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Summary

This on-demand teaching session on nephrology covers critical aspects of kidney anatomy, physiology, common disease conditions, testing, and medication impacts. The live interactive presentation contains Single Best Answer (SBA) questions, followed by an in-depth explanation of the correct answers and disease process. The session will also provide a review of various renal ailments such as AK, ICKD, and glomerular diseases and delve into the concepts of renal replacement therapy, transplants, and diabetic nephropathy, with emphasis on the UK MLA condition map and presentation map. However, attendees were informed that not all the outlined topics would be covered in depth, such as renal replacement therapy and transplants due to time limitations. The class was led by a doctor with extensive experience and training in cardiology and gastroenterology. Anticipated benefits of this online lecturette include an enhanced understanding of the renal system, improved examination preparedness, and the practical knowledge of how to manage renal-related complications. Attendees' questions and concerns are addressed, with the promise of ongoing support for questions arising post-session.

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Description

The 17th session of a 4 month Mind the Bleep Final Year Series! Dr Eamon Dhall (FY1) will talk you through a summary of Nephrology for finals! We hope to break down these often-feared topics & refresh your minds on the most common renal diseases, including AKI, CKD and glomerulonephridities.

Event date is 18/12/2023 from 7-8pm and we look forward to seeing you all there!

Please also remember to fill in the feedback form. All feedback is very useful for us and you will get a certificate of attendance after completing it!

Learning objectives

  1. Understand and summarize the key functions of the kidneys, discussing how these may be affected by renal diseases.
  2. Examine the structure of the kidney and key elements such as the nephron, using this knowledge to understand the processes of filtration and reabsorption as well as the potential impact of disease.
  3. Analyze diagnostic criteria for Acute Kidney Injury (AKI) and Chronic Kidney Disease (CKD), demonstrating the ability to stage these conditions in a clinical setting.
  4. Discuss common renal disorders such as glomerulonephritis and nephrotic syndrome, explaining their presentation, complications, and some potential treatment options.
  5. Assess the impact of electrolyte imbalances in renal diseases, explaining their causes and potential management options.
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Computer generated transcript

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The following transcript was generated automatically from the content and has not been checked or corrected manually.

Hello, everyone. Welcome to our talk on nephrology. Renal medicine, whatever you wanna call it. Just to let a few last few people trickle in and then we'll begin while that's happening. I'll just introduce myself. My name is Mon. I'm the mind the bleed final year lead F one did cardiology. Now doing gastro, always quite enjoyed Renal and have produced for you guys this presentation with another registrar doctor who is a lovely guy. He's checked for it all as well. Should hopefully be an hour. We'll have a few SBA saa little bit about what's, you know, the anatomy of the kidneys and the common things that come up in ss ba S os less so, but we'll try and hit osk later on in the year. We have some various other lectures too. As always, if you guys have any questions, just pop it in the chat. We'll try my best to answer them or if not, then I'll get back to you later. And yeah, I think let's get going. So we've got an hour and today, what we're gonna try and do is basically cover the main things that you're gonna find from renal and SBA S and that's going to be, first of all AK IC KD and a little bit of glomer diseases as well. We'll do some anatomy and function very briefly at the start. Just so everyone's kind of familiar and the rest of the talk makes sense. The bits that we won't cover. But I think are really, really important are renal replacement therapy, transplants and diabetic nephropathy as well. We'll touch on them, but we're not gonna cover them probably to the level that you will be tested on. So I would recommend that, you know, from this talk, do a little bit of that other stuff in the background as well. We also have, I know I've drawn up the UK MLA condition map and presentation map. This is basically what they're expecting you to know. The key thing obviously from a renal perspective rather than urology perspective are AK IC KD diaphragm nephropathy as well. Nephrotic syndrome. Two, I think nephrotic syndrome kind of includes all the glomerulonephritic as well, which we will touch on today. Nice. So let's get going. The kidney generally is made up of a number of different layers on. As you can see in the picture on the left, the out outermost layer, there's a fibrous capsule which kind of provides some protective layer of PL element to the kidney. You then have the renal cortex, the renal medulla, and then you've kind of got all the little bits of minor major ca renal pelvis and ureter as well. Generally, the majority of nephrons are found in the renal cortex with the collecting ducts then going down to the renal pyramids. The renal medulla generally includes the renal pyramids and the renal columns as well. The renal columns are where you get the blood vessels that's going to be your arteries and veins, supplying all the blood to the nephrons and the glomeruli where all the filtration happens from the collecting duct. You then go into the M minor and then the major caddock and then you go into the renal pelvis and then into the ureter. So very basic overview of what the kidney involves. I don't think you need to know anything more really for exams in terms of the Nephron itself. Now, this is important and the reason why this is probably important is because there's a clinical aspect to this where it, this is where it's, it helps to know where di where diuretics affect the Nephron. The reason being you can then work out what electrolyte abnormalities you should be expecting. So the most common, one more, most common ones that we use are furosemide. These are loop diuretics and they work on the N KCC two channel on the ascending loop of Henley N KCC two is sodium potassium, uh chloride, I think calcium as well. But basically, you're gonna get low in all of those different channels because you're not reabsorbing them. OK. Um So you get hyponatremia, hypokalemia, very, very classically with furosemide in the early part of the distal collecting tubule, that's where thiazides work. The later part is the spinal lactone. The thiazides kind of work on the sodium chloride channel. Um and this causes increased potassium excretion as well. Later on through the sodium potassium channels, we call spirolactone or other meno corticoid receptor antagonists. We call these potassium sparing diuretics because they actually don't cause hypokalemia. You got spiro aenone as well and these block aldosterone. So these are aldosterone, um receptor, mineralcorticoid receptor antagonists and they kind of inhibit some of that ras e that ras effect as well. Cool a little bit about function. And this is important because when you get diseases to the kidneys, you can actually very easily work out what you're expecting. What you need to be testing for specific. I mean, there, there's loads of acronyms out there. One I've just picked up is a wet bed and the different types of function to be aware of are acid base balance. So if you get impairment in that, then you get metabolic acidosis. Typically water removal classically kind of, we expect this patient is not passing urine, then you become edematous and often present with a patient who is, you know, very overloaded, swollen and anuric. The kidney is involved in erythropoiesis. It produces erythropoetin the hormone and this can present with fatigue, tiredness and lead to anemia. An important function of the kidney is removing toxins. The one of the main ones here that we're focusing on is urea. When you get high urea, then you can become pruritic confused. You can get a flap, you can get uremic pericarditis encephalopathy. So it's a very, very important complication to be aware of BP controlled as well is crucial. And you know, you can get ros activation to the renin renin angiotensin aldosterone system activation when it shouldn't be activated. This can then cause hypertension, electrolyte balances as imbalances as well. So you can get hyperkalemia and this can lead to arrhythmias and ECG changes. And one of the classic KD complications is mineral and bone disease and this can present as things like fractures, bony pain and often you may see hyperparathyroidism as well. Soap first SBA for you guys. Uh I just saw Paul's message. Can't remember. Will these slides be available afterwards? So we'll put the talk up onto youtube afterwards. The slides we're struggling to kind of get them sorted. So screenshot what you want. Um but this talk will be put up onto youtube afterwards regardless. Alright, cool. Um So let me just create a pole. OK. So on are away, quickly read you through it. 68 year old lady presents to A&E with four days of worsening nausea and vomiting her blood show creatinine 156 baseline of 64 potassium 6.18 0.7 sodium 135. OK. Routine bloods and then her observations show she's quite tachycardia. Um, normal is BP. All right. Last responses and stopping the party. Oops. Ok. So 52% of people have chosen one and 47% of people have chosen two. And that is generally the, the split that I was expecting. So what's going on here? This is a lady who has presented with four days of sudden more acute nausea and vomiting. Her heart rate is raised and her BP is the normal side. So you can suggest from this that she is slightly dehydrated. Ok. Her BP is holding but she is tachycardic and she is vomiting a lot as well. So that are all is risk factors for AK I isn't it? And we know this is an AK I because number of things, one, her creatinine two months ago was 64. This is less than three months, which is not within and more than three months is required for it to be d so it's less than three months of quite a big jump, actually, more than double lobe of hyperkalemia as well. And the urea is typically high too. So everyone genuinely has been able to establish that you need IV fluids, they're dehydrated and they're hyperkalaemic as well. So we need something about that. Generally initi look at the question, the best initial management, you would not give calcium gluconate one without at least doing an E CG and preferably actually, they should be on cardiac monitoring as well. OK. So the first thing you will do is look for E CG changes. If there are ECG changes, then you will give calcium gluconate. If generally the algorithm says, if potassium is more than 6.5 then you would also give calcium gluconate. But again, that can be argued otherwise as well. There are some doctors that would only wait for E CG changes. So that really is dependent up to the clinician, probably be safest to give it, especially as an F one, you know, potassium more than 3.5 or 6.5 give you a calcium gluconate. So, Rai's question, if it's more than 6.5 then you wouldn't do eg you would still do an E CG anyway, just what I just said, you know, you want to look for E CG changes. Um And if there aren't, then you know, the inclination for you to do the, to give the ca gluconate is less, but you can still give it. And yes, thanks Rajat. We know that this patient is dehydrated because uh the urea is raised and they are tachycardic as well with a known cause of dehydration, nausea and vomiting. All right. Nice. So AK I ATI is defined by an acute decline in renal function and this is either through a rising creatinine or decline in urine output. With the table being over here on the right generally stage one is 1.5 to 1.9 times. Stage two is 2 to 2.9. Stage three is more than three times with a few other different caveats or look at the urine output as well. I'm not going to read them out to you, but I would be very familiar with this table. I think it's an important table and does come up in exams. Um, and he said the DARS in terms of being able to stage an AK a little bit as well. All right. And generally we classify it into three types. I'm sure, you know, prerenal, intrinsic and postrenal. And we'll talk a little bit about all of that individually a shock. So the first option is correct then for the SBA. Yes, sorry. So we always want to do IV fluids and E CG. OK. That's the initial, that's the best initial management. Once you've done that, then you will start the calcium gluconate. So prerenal AK I is caused by a decreased perfusion to the kidneys. And generally what people assume is it's hypovolemia ie someone who's very dehydrated. But it is important to also consider hypertension. And there is a distinction between the two hypovolemia being lack of fluid in the, in the blood vessels and hypertension being a low BP, subtle, but there is a difference and we'll, I'll talk a little bit more about that. So if someone is hemorrhaging lots of blood, they're losing fluids in other ways such as vomiting, diarrhea, sweating lots or burns, we get huge extravasation. This can also cause reduced fluid in the blood vessels. This then causes reduced perfusion to the kidneys. And that in itself causes damage for raising the creatinine and reducing the amount of excretion that you can get from the blood vessels. Hypotension is a little bit different. And for example, take heart failure, ok. If someone's got heart failure, you have a poor ejection fraction, a poor cardiac output. And this then causes a backlog of blood into the venous congestion. So actually in the blood vessel, there's a lot of blood but the BP is low and that in itself is causing decreased perfusion to the kidneys. Ok? Because your cardiac output is inefficient. So there is a slight distinction. Another thing to consider is renal artery stenosis. This is where the main artery supplying the kidney is blocked, not fully blocked, but often can be. The lumen can be reduced in size. When that happens. The kidney thinks that there's hypovolemia because well, it's getting reduced supply and then acts as such and you get a prerenal ak I other drugs are also important. So things like NSAIDS and ace inhibitors, we all are aware of often it's confusing to remember which one does, which nsaids cause constriction of the afferent arterial. What this does is similar to renal artery stenosis. You get reduced perfusion to the G to the glomeruli and the kidney thinks that it's hypovolemic ace inhibitors reduce constriction of the efferent arterial. And what happens is when you, the excretion of all the the waste products from the blood is effectively through the difference in pressure between the efferent and the afferent arterial. And if you're reducing constriction of the efferent arterial, well, then you're decreasing that pressure gradient and you've got reduced. Um We, we, we, we have, we've taken out fewer waste products from the blood due to that. The next type of AK I is an intrinsic AK I. This is where you get severe direct damage to the kidneys. Acute tubular injury is the commonest and we'll talk about that. But other things are also glomerular diseases which will have a section to itself later and also acute interstitial nephritis. No. So, acute tubular injury used to be known as acute tubular necrosis. So often notes, you'll see both in questions, you might see both as well if they haven't been updated. And then my med school wasn't. What happens here is you get damage to the epithelial cells in the tubules of the Nephron and the kidney. And these then necrose and slough off sl ca kind of blocking the tubal lumen. OK. Typically, this is caused by two main different categories, either ischemic or nephrotoxin ischemia where let's say you have a prolonged prerenal AK I and you're decreasing perfusion to the kidneys, this in itself whilst causing an AK I can actually also, you know, reduce blood supply to the tubular cells, which are actually some of the most energy hungry cells in the kidney. And these are one of the first to die. These then fall off effectively and necrose blocking the tubules and causing muddy brown casts, which is pathic of acute tubular injury. Ok. So in a question, if you ever see muddy brown casts, always, always think acute tubular injury, The other main cause are nephrotoxin. And there's quite a few of these often, we think of things like gentamicin contrast dye from, you know, ct scans, et cetera, but also think about rhabdomyolysis, hemolysis and raised uric acid. So in patients, for example, who have a history of gout in those three diseases, you often also can see acute tubular injury and it can be quite common. OK? I've put here, reduced reabsorption of water urea and sodium. We'll come to that a little bit later, but it's helpful in differentiating ready acute tubular injury from prerenal ati S and A A two injury is not easily reversible. It's quite hard to treat. Generally, we just to give supportive management, acute interstitial nephritis is a sounds very similar, but actually, it's quite a different in terms of quite different in terms of what's going on with this one. Always think an allergic reaction to the kidneys effectively. Ok. And this is how it present generally in your SBA S the four things to remember are if you get AK I with a fever, a rash and eosinophils in the urine. And that's it. That's your, this is going to be acute incision, nephritis. Ok. Often it's a type one or type four hypersensitivity reactions. So I ge or cell mediated can be caused by drugs such as those that we've got there. Diuretics, nsaids, penicillins, PPI s antiepileptic drugs, sarcoidosis and also a number of infections can also cause acute nephritis. Remember your, your symptoms are always, you know, pyrexia rash. And although typically people say eosinophils in the urine that is apparently in clinic in clinical practice a bit rarer and generally what you do see is white cell casts in the urine. Ok. So and then SBA if you see raised eosinophils in urine or serum with a patient with AK I fever and a rash, think acuteness of nephritis in real life. If you don't see the eosinophils in the urine, that doesn't necessarily mean that's not look for white cell casts too. Treatment for this is to stop the drug. Give supportive measures, give steroids as well. Ok, I've got a little bit on the urea creatinine ratio and now this is not necessarily something that gets used a lot, but you do hear it on the wards and it's kind of just to, you don't need to know it effectively, especially not for exams, but it's useful to be aware that in a dehydrated patient. So I ea prerenal AK I, you're more likely to get a uh increased urea to creatinine ratio in the blood. Uh urea goes up higher in dehydration. Whilst a renal ak I actually is going to be a much lower urea. Ok, if you look on the right this table, um I don't know if you can see my mouse. So if someone can let me know if you can, if not, don't worry. Oops, sorry. Um but let's if we look at the differentiations between prerenal AK is and acute tubular injury or necrosis, there's a few things to note here in prerenal AK, you're dehydrated, your body is trying to reabsorb as much fluid as possible. And we have reabsorbed fluid as it remember as it follows the sodium. So we're going to reabsorb lots of sodium, lots of fluid and therefore in the urine, you're gonna get a low sodium in the urine. All right. Likewise, you're gonna get a high osmolality in the urine because you reabsorbed as much as possible. However, in acute tubular injury, the cells that reabsorbing are damaged. So you're going to get a quite a high urine sodium and a low urine osmolality because you're not able to reabsorb much fluid. Ok? And that's um helpful distinction between the two alongside the urea creatinine ratio. Right. Then the other third main classification of AK I are post renal AK is and these are effectively where you get obstruction to the urinary tract. And these can be through extrarenal or intrarenal causes extrarenal, typically are more common. So things like BPH, tumors, retro protein fibrosis, whilst intrarenal can be things like renal stones and blood clots. I'll come to a, I'll explain after this slide. A um so generally, if someone has an acute retention of urine, that's going to be very, very painful. Ok. And that's a helpful way of differentiating, whether it's chronic or acute. If you get complete obstruction, then you're going to be anuric. So, you know, just generally ask, are you even passing any urine and the key diagnosis to a post renal ak I is ultrasound. Here, we're looking for hydronephrosis or hydro or er hydro basically increase in the size of the ureter. Ok? If you see those, then you can expect that there is a blockage somewhere. So note you're not looking for actually the thing that's blocking the urinary tract. You're looking for signs that the tract is blocked by swelling of the upstream segments. This doesn't however exclude, exclude a blockage. Ok. And there are cases in the literature et cetera where actually case, you know, postrenal ati S have been missed because of this treatment generally is treat the cause. So for example, if you have B PH and you need to treat that, if you have a tumor, then you know, go, go down the the tumor treatment route as well. In the meantime, well, it depends on where the blockage is, but often catheterization can help. There's things like B ph if it's a bit of a higher up blockage, and you can consider things like a percutaneous nephrostomy or an endoscopic ureteric stenting. This is where you kind of go through the urethra, put a stent into the ureter and open up that way. Yeah, with the sodium bit. So in a prerenal ak I you're very dehydrated. Your body is trying to reabsorb as much fluid as possible. Fluid follows sodium. So your body is reabsorbing the sodium and the fluid is following that in with it. Therefore, in the urine, you're gonna have very low sodium in a prerenal AK I and a high urine osmolality because it reabsorbed as much fluid as possible in acute tubular injury, your sodium is not able to, you're not able to reabsorb as much sodium due to damage to the lining of of the of the tubular cells. The tubular your cells, this means like there's quite a high sodium in the urine and a low urine osmolality because you're not able to reabsorb as much fluid as you'd like. Ok. So that's a helpful distinction and just trying to work out the differences between two different causes of AKI which actually have a very similar presentation. Cool. So AK I investigations remember always split into bedside laboratory and imaging. Bedside are basic stuff. So a urine dip, a urine acr so albumin creatinine ratio and M CS if you're worried about an infection, consider doing urine electrolytes and os modality. And that again will help you with what we just described in terms of differentiating prerenal and renal a bladder scan can be helpful as well. This is a bedside test. I don't know if you guys have seen it done. It just tells you how many mils is in the bladder. If it's a lot, you might consider a post renal blockage such as B Ph, then do your bloods, your basic bloods and imaging such as your ultrasound K UB are helpful to. Again, look for blockages. Renal biopsy is the gold standard. If you have causes such as glomerulonephritis causing your AK I, this is where you're gonna pick it up. Now, generally for most patients, it won't get to this stage. But if you're at a tertiary center, you're more likely to get it done. And yeah, it's, it's generally the best way of working out what the cause of this AK I is in terms of management, I use the acronym Stop AK I I think I got this from B MJ. Best practice. But what it is is effectively uh query. Is there a septic screen required because dehy sepsis can cause dehydration or reduce perfusion to the kidneys? Ok. Good question, Paul, we'll get that. Um then look what drugs do you need to stop? So what are the toxins that you're giving? OK. Things like NSAIDS, ace inhibitors, aminoglycosides contrast, et cetera. Try and reduce as many of these as possible, optimize patient's fluid status. And again, this comes down to what we are talking earlier about hypovolemia versus hypotension. Do you need to give someone fluids? Do you need to give somebody um, diuretics? Ok. Because someone's got heart failure, you're gonna give diuretics and fluids will actually worsen the problem. So this is, this is why I was making that distinction at and the last one is p prevent any harm. So, treat any reversible causes, manage any complications. Bianca Crowder is a feedback form. Yes, there is. I think I've just sent it. Um, Paul's question. What happens? What would you do first? Well, do the bedside investigations first. Ok. Generally that's, that's the best thing to do in any exam question. So that's for here. It would be a urine dip A C RMC S et cetera um and consider a bladder scan as well. Ok. Then you want to, you know, but the difference is here, typically, if you're suspecting an AK I, it's because not necessarily the patient's symptomatic but because actually the using these have come back erroneous because often AKI I is asymptomatic and this is quite bad. So, yeah, um Doctor Adi's question is have more prevalent in women and given the hypertensive treatment, potens of angiotensin receptor and nely inhibitors um treatment with diabetic hyperkalemic resistant with diabetic hyperkalemic treatment, resistant hypertensive females clinically benefit from entresto in the absence of heart failure specialists that lowers HBA1C. Uh I mean, II don't know that's a very specific question. Um And also more cardio than Reno Sorry about that. Um Yeah, II, I'm not able to help with that doctor. Sorry. OK. So ak I complications, one of the most feared ones, the one of the ones that actually is probably an emergency, I mean, they need to definitely treat as soon as possible. Is hyperkalemia. OK. And I would especially for exams, be very, very familiar with this treatment algorithm. So someone's hyperkalaemic, as we said earlier, we need to do an E CG if we can, we're gonna put them on a cardiac monitor to monitor them. And if they've got ECG changes, if their potassium is more than 6.5 then we'll consider calcium gluconate. OK? This is gonna be 10 mils, 10% calcium gluconate and this is cardioprotective. So the point of this is you're protecting the cardiac membrane, you're stabilizing it and reducing the risk of an arrhythmia, which can be life threatening hyperemia. OK. In terms of the ECG changes that you're looking out for, they can be found on the set of life in the fast lane diagram, I've got on the top right corner, you get initially peaked T waves, which is, you know, the first signs of hyperemia. But then you can also get P wave flattening pr prolongation and a wide QR S complex eventually that can become quite a sinusoid passion uh pattern. So it looks like a sine wave going up and down. And that's, you know, that's where you're in real bad territory and you need to kind of urgently treat this hyperkalemia. The other thing is insulin dextrose. And actually what I found out making this powerpoint is the insulin is only given. If your patient is diabetic. If you just give dextrose, then actually the patient produces endogenous insulin themselves. And insulin increases the shift of potassium extracellular to intracellular spaces. Therefore, reducing the the amount of potassium in the blood. So that's quite interesting. Not everybody actually needs to be given. Insulin. Salbutamol works in a similar manner. The key thing to note about insulin, dextrose and salbutamol are you're not actually reducing the amount of potassium within the body. You're just moving it from one space to another to effectively reduce the impact on the heart. Ok. So it's a temporary measure and it's something to keep an eye on definitely in the future, but that high potassium might still come back. Um Cool furosemide. Its indication in AK I is a little bit more contested. It's given in sorry, in hyperkalaemia, it's a little bit more contested given le less commonly often because you know, patients are dehydrated, especially if they're prerenal, but furosemide does increase potassium excretion. Likewise, metabolic acidosis, sometimes sodium bicarb is given again, this is a bit debated in the literature and pulmonary edema. So where you've got your fluid overload is treated like you've got heart failure, diuretics, oxygen sit them up, give them CPAP if need be OK. One question, if urine sodium is high in atn surely the urine osmolality should be high too because you have more sodium in the urine. Um Yeah. So the thing about that is you, yes, but you've also got lots of fluid in the urine that you haven't reabsorbed and that makes more of an impact on the urine osmolality. So ultimately, it, when you're reabsorbing the sodium in a prerenal ak I you'll, there's a whole gush of fluid coming with it and that really concentrates the urine. But if you don't reabsorb that urine like you do in ATM, so that you're not reabsorbing that fluid in the urine, then actually you get quite a low urine osmolitic cos it's very dilute even though there is still lots of sodium in there. I hope that makes sense. I think basically the answer to that question is the, the fluid makes more of an impact on the urine osmolality than the sodium. Yeah, basically cool and indications for renew replacement therapy. Now, there, there are some cut offs here. For example, people say acidosis P HS and 7.2. But clinically there used less frequently. But the, the nice little acronym to use is ei ou or your vowels. A standing for acidosis, which is refractory. So it's not going, you're not managing to raise the ph back up and again, the numbers thrown around the 7.2 ph 7.2. But yeah, electrolyte imbalances. Again, refractory hyperkalemia. You've tried to bring it down, but you can't, again, the number here is 6.5. But clinically that's relevant intoxication. So, if you've got lots of drugs in the blood that need to be removed, edema. So they've got refractory overload. You've tried diarrheas and then we tried getting this fluid off and you can't and uremia causing or end organ complications such as pericarditis, encephalopathy, et cetera. These are all the reasons why you would do renal replacement therapy. OK. So our next SBA let me create a pole. OK. I'll give you guys 30 seconds. Take 10 more seconds. Get your last, get your answers in. All right. 54321. OK. Stop the pole. Polls closed. So a bit of a mixed bag here. 41% have gone for secondary hyperparathyroidism and then a little bit more of an even split between answers. 23 and five. So what do we have here here? We have a 70 year old male. So he's, you know, quite an elderly gentleman who's presented with a risk factor from quite a, not a high energy impact. Yeah. So he's just slit from a sofa to the floor. He also has generalized bony pain for a few months. That's important. He's got C KD likely secondary to diabetes and his blood show. He's anemic his eg fr is very low, potassium is normal, but on the higher side, it's got a raised calcium, erased phosphate and a raised parathyroid coma. And what we're asking really is, you know, which complications is he suffering from? Well, he's suffering from anemia. That's one we know, but that's not an answer here. The other one is, there's something going on with his po potassium, his cal sorry, his calcium phosphate and parathyroid hormone with parathyroid hormone. That's your primary secondary, tertiary, primary, your parathyroid glands are producing loads and loads of hormone. Here you get. And that's, that's the problem. That's where your, um that's what's causing the issue and secondary. It's in the name kind of your calcium is low and it's a low calcium that then causes an increase in hyperthyroid excretion from the glands in CKD. What typically happens is your calcium is low and this is due to a lack of activated Vitamin D being produced because of the lack of a activated vitamin da lot of the calcium then has to come from parathyroid hormones. So your parathyroid glands go into overdrive, they start producing lots of the hormone, this causes lots of bone resorption, um and lots of calcium gain released into the blood that way. However, at some point, your parathyroid hormones go into such a state of overdrive that actually they completely decouple from the calcium levels and they're just constantly pumping as much hormone as possible. And at this stage, you become hypercalcemic and hyperparathyroid hormone as well. And that is a late stage complication of C KD. So the answer to this question is going to be number five being he's got a high calcium and a high parathyroid hormone. And therefore he's got tertiary, high parathyroidism. And this brings us on to d right. So defined by abnormality in kidney structure has to be more than three months. That's really important. So you need to do two blood tests more than three months apart. Egfr less than 60 or markers of kidney damage. Typically we use ACR album and creatinine ratio that table there. You can see on the right. I'm not gonna go into it for time's sake, but do become familiar, do become able to diagnose on stage D depending on the numbers. Ok. The causes generally generally are well, diabetic nephropathy is a big one, hypertension is a big one. Glomerulonephritis, which includes IGA nephropathy is a big one. But actually, often we don't even know the answer of why a patient has CKD. So it's very, very varied, very, very broad as well. Remember things like Polycystic kidney disease too and a patient with C KD often actually won't have any symptoms really. Ok. It's only when you get to the very late stages, when all these things like fatigue, edema, et cetera come along and here you've got the symptoms, you know the cause. So if someone's fatigued, it's likely due to low HB but also it could be due to uremia edema because you get reduced urine output, causing salt and water retention. You can become uremic again, which causes pruritus and also anorexia and nausea too. So it's uremia that really causes a lot of problems here. Another important distinction to make is being able to differentiate KD from AK I A good way of doing. It is through an ultrasound. If you look at the kidneys through imaging, then you can see actually in C KG. Generally, you get smaller kidneys. The one exception to this being diabetic nephropathy, where at the early stages, you get very large kidneys and very swollen kidneys and then they start to shrink later on down the line. The other thing is in KD endocrine uh function is, is impaired. Ok. And this is what leads to your anemia and your D and your uh mineral and bone disease. The other thing is if you have a patient with a urea of maybe 3040 is sky high and they're, they're just chilling, you know, they're not encephalopathic, no opathy whatsoever. That's a sign that actually they've had this high urea for a very long time. And that, that is probably d investigations are very similar to what we said for AK I, I'm not going to go into them too much note the bone profile. We want to be looking at parathyroid hormone, calcium, etcetera because that is a complication of CKD. And you know, I think of spend a lot of time talking about this slide without, before you've even got here. But I think that's because this is really, really important. OK. The complications of CKD, uh um uh sodium imbalances. So often you get fluid overload. And this is because you're retaining lots of fluids and lots of sodium treated with diuretics and a low salt and a diet. You can also fluid restrict as well, but that's uncomfortable for the patient. Especially long term. You can get hyperkalemia. Long term. In KD. Often patients can become a little bit more tolerant to hyperkalemia. This is again treated with dietary restriction. Generally, other things like lokelma have come into play and they're very good drugs in um actually helping with hyperkalemia. Then you also you can get metabolic acidosis. This can be long term. Again, sodium bicarb can work. I think it's a little bit more debated and we'll, we have further information on the last two upcoming doctor s question, reduced urine output and AK I, yeah, you get reduced urine output and AK I um yeah, you do. So, Roger's question, what is the reason behind hyperkalemia? And do you also get hypernatremia too? So the kidneys are involved in reabsorbing sodium and excreting potassium? Ok. So when you get damage to the kidneys, you're excreting less potassium and therefore you've got more potassium in the serum and you get hyperkalemia. So you wouldn't necessarily get hyponatremia as well if that makes sense. OK. Um Cool. So, and another big complication of C KD is anemia typically appears when you got T fr less than 35. And it's because you're producing not enough erythropoietin. The main thing, the main thing here is, I think that, you know, you kind of learn KD anemia. Ep O don't do it necessarily always replace iron if iron deficient. So if you get a question that says, what's the first thing you do? Iron and or at least test for hematinics first and look to see if they're iron deficient. OK. Then you know, if you do a cost benefit analysis and a risk benefit analysis and you think, well, ep O will help with quality of life, then fine you can give it. But there are a number of side effects. It can cause hypertension, it makes the blood very viscous. So you can get strokes, mis it can cause recurrence of cancer as well and those who've had it previously. So, you know, we don't give it lightly. There is a analysis to be done for every patient that does get it and always, always replace iron fest. Then you've got mineral and bone disorder. The key thing here is you have it, it's caused really by two things. One, decreased vit activated Vitamin D OK. This then causes decreased calcium absorption and over stimulant and decreased calcium causes parathyroid hormone to go up. Likewise, the kidneys are involved in excreting phosphate. And similarly to to potassium. Because of that, when you get kidney damage, you're excreting less phosphate and phosphate in the blood goes up. Raised phosphate also causes parathyroid hormone or stimulates parathyroid hormone release. The combination of these causes bone reabsorption. You get bone pain, you get weak bones, easily fractured. The treatment for this is low phosphate. Give activated Vitamin D if especially the Vitamin D is low consideration of phosphate binders. So reduce the phosphate in the blood calcium emetics, which effectively mimic calcium and reduce parathyroid hormone stimulation. And in specific cases where you know it's gone quite far down the line. You've tried other treatments, the patient might have tertiary parathyroidism, then you can consider a parathyroidectomy in terms of management. Well, it's often really depends on where we are in terms of how bad the KD is if there's a cause identify and treat it. So if someone's hypoglycemic or very bad, diabetes treat that hypertension treat that nephritis try and treat that problem with things like diabetes are diabetic nephropathy is once you've got it, it becomes a self offending prophecy. And even if you treat the diabetes, the protein urea and all the damage that you get from that can really worsen kidney function itself. So it's very hard to treat. Once it's already begun stopping nephrotoxic, you want to try and protect the kidneys as much as possible and dietary modifications is really important. So things like a a normal protein diet, but low phosphate, low potassium and low salt is very, is crucial. And actually, this could be something like a a case scenario. To be honest where you have to talk to a patient about and counsel them really about how we're going to treat their C KD in terms of lifestyle measures, as well as medicines. Often, you know, treat them, give them statins, you want to control their BP. Ace inhibitors are very good, especially in anybody with protein urea vaccinations, pneumococcal influenza. Um and when somebody hits stage five, so EGFR 15 or less, then we go for consideration of dialysis or transplant. These are the ultimate treatments for CKD. Sorry, I'm rushing a little bit. We're running out of time. Wanna get, wanna get you guys out on time in terms of dialysis, ma two main ones very briefly, peritoneal, hemodialysis peritoneal can be done two ways either overnight or kind of while you're walking around. Um can be performed at home. So it's good for people who you know, are quite active and their lives don't want to spend three times a week coming into clinic or into the hospital. You insert a catheter into the abdomen and use the peritoneum as the exchange membrane with hemodialysis. You go to hospital three times a week. Long term requires an arteriovenous fistula. Although if it's an acute scenario, then you can do things, you can insert lines and get around that elsewhere, arterio venous, especially that requires a surgery as well. Ok. And it uses an external membrane for gas exchange or for exchange of waste products. A little bit about kidney transplants. The best kidneys are those from living donors. These last the longest and have the lowest rates of rejection. Then it becomes donor after brain death and then donor after cardiac death. It's not an option for everybody but it is generally the best treatment and it will provide the best kidney function for you long term. Ok? The issues are one, not everybody is fit for the surgery. If you've got very bad C KD, likely you've got a whole number of different comorbidities which makes you unable to tolerate surgery. And also you have to be able to tolerate immunosuppression life long. Ok. So for example, if your patient isn't going to be compliant with the medications and you know, has a very itchy sketchy record and background, then you, you might not consider them for a renal transplant. But again, it's a very nuanced decision. No one's gonna expect you as a medical student or an everyone to be doing that. Ok. Next question gonna make a pull. Ok. And I'll give you guys 20 seconds, only three responses so far. Ok. Whole host will come in last 23 seconds, get your answers in closing the pole, closing the pole because Nepal. Great. Ok, fine. So I don't know if you can see the results. I hope you can. 68% of people have gone for three. So majority have gone for three with a few scattered going for 12 and four. Really good job. Three is the right answer. Well done guys. Um So this is a patient who is a 42 year old European woman with cancer, January and the SBA any information you're given is relevant. They develop sudden onset, peripheral edema of her face, legs and abdomen. Ok. So generalized edema, noticeably, it's not gravity dependent. So things like heart failure, it starts in the legs and works upwards here. It's her face as well and abdomen. So it's kind of, you know, it's likely to be something like heart failure, lots of protein in the blood. So in the urine albumin is low, you've hit your triad of nephrotic syndrome, haven't we? Now with nephrotic syndrome, let's look at our answers. Well, actually good postures is not, it's nephritic. Minimal change is nephrotic. Remember this is nephrotic. Lupus is nephritic and ig nephropathy is also nephritic. So just from that, we can really rule out 14 and five, we know it's gonna be two and three. The the key thing here actually is minimal change. Disease can occur in adults. It's kind of glossed over. You will always think Children and Children, but it can occur in adults and it's fairly common in adults as well. Um However, this is a European person with cancer and when you see malignancy and commode nephritis, do t do think membranous nephropathy because often, I mean malignancy is a big risk factor for membranous nephropathy. Ok. So number three was correct. Well done guys. Now this is a good slide. I would screenshot this. I'm gonna talk you through it. But what it does do is it helps you understand some of the terminology behind the names we're giving these these diseases. So for example, focal um sclerosing glomeru nephritis, focal means less than 50% of the glomeruli are affected. Sclero means you've got scarring of the glomerulus and then you have a glomerular nephritis. Ok. I would just pore over this kind of get a bit familiar with it. It can help with some of the histology as well. And I don't know if that comes up in your SBA s or not, but they didn ours other thing to notice neuro diseases can be primary or secondary secondary meaning it's caused by another disease process. So, for example, lupus or diabetic nephropathy. Right now, nephrotic versus Nephritic syndrome, people generally tend to be very comfortable with nephrotic syndrome. It's your, you know, the triad people know. So, hyperalbuminemia protein, urea and edema caused by reduced oncotic pressure, other things to be aware of. And this is helpful when looking at complications of nephrotic syndrome. Uh you get hyperlipidemia um in you get lots of antithrombin three, which means you're at increased risk of venous from of VT. So DVTs or PS you get loss of I GG. So also you're at an increased risk of infection as well. Ok. Nephritic Syndrome, you use less, frequently, less important to know, but generally you get your hypertension, your hematuria, an AK I of uria red blood cell casts in the urine as well. Some mild features of nephrotic syndrome. But the main thing here is hypertension hematuria. AK I, no, the main, to be honest, I didn't think I knew much more than this slide for my finals on nephrotic syndromes, minimal change, disease, you know, commonest and it's the commonest disease of gon nephritis. In Children, you get podocyte effacement seen in an electron microscope. Whilst in a light microscope, you don't see anything and 90% idiopathic focal segmental glomerulosclerosis um can be split into primary versus genetic versus secondary versus undetermined. This is a new classification. Secondary often is caused by things such as viruses or drugs. Often in the stem, you will see something about men or african-americans and it's actually quite bad. 50% of people will develop end stage renal disease in a few years, membranous nephritis, what we just had. Now this one is kind of really expanding the past few years in terms of the number of antibodies we found. So typically what people? No is anti pla two R. Um I would remember that one. That's the big one, but there are these other ones here that are all very new, can also be caused by infection. Um malignancy, especially renal cell carcinoma and drugs like gold as well of has an insidious onset. And you can remember the prognosis in terms of thirds, one third re have go into remission. One third develop chronic derma nephritis and one third develop end stage renal disease. The good thing about nephrotic syndrome is generally there is a generic treatment plan or pathway. Ok. We're going to salt restrict fluid restrict. If they're overloaded, then we want to then furosemide can help. And um other things such as ace inhibitors, statins for the hyperlipidemia anticoagulation is really important. Cos remember that risk of VT E and consider steroids. That maybe depends a little bit more in terms of what the disease process is. Complications. We've spoken about earlier but they are venous thromboembolisms, mis strokes, renal vein, thrombosis KD, recurrent infections, hyperlipidemia. So you're getting venous and arterial clots become very hypercoagulable. Ok. In terms of Nephritic syndrome, it's not used very frequently anymore. Typically involves these five that we've got here and we'll talk very quickly about them. Two of the most common ones that I know especially on passed um or as a hoard of questions is the renal function by Mark Cystatin C independent of body mass are more reliable than G fr and creatinine getting false re apparently. Um So cystatin C is it can be used when you are expecting problems with the creatinine. So where you, you're expecting creatinine to not be a representative of patients renal function. Again, that can be in very uh in patients who are very thin or not eating very much or big bodybuilder as well. Then you can consider using Cytin, see if that is an alternative. Although generally we do use creatinine and EGFR from that. OK. I wouldn't say it's more reliable though, although I am not sure on that. To be honest, ma's question, how do you know which is nephritic nephrotic? Do you just have to memorize that? Um in terms of, I don't know what you mean by that. Uh Sorry, I think II didn't see it when you posted the question but yeah, if you want to just explain a little bit more. Um Maica in the meantime, like the syndromes. Yeah, you're gonna have to basically memorize. There's no the names. Um There is no easy way otherwise. Yes. So minimal change FSG S membranous. These are your nephrotic syndromes. These are the ones done, you know, present in the lower albumin swelling, et cetera. Nephritic generally is everything else. To be honest, you're not gonna get anything else like that. You're gonna get a, you're not gonna get tested on a Glomeru nephritis, which is not on these slides. I would say I would hope I'm not gonna say that conviction. I would hope five. So the two main Nephritic syndromes or two of the big ones that we want to, that can't be on SBA S are iga nephropathy versus post streptococcal glomeru nephritis. These both typically occur post infection. IJ nephropathy can be seen as the adult version of IJ vasculitis also known as HSP, but that's the old name. Um and you get the presence of mesangial iga deposits. So if you ever hear that's no question, just think IGA nephropathy happens in quite younger people, Asians especially again, happens, you know, 2 to 3 days after an infection and affects the kidney area. Post streptococcal glomer nephritis, however, occurs 1 to 2 weeks after a throat infection or 3 to 6 weeks after a skin infection and often the skin infection gets forgotten. So do remember cellulitis as a cause of postal glo nephritis, antistreptolysin, antistreptolysin O titer is raised in a pharyngitis strep infection. So if you've got a throat infection that will be raised and it's important to test for and recovery is usually 6 to 8 weeks, although it's quicker in Children and longer in adults. Now, I think very quickly. Last two slides is rapid progressive glomerular nephritis. This isn't a disease in itself, but it's kind of, it describes a number of disease processes where you've got a very sudden decline in renal function can be split into three types. Type one, type two, type three, type one is anti GBM or anti glomer replacement membrane disease. Remember this triad glomer, nephritis, pulmonary hemorrhage, anti GBM antibodies. Ok. If you remember those three that should hopefully help you answering those in SBA S if you see linear I GG deposits in any kind of biopsy that will point you towards that. Um and is treated with plasmapheresis and immunosuppression type two is immune complex so often uh post infectious from strogen. But also IJ nephropathy can cause this and lupus nephritis as well. The little bit at the bottom wire loop appearance on histology is also important. Again, that's just a spot diagnosis. A lot of these can nephritis things. You either know it or you don't really. Um And often they just tend to be spot diagnoses. The last one is partial immune nephritis. So small vessel vasculitis and these are going to be your anchor positive things. So it's gonna be your granulomatosis with polyangiitis or your E GPA eosinophilic gois with polyangiitis. Um anti MPO is also an important antibody alongside Anchor that's typically positive in microscopic polyangiitis. And you know, I'm not gonna go into how to differentiate GPA from E GPA. Here, vasculitis is horrendous. In my opinion, it just takes ages to get a head around, but you've just got to memorize it, I guess. And at some stage, hopefully it clicks. That's all from me. Thank you guys so much. I hope if you have any questions do let me know. I hope that was useful and let me just post another feedback form. How do you differentiate anti GBM with granulomata granulomatous polyangiitis, right? Um So with granuloma, granulomatosis with polyangiitis, you're going to have anchor positive antibodies. Um whilst with Good Pasture Syndrome or anti GBM, you're going to get your anti GBM antibodies. Ok. So look at antibodies also, you know, if you've got a pulmonary hemorrhage, that's gonna point you immediately towards anti GBM. Typically these kind of diseases. No one or I won't say no one, but they're very hard to diagnose clinically. You're going to need to do a biopsy, do your blood tests and that's going to give you the answer. Differentiating between the two I don't think is necessarily so important. Ok, please fill out the feedback. Thank you all for coming. I hope this was useful and have a good evening. If you have any questions, let me know I'll stay on for another few more minutes and sorry about rushing the end, but we managed to get it in an hour. So that's what matters. Sorry. Could you clarify when you're fluid restrict and get fluids in an AK? I uh Yeah, sure. So generally um to the fluid status assessment that's going to be critical. Ok. If somebody is fluid overloaded, they've got peripheral edema, you know, pitting edema in the calves, um crackles on the chest and by basically, and then you may think they're overloaded. They need to be diarrheas. If the fluid deplete, then you would think. Well, actually let's give fluids in terms of, you know, your skin turgor, dry mucous membranes, et cetera. That's when you get your fluids. The challenge comes when you've been diuresing a heart failure patient and they then become uh then, then go into AK I and that's why you have to kind of use things like creatinine ratio. Try and work out how we over diaries, how we under diaries. Is it fluid overload causing AK I? Is it the lack of fluid causing A II? Um That is all clinical judgment really. But your main thing you want to do when you're fluid strict or give fluids is do a fluid status assessment. Is that prerenal causes? Yeah, that those are all prerenal causes. Ok. Um So typically, typically you will be giving IV fluids, especially in exams just if you want to give it an extra level of kind of understanding you would fluid restrict in patients with heart failure because it's the overload causing increased preload. And if you remember the Frank Starling curve when you've got increased preload and it goes too far, then you've got reduced cardiac output and that then causes reduced perfusion. How much fluid would you give again? That would vary on the on the fluid status. You won't go wrong with 1 L over an hour. Generally, if you've got heart failure, you might go a little bit less. Yeah, I hope that answers all your questions. Can you give 500 M? Yes, you can. It doesn't really matter necessarily how much you give. Um and then if you're like an at e just give 100 ma there's no no harm in that and then reassess. Um Yeah, no worries. Ok. It off now. All right. Thank you guys.