has to 10 D waves showing on his ECG. So we've given him some calcium gluconate. What else do we need to do for this patient at this point? Got some suggestions of d so acute dialysis. Yeah. So now we've got, um, we've tried the, the sort of medical treatment and it's not working. So there's no point in increasing the dose of insulin um, or repeating more of the same thing and the patient doesn't need cardioversion. They're not in, you know, VF or anything, they haven't had an arrest, but they're heading that way if we don't do something quickly. So the correct answer is absolutely. As you guys have said, acute dialysis, we've tried several rounds of treatment we've monitored the whole time and the V VG is just getting worse. Ok. So what apart from obviously treatment resistant hyperkalemia, what are the indications for acute dialysis? And does anyone know any nice acronyms? Ei ou Absolutely. It's nice that there's one that's fine. Not ABCD. Um Yeah. Has anyone got any ideas what the letters stand for? Acidosis for the A? Absolutely any more for any more or should we move them? And I'll show you acidosis, electrolyte, imbalance, something. Yeah, I like the something fluid overload and uremia. Oh, top marks to you. Absolutely. Um So the only one that was missing there from your answer, she was um intoxication. So, any sort of certain poisons, certain drugs can be filtered out with um dialysis as well. So, the important thing for all of these is that um it's treatment resistant. So, or persistence persistently there. So it's a ph persistently less than 7.15. Um for electrolytes, it's hyperkalaemia, it's persistently either above 6.5 or seven depending on the guidelines. Um Despite treatment intoxication, um tox space will tell you whether or not a medication can be dialyzed um to remove it from the system. Um, edema is ref treatment, refractory, pulmonary edema. We don't care about legs being swollen, but if the patient can't breathe, um and nothing we do helps, then we need to get rid of that fluid somehow. Um because with dialysis, you can alter the fluid balance and then uremia, it's it only if it's symptomatic. So the number can be pretty high um with without symptoms. Um And we wouldn't usually dialyze dial, dialyze. Um But for these patients, you're gonna be discussing with the renal team and the it team um depending on what you have in your hospital, um whether or not it's indicated. So, some symptoms of uremia on the screen. So, encephalopathy, seizures, pericarditis, et cetera. Those would be reasons to acutely dialyze the patient really good answers guys. So, moving on to my last question before I hand over to Ryan. So we've now got, um, an elderly gentleman referred to A&E by his GP because he might need a blood transfusion based on some recent blood tests. He's been feeling a little bit tired and having some back pain, but he thought that was due to gardening. Um, and his past medical history, he has, he's got af hypertension and he's had a hip replacement. His observations and bloods are on the screen have a little read of them all, all the way down to the bottom and then tell me either what diagnosis do you think it is or ideally answer the question, what investigation would confirm the diagnosis? I'll just give you a few minutes. Yes. Ok. So someone suggested D is anyone? Oh, ok. We've got ac any other options? Oh, we've got a B ok. So BC or D I like I like the spread. So before I show you the answer to the question, can anyone tell me what diagnosis they think this is? Ok. We've got another vote for c majority of ac I got a suggestion of multiple myeloma. Excellent. Um So the answer here is a bone marrow, but obviously I'm going to go over on the next few slides. Um Why that is? Ok. And um Eric's what the answer the most like differential here. Um We're going for multiple myeloma. So what are the features of multiple myeloma? What are the sort of things you look and look out for in an exam and any patients or Ryan's giving away, please? Ok. Well, Ryan's giving you the acronym crab, but now I want, I want some suggestions of what the letters stand for C ra B hypercalcemia. Yeah, that's the C the R is to do with the topic of the talk. I can go back as well if that helps anyone. Actually, I've highlighted it renal impairment for our lovely anemia. And what's the b back pain? Yeah. Mo most likely um bone pain in general. Um but most commonly you see sort of back pain. Absolutely. But any kind of bone pain be worried about. So what actually is um multiple myeloma? Um It's called um oh I can't um I can't see if my slides have moved on. Can, can you guys see my slides? I think so. So multiple myeloma, you've got an over proliferation of your plasma cells, which means you're mass producing one single antibody and that's gonna cause your features of hypercalcemia. Your crab features in a couple of different ways. The excess plasma cells are gonna crowd your bone marrow, impairing production of your other types of blood cells. So you can actually get a pancytopenia, not just an anemia, but the anemia is the sort of most common thing we see. So that's the cells crowding out the bone marrow. Then the abnormal immunoglobulins or the paraproteins that are being produced by these plasma cells are gonna cause damage to the kidneys, reducing your kidney function. And they're gonna activate your osteoclasts causing breakdown of bone, which leads to your hypercalcemia and your painful osteolytic bone lesions. Ok. So that's how you get the different features, your investigations. So initially, you're gonna do, you're gonna do your routine bloods if you're suspecting it. So you will see, you'll see a pancytopenia and the FBC, you'll see a hypercalcemia, um reduced renal function. And then they're gonna have a raised E sr and plasma viscosity. These paraproteins basically clogging things up. The, the reason my question was a little bit, a little bit mean. Um I put in serum electrophoresis here. So that's part of a multiple myeloma screen. If you wanna sort of rule it out, you do serum or you, you're thinking it's a possible differential. You do serum protein electrophoresis and you do new urine Ben Jones proteins. Um which is basically looking, are there weird paraproteins coming out in the urine? The actual confirmatory like proper diagnosis is done with a bone marrow biopsy. So that was the right answer in this question. So it's really important in your finals to sort of read the questions. Are they asking for initial management steps or definitive treatment? Are they looking for initial investigations or how to confirm the diagnosis? Ok. And then, um ideally you do sort of imaging for bone um lesions. The best option is a whole body MRI. Um, but you can also do a CT or a skeletal survey as well. Um Treatment, it depends if they're fit enough. But um, if so they'll get chemotherapy plus or minus a stem cell transplant. Um for the bone pain, um, radiotherapy can help, um, bisphosphonates can suppress osteoclast activity. Um, but ultimately, they might need or orthopedic surgery involvement. Um in terms of asking your history for these patients if you don't have the bloods and stuff, um, your, your anemia and pancytopenia symptoms is going to be, you know, the shortness of breath, fatigue, increased infections, bruising, et cetera. Um, bone pain is obvious you can ask about that. What other symptoms of hypercalcemia? So I've put on stones, bones, abdomens and psychic groans. But can anyone sort of tell me what kind of what, what does that actually mean? What, what would you ask the patient about? Would you ask them if they have stones and bones constipation? Absolutely. So that comes under the abdomens along with nausea and vomiting and indigestion. But constipation is probably the biggest one, renal stones. So you probably wouldn't ask them, do you have renal stones? But you could ask, do you have, you know that radiating back pain? Have you had any blood in the urine? Um, sort of long to groin pain? Ok, thirst and polyuria. Absolutely. Um, with hypercalcemia and then psychic groins might be um, sort of things like psychosis, depression, lethargy memory loss, fatigue, et cetera and get ounces everyone. Ok. Yeah. Um and it's just called multiple myeloma because it's myeloma affecting multiple areas of the body that confused me a bit. Um when I was in fifth year. So to summarize my part before I hand over to Ryan, um acute renal impairment has loads and loads of differentials and in your exams just break it down. Um whether that's in an osk or if you're trying to figure out what the answer is, it's, is it a prerenal cause renal or postrenal? And then you can go from there, look at the patient's clinical picture. Can you get any clues from that? And what additional tests might help? You figure out the underlying cause? Always look at the creatinine ratio as well when you're treating an AK it helps to know the course so that you can address that fluids might help. Um But if it's, you know, if it's urinary retention, that's not going to make much difference and then review their medications. So you can either use the shortened sort of dam acronym or diamond, which I quite like if they um if they have hyperkalemia, you always want an ECG and monitoring, then um pop them on monitoring, reverse any underlying causes and then treat as per your algorithms. But if it's refractory, they're going to need acute dialysis. So let I know early on the EI ou is the nice acronym for acute dialysis um And just remember renal impairment can be seen in a really wide range of pathologies. So don't miss a cancer like multiple myeloma. I've summarized here on a little table, the difference between acute interstitial nephritis and acute tubular necrosis. So you can try and remember which ones which, when it comes up in exams. Ok. So if no one's got any questions about any of the things I've talked about, I'm gonna hand over to Ryan. Thanks. T that was amazing. I'm going to try and keep up and be equally good. I'm going to quickly skip through. Unfortunately, I've got to now bring it all up to where we were previously. You can type in the slide number if you got it. Oh, can you, me being technologically impaired any of, you know, the light number otherwise just keep going. Oh, yeah. Question eight. That's you. Yes. Lovely. Ok. So next question guys. So we've got a 52 year old woman seen by a GP for bilateral leg swelling. She's been feeling tired a little bit short of breath and she's been having frothy urine. She also feels a bit itchy. She's been putting it down to allergies. Um, she's got diabetes. She's got s les a bit of lupus and asthma. Um, and there's her observations and her bloods. Um, if you just want to put in the chat, what do you think this could be? I'll give you another 10 seconds and then I'll move on in the interest of time. So this one well done Eric, it is indeed chronic kidney disease. So she's got a lot of these classic features that I'm, we're gonna go through now and, and discuss KD in a bit more depth. Um So we're gonna go over what the criteria are for diagnosing C KD and what are some possible symptoms. And I think the best way to go through this is to start off broad and think about the functions of the kidney. So we can work out what sort of symptoms you're gonna get when the kidney goes wrong by thinking about those functions and what happens when we lose that functional ability. So just to start off just to wake you guys up a bit again and for a bit of fun comment, what your, what the best organ in the body is. What do you guys think the best organ is could be the heart, brain, liver, lungs, gi tract, stomach, kidneys, bladder. Ok. So the test is saying kidneys cash obviously saying heart, I knew she'd go for that. The useless muscle that just pumps over and over again and doesn't do anything other else. That's interesting. Spleen. That's an interesting one. Sarah. Ok. Seeing as we can live without it though, I wouldn't say it's quite an s tier organ. But um but you're very right skin. That's interesting one. Aaron. Yeah, I think that's pretty valid test. I feel like brain is a bit biased because your brain is making that decision to say it is the best organ. So, you know, it can never be a, a truly valid opinion because it's got so much bias involved. Um, but, yeah. Ok. So we've got some good ones. Um, everyone that didn't say kidney, I'm afraid you're wrong as far as I'm concerned. And we're gonna go through why? So, what are the functions of the kidney? Can we throw some uh kidney functions into the chat, please? Yeah, exactly. I'm very biased as well. So I'm obviously gonna say it's the kidney. But um you know, I'm going to try and make my case to you. Now with this the rest of this teaching session. So anyone got any functions, filtering stuff? Nice, nice broad, broad start there, activating Vitamin D acid balance producing ep I. So already we're seeing that the kidney is amazing because it does all these um different things that involve loads of different systems around the body. I'm so glad no one's written makes we because that is often one that people think of the kidney. They usually think it's just the the urine producer. But the thing about your kidneys is they don't make urine, they make clean blood and the byproduct is urine. So, yeah, we got some really good ones there. So there's five key functions. They are maintaining BP, excretion of waste products, acid base balance, bone regulation and red blood cell production. Those are the sort of broad ways you can classify into the five main ones. So, what happens with each of these things when they disappear? What kind of symptoms are we gonna get? Cos then you're gonna know without having to think about it, what the symptoms of KD could be. They didn't wanna put them in the chat. Fatigue. Yeah. Very good. So, that's kind of related to a lot of the things it can be because of the build up of waste products. It can be because of anemia and the bee has written an anemia straight up there. So, yeah, that's the red blood cell production. If that's not being produced, we get anemia. Um any others or should I move on edema? Yeah. Very good. Eric. So that's again, sort of like us. Um We'll discuss a bit more about why we get edema and hypertension. Yeah, perfect. Yeah, these are all really brilliant. So well done guys. Um So yeah, so II put the main ones sort of next to where the, the the function is. So obviously, if we don't have good water and sodium retention or we have too much water and sodium retention, then we're gonna get hypertension. Um We don't excrete the waste products. They build up, they make us feel sick, they make us itchy and I've put in brackets retention of desired products cos this is why we get edema and we get um frothy urine is because we're essentially pissing out all of our proteins. So, um the reason we get third spacing is if you think about it, we get edema when we've got increased hydrostatic pressure. So, hypertension is one aspect and that's partly the kidneys fault. Sometimes it's the heart's fault. Sometimes it's, you know, something else, but then also loss of oncotic pressure. So that's things like if your liver's failing, it's not making the proteins. So there's nothing to hold on to that fluid that's in the blood vessels. So it leaks out into the third spaces. We get pleural effusions, we get ascites, we get peripheral edema. But then similarly, if the kidneys are all leaky and all, you're losing all of those proteins that the liver is making, then you're gonna have um you're gonna have proteinuria, you're gonna have that froy, but you're also gonna have edema. Um just because of that loss of oncotic pressure, uh acid base balance. So, yeah, we get a metabolic acidosis cos our kidneys are um holding onto acid and not producing bicarb. Um And then bone regulation, we'll get osteoporosis, we'll get dodgy, calcium and phosphate levels. Um And yeah, anemia and fatigue for the uh for the um red blood cell production. So, yeah, just going over chronic kidney disease. So it's when your eg fr is less than 60 for three months or more or you've got album albuminuria um for three months or more. Um So, yeah, you'll have low albumin in the blood. So I think it's a bit of a typo. Um But yeah, there's, there's, there's albumin in your urine and there's too much that should be there. So, urine acr is a really good way of detecting um, d we always diagnose it too late. And that's because creatinine is um um basically the way we measure kidney function and you lose the vast majority of your nephrons by the time your creatinine starts to tick up. So, um, urine a cr is what you need to think about when you're looking at any patient who's at risk of CKD. Um So yeah, symptoms we've gone through. Um, let's move on. There's a classification there. You wanna look at that later. So yeah, main sort of main two causes you need to remember. Um, for finals, the first ones, you should be rattling off and the ones you, you might potentially, if you're in an ay station, the examiner won't be very happy if you don't think of uh diabetes and hypertension. Um, other things though obviously are nephrotoxic medications. There we go. So, tests showing case in point urine acr doing very well. Um For mi for catching the, the things we might otherwise miss. Um, so nephrotoxic medication. So you might have people who've been popping Ibuprofen for their arthritis for years now. And then now that's probably led them to having a bit of D or glomerular nephritis congenital stuff and autoimmune stuff. So, yeah, diagnosis and we do a nice urine d that's a nice dirty way of seeing, um, straight away if there's any, any protein or blood there acr is a bit more fancy up to date, um, accurate, um, and sensitive. Um, and using these obviously. Um, so we've got to look at the, the causes. So, um, you can look at doing a renal ultrasound. That'll tell you if there's any sort of genetic causes like P CPC KD or um if there's an obstruction there, um renal biopsies um management. So, yeah, there's lots of different uh management. But the main two you need to remember are optimized, hypertension and optimized glycemic control. Uh Those are the two big ones in all CKD patients. Um And similarly, um ace inhibitors and ARB S and Dapagliflozin or SGL T two inhibitors are renoprotective regardless of their um BP or glycemic status. So we will probably, you know, in the future, be giving every single patient who's got early CKD, a Dapagliflozin and an Ace inhibitor or an ARB because they, we know they are renoprotective. Um So the, the big ones and then statins very important. So, Aaron, the um the main reason for good glycemic control is because basically that sugar in your urine is, is shouldn't be there and it's lots of big molecules that are passing through. Um this very fine filter if you think about it essentially as that sugar is going through, it's just punching holes in that mesh and then proteins and other things can leak out behind it. Um So that's why diabetes diabetics. So at risk of CKD and why it's really important that we optimize their glycemic control because if it, if we're not controlling it with insulin and moving it into their tissues, it's going to end up in their urine because it's floating around in their blood and that's going to damage that lovely fine filter that we've got in the kidneys. So, next question. So we've got a 66 year old here. He's having routine bloods. Uh, he's got sort of like a classic, um, medical history of someone of that age. There's his observations, there's his bloods. Um, what do we need to do with this chap? What's the, what's the best thing to do? So, D stage three EP O injection is what Eric's saying? Ok. And that seems that seems very reasonable. He's a bit anemic. There's a, there's another thing though we might be doing beforehand with this chap. So I'll, I'll give you the answer. So it's, it's iron and the reason is that we, yeah, we always, as Nabila said, we do the iron first and then we do EP O. so, um, it's, it's always best practice to make sure that we're, um, giving er the body everything it needs to make these red blood cells before we start. Um, putting in that EP O because obviously if we give them the EP O and they don't have the building blocks to make red blood cells, we're not gonna really improve the anemia. So that's why that's the correct answer. Um So yeah, here's the consequences. So again, we've kind of gone through a lot of this stuff already. So you get dodgy, fluid balance, you get edema, you get hypertension, metabolic acidosis, your electrolytes are gonna go off. Your bone disease is gonna start setting in. Um we're gonna get um osteoporosis osteosclerosis. Eric saying, can we give oral iron tablets first? I suppose it depends on um how bad the anemia is, Eric and how, you know, um replete they are. So you don't really need to go for iron infusion. I think if um if, if you're not too concerned about the patient, but I'd go on a case by case basis. The one thing to remember about all iron tablets, especially in older patients who often, you know, the ones that have CKD is that it's very constipating. Um So we need to be a bit careful with it. But um but yeah, similarly, if they've got a bit of an on online infection or something like that, you don't want to be giving them iron because it will IV because it feeds the bacteria. Um So yeah, just case by case really. Um So yeah, hyperparathyroidism is something just to chat about in terms of um bone turnover and another important function of the kidney. So, um the most common cause of raised calcium in this country is primary hyperparathyroidism. So, there's no obvious cause. It's just your parathyroid gland is a little bit overactive. Um And then you get raised calcium and low phosphate. Um and then with secondary hyperparathyroidism, you have a low calcium um and then your parathyroid um gland responds to that. So you get a raised P TH and your calcium becomes low or normal because of the fact that the P TH is causing uh the bones to leach out calcium. Um And yeah, the phosphate can be raised low or normal tertiary hyperparathyroidism. You see right at the very end um of C KD. Um So it's been going on for ages and ages and ages and that hyperparathyroid gland has been stimulated by that um that lack of calcium for ages. So you get this raised calcium and raised phosphate because um the kidneys are again, not very good at sorting out the electrolytes. So the phosphate goes up. Um And also, yeah, there's, there's a lot of absorption from the gut because of that P TH secretion. Ok. So question 1064 year old man, he's having dialysis. He's got C KD. He's got diabetes, he's got hypertension. So it sounds like they're all contributing towards his um kidney disease. Getting worse, got a tunnel lining him. What do you reckon is the most common side? Effects of dialysis. Ok. So we've got everything is nausea and vomiting from Aaron. That's a very, uh, very good response. So, yeah. Um, no, so basically all of these things, um could potentially be an issue. Um, especially depending on, on the complications. So, nausea and vomiting. Yeah, you, we're massively messing around with these people's electrolytes. So, not, unfortunately, the KD itself can cause this nausea and vomiting but also ha having this huge shift in, in electrolytes and, and you know, um the concentrations of all of these um sort of things can cause some issues for them, but blood clots are a big one. We need to look out for infection. Um is a big one. steal syndrome, high output heart failure, disequilibrium syndrome. Um And then peritoneal dialysis as well. Obviously, same for um, if you're putting in peritoneal drains in people for um for liver ascites, you need to worry about SPP um So on. So I look back here. Well, to be fair, I don't think it's highlighted it. Yeah. No nausea or vomiting. Nora Robson is the, is the top one. Thanks. T um So yeah. Um So these are the sort of ones you'd think of. Um But the one you're most commonly gonna see is, is them feeling, is them feeling sick? Uh OK. Oh, and Tessa's put a lovely little paragraph there on Steele Syndrome which I think I, you should all have a read of. Um, and er, and all the other sort of jobbies, um, whilst that you guys are having a read of that have a look at this question, um, and stick an answer in when you've got a chance. So, just as a clue for this question as well, there's only one of these really that is going to cause, um, or, you know, can induce an Addisonian crisis, um, depending on what sort of medications it's having. So A has put D hips, has put D yeah, you're right. So the things that sort of give us a clue here is um you've got that low sodium and that high potassium. Um So that means that the, the mineralocorticoid effect of um of, you know, endogenous steroid or exogenous steroid, which is that it causes absorption of calcium and excretion of potassium has disappeared. So we know then that this is a steroid kind of issue. Um And obviously if, if this patient has been on prednisoLONE for ages and then he's suddenly become unwell, he's got, you know, pain nausea, vomiting, maybe, um maybe he's got a bit of an infection going on there or something like that. Um It could be all, all those, those millions of causes. Um Then yeah, it's, it's probably that he's not got enough steroid going on. Um And we need to give him more. So, potential post transplant complications, anyone think of any. So, generally classify them into sort of like immediate early and late. There's a big one that kind of broadly fits into all three that begins with an r, that kind of covers most of them. Yeah. So, rejections sort of like the, the big one, that can happen immediately or it can happen, you know, 3040 years down the line. I've seen a, a few on the elderly medicine, more than one currently where they've had this, um, they've had this transplanted kidney for ages. And then, unfortunately, sadly, um, they might have stopped taking their tacrolimus or something like that. And, um, and then suddenly they've gone into, into having a rejection. Um, so, yeah. Um, so you have the sort of effects of surgery, so, infection, bleeding, um, leaks where they, you know, it hasn't been anastomosed, the ureters or, um, or the arteries or the veins. Um, you can have the immediate rejection, which is normally because there's like, you know, an issue with cross matching and, you know, a bo incompatibility, um, or over time it's that the body starts to recognize the, um, oh, I've forgotten the name of the, um, oh, God, it's gonna really bug me. Um, the receptors. HLA, thanks Cash. Thanks for saving me. Yeah. HLA, er, antigens, all that sort of stuff. Um, they, they tend to pick up on that's what's the mechanism for, for the more longer term rejections. It takes a little while for the body to get sensitized to those foreign HLA a antigens. And then, and then start attacking. Um Yeah, they can have a, a massive electrolyte imbalance or they can have a big clot that gets thrown off into the, into the renal artery just because of the trauma of the surgery, endothelial injury. Remember from Biko's triad, um is a big risk factor for clot formation. Um And obviously we're slicing up all these big vessels that then means they're at risk of clots um in terms of immunosuppressants. So, um you, you, you know, we're gonna put these people on immunosuppressants for the rest of their lives, pretty much to make sure that they don't reject um their kidney. And then that means that they're more prone to these very unusual infections. So, Pneumocystis cytomegalovirus, which normally is not a problem for most of us, gives us a bit of a bit of glandular fever or something like that. And it can become really widespread systemic or TB, especially in at risk populations in urban areas. That's, that's always a big one to think of. Um, you can also get reactivation of them if they might have had them previously in that, we haven't done a chest X ray on them, these kind of things. Um And then they're also are at risk of skin cancers, um like Kaposi sarcoma and all these other things or non hodgkin's lymphoma. Um that's from um basically er immune system not being able to detect the malignant cells and kill them off themselves. And then there's the, the big, the big four medications we give that are anti rejection um for transplant. So, tacrolimus, Ciclosporin, prednisoLONE and mycophenolate. And obviously they all come with their classic side effects. Try and remember a few of those for, for the A KT that'll probably do you good. So it causes a KD. So you had diabetes. Big one. This is, this is the big one. So good. Glycemic control, treat their diabetes, start them on an ace inhibitor um and start them on dapagliflozin. Um We're moving towards now. Um it'll probably be that we don't even need the ACR to be too bad or we don't need the G FR to be too bad. We're just going to start putting people on it constantly. The KO KD guidelines have come out recently. Um and they're now starting to suggest even things like um your Wegovy, your Ozempic. So your G LP one analogs that we're using. Would you develop for diabetes now becoming good for weight loss? Now also seeing the are, you know, protective. So yeah, ace inhibitors and SGL T twos, but probably G LP ones are going to be on the horizon as well. Um And yeah, make sure you're doing regular check ups on these patients, do their EGFR every year, do their ACR every year. Um in addition to, you know, checking their eyes, checking their feet like we all do full diabetics. Um ok. Question 12. So this lady's 39. So quite a young patient, she's had quite a lot of blood um in her urine. She got this chronic flank pain and recurrent uti s not getting any dysuria or urinary frequency at present. She had a stone five years ago. Um, she's adopted but she knows that she probably has some sort of genetic issues with her kidneys. Um There are bloods, what do we reckon the most likely cause of our hematuria is? So I'll move on in the interest of time. So, yeah, uh Polycystic kidney disease is um, the, there's some of your clues. Um So you get quite frank hematuria. Um The, these patients just keep having UTI S. Um, their creatinine is very high. They're very young as well. Normally when they start getting all these problems. Um, and they'll be losing a fair bit of blood and becoming a bit anemic with it. Um And that's, that's sort of like your main clues here. That, that, that's what's going on. Also, if you examine this lady, you're gonna feel the kidneys, you know, when we blo the kidneys, you never should find anything if they're um, if they're healthy, but polycystic kidney disease patients, when you blo a Polycystic kidney, you know about it. It's, they, they're just, they're huge, absolutely massive. Um So yeah, they end up getting these horrible fluid filled cysts. Um, yeah, Tess has put a very good point in there about secondary causes of hypertension. We should always be having a look at that in, in young people. Um So yeah, so she's got, so yeah, the, the big ones for autosomal dominant P CPC KD. Um Yeah, the flank pain hypertension, hematuria, uti S and stones and they're getting in a renal failure and they're, and they're very, very young. Um And yeah, um you diagnose it with an ultrasound and then subsequent genetic testing. Um and then the treatment is really just transpl. Um But you can slow it down in the meantime, like the gold standards, the definitive management is obviously to transplant. But in the meantime, Tolvaptan is pretty good. Um can slow it down a bit, give them and then you do symptomatic treatment. You do good um BP control. Um you treat, you know, the sequela of it. So give them analgesia, give them antibiotics. Um You can drain them. Um But yeah, those are the, the main sort of things, but at, at the end of the day, they're always probably gonna need a, a transplant sooner or later. Next question. So we've got a five year old here who should immediately if you, if you know your um your kidney issues, um you'll have, you'll be starting to think about what this could potentially be. Um So his legs and face are looking a bit more swollen, urine looks a bit funny. Had bronchiolitis a baby. So he's got no blood in his urine. No leucocytes in his urine, but he's got loads of protein, no nitrides. He's got low albumin, so low protein levels in his blood, high protein levels in his urine. So that gives you a clear as to what's going on in terms of where that protein's going high cholesterol and reduced. Eg fr what do we reckon? The next step is everyone is saying steroids very good, very good. And anyone wanna hazard a guess as to what's going on here? Minimal change. Very good. Ok. This one here, another 1, 25 year old man presents an A&E with hemoptysis and hematuria. There's his obs. So this guy's got no nitrites, no leucocytes, loads of blood, a little bit of protein seems quite concentrated and he's coughing up blood and he's weeing blood. So this again is another sort of one where I'm sure a lot of us should hopefully recognize it pretty quick. Um in terms of the diagnosis. But what do we, what we taking that one step further? What are you gonna see on the biopsy? And if, if you don't know what the answer is for this, you can, you can throw out the diagnosis if you want if that's easier. So he's just saying a and that is correct. So yeah, this is good postures. Um So anti glomerular basement membrane. Um So you get these I GG deposits because there is anti GBM antibodies. So these, these antibodies deposit along the basement membrane of the glomerulus. And that's why you get all this hematuria. Um But similarly, there's um uh it binds to it in the, in the lungs and that's why you get hemoptysis. C. Can anyone give me a nice, hard and fast rule between nephritic and nephrotic syndrome? And we've kind of gone over it just now with those two, those two sort of examples. With one, you get lots of one thing and with the other, you get lots of another thing in the urine. So, and Nabeel is saying nephrotic loss of protein. So, yeah, so we get lot, lots of protein loss in nephrotic syndrome and nephritic. Yeah. You know, it's a nephritis irritation. Think about it that way you tend to get lots more blood. Very good, well done guys. So, yeah, the big sort of way we distinguish between the two is the amount of protein in their urine. Um So, um, it, it's nephrotic range proteinuria when it's over 3 g in 24 hours. And at that point, um their urine should look really frothy soon as um they're in that range, it's, it's probably nephrotic syndrome. Um But obviously you might have a few clues before that point if you've done a urine dip. Um, and it's like loads of protein, barely any blood or loads of blood, barely any protein. Um, they become a lot more edematous in nephrotic syndrome and we've discussed that before. It's that they're peeing out all their proteins, they get that loss of oncotic pressure and then they start swelling everywhere. Um And you should always sort of can think about it in um like, you know, older patients where you're thinking, oh, this is heart failure. A lot of people get treated for heart failure. They put on these diuretics for ages and then actually, um no one realizes that they've got an underlying nephrotic syndrome um very easy to spot. Um, if you know what to look for. Um And similarly, yeah, they, so they'll have, they'll have low albumin um because they're losing it. Um, and then with the Fritz syndrome, yeah, it's the, the blood in the urine is the main one, but they'll also have reduced output because obviously they're um, er, their nephrons are clogged up with blood. So they're not really, they're able to make as much urine. That's why they get less urine. Um, and they'll get high BP as well. Um Yeah, nephritic conditions. So, try and remember a couple of these for finals, there's certain ones that are a bit more important and a bit more common. Um, but yeah, Buerger's disease, uh post strep glomerulonephritis, er, rapidly progressive glomerulonephritis is a very nasty one, but also I think a bit more rare um, good pastures we've already been through. Um, so they get that kidney failure that hemoptysis. Um Alport syndrome, another one that past med loves to throw up, I think. Um, from what I remember. Um, but it's, um, again, relatively rare, um, lupus nephritis. Yeah, lots of lupus patients that you see on, on kidney wards and your vasculitis or your panca or your canker. Um, all those job, the nephrotic. So, nephrotic is pretty easy in terms of, you can classify it by the sort of patient that sat in front of you. So generally when they're kids it's minimal change, disease, treat them nice and easily with steroids, tend to get better, pretty, um, tends to just get better with age with adults. Big one to remember probably is membranous nephropathy. It's the most common. Um especially in older patients, you need to be like looking at their CT scans, looking to see if there's any obvious masses or lesions because a lot of the time they might have a bit of underlying cancer going on. Um So, you know, just, just keep an eye out, do they have any lung nodules or anything else that could suggest there's um a secondary cause for this membranous nephropathy. Um and I'll have a thickened basement membrane. Um FSG S is the other one that um, that we see quite a lot of and probably those two I'd say are the most important ones to remember. Um for finals. Um And then, yeah, FSG S you see with um a lot of sort of infective er kind of patients HIV sickle cell sle et cetera. Um So yeah, important takeaways. Just to summarize then for C KD cos that's probably the big one that you're gonna ask the most amount of questions on for the A KT and is more likely to come up um in a finals oy station. Um So it's very common. It's often diagnosed late the reasons why are, um just because again, creatinine is what we use. It's the gold standard. Um Well, it's the, not the gold standard, but it's the, it's the one that we use the most commonly. And actually by this point, they've already had quite a lot of loss of their nephrons. Main two causes, you have to remember, diabetes, hypertension, and therefore we need to get on their glycemic control, get on their BP control the best way to investigate. You're in acr um se LT two ace inhibitors, ARB S, those are mainstays and pretty much everyone is also gonna need to be on a statin because they're gonna be older. They're gonna have, you know, if they, if they're diabetic, they, you know, it's often type two, they'll have um metabolic syndrome, therefore, they're gonna have hypercholesterolemia. Um, you know, all these sort of things, but yeah, you can do cure risk and these sort of things on them if you're not too sure. Um And then the extra management just based upon sequela that we've mentioned. So when they start to get in those more advanced stages of D and they start getting anemia, we give them ep but make sure to fix their iron first when they start getting the calcium dysregulation, phosphate binders, diet changes, Vitamin D metabolic acidosis give a bit a bicarb that's probably gonna change. You know, there's less the, the evidence for that is getting weaker and weaker as time goes on. And then when they're really late stage, it's dialysis and transplant. That's about me. If there's no questions, you guys are free to go. Hope you found the session useful. Thank you for coming everyone and um answering questions and answering, asking questions in the chat. Really good engagement. And thank you Ryan for an excellent talk. Very knowledgeable.