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Hi. Yeah. Can you hear me? Yeah, I can. Yeah. Ok. So your audio is ok as well. So, um, I just shared the link into the peer share, like whatsapp group. So hopefully more people will join. I think we can start like, two minutes past three minutes past. Do you, do you want me to share everything from? Uh, yeah. So you will share the slides and I'll just keep an eye on the chat and I'll put the feedback link at the end. Yeah. And I'll tell you if there's any questions or anything. But, uh, yeah, if you could share the slides you can try to do that. Now, see if there's no issues. Yeah. Does that work? Yeah, I can see Renal medicine. How do I make it go there? Yeah. Both sides. Yeah. And are they moving? Yeah, that's fine. Cool. Mhm. Just wait one more minute. And then, and so, yeah. So it was just you tonight? Um, yeah. Sure. That was supposed to do dermatology. She can't do it anymore. Ok. Ok. Yeah. So, so, so don't rush through it. No worries. Yeah. All right. Right. Well, we get to start. Yeah. Oh, yeah, you can make a start. Yeah. Ok. So, hi guys. Uh, my name is Yan. I'm one of the, um, final years. Um, and today I'm going to be delivering a talk on renal medicine. Um, just before we start just a few things on reading medicine. I think that, um, sometimes doctors tell you, you know, it's good to go back to first principles and usually take that with a pitch of salt. Um because it can get really complicated if you get too deep into the weeds. But I think that um with renal medicine, especially when you come across questions, which may, you know, test you a bit deeper, it's good to have a good fundamental knowledge of how everything works at base level and then kind of build from there. So, um with that in mind, I decided to go over these topics today. Um chronic kidney disease and acute kidney injury and then um a few things on glomerular disease. So, um glomerular nephritis and nephrotic syndrome and then I'll be going over some um slides on renal interstitial and tubular disease. Um I will not be covering urinary tract infections and I will not be covering anything like um neoplastic disease um in this lecture and they kind of overlap with uh urology, which is the surgical side of renal medicine. So I decided to stick to these and discuss these on a more in a bit more fundamental level. Um Two sides. So uh moving on to kidney in uh acute kidney injury. So, the thing about acute kidney injury is to, is to have an understanding of um how to recognize it. So, it's defined as an acute drop in kidney function. So if somebody has an already reduced kidney function and it drops even further, um that can be uh uh AKI or when somebody has a normal renal function and it drops um that's also ak I um numerically is, is it's um described as a rise in creatinine of more than 25 and 48 hours or 50% in seven days. That kind of, that doesn't really tell you much if you're on the ward or um I mean, if you're reading a question, you might go ahead and calculate it. But um the big one here in bold is a urine output of less than 0.5 mils um per kilogram per hour for more than six hours. So by that, you know, that if somebody weighs 70 kg and their u urine output is 35 mils, um it should be 35 mils over an hour. But if it's 35 mils over two hours, you know, that's less, that's, that's that you're starting to enter acute kidney injury kind of um definition and the symptoms are oliguria. So um very infrequent passing of urine and urea. So complete um lack of passing of urine, hypertension, pulmonary edema and hyperkalemia. So, pulmonary pulmonary edema is secondary to um fluid retention. So, you're not, your kidneys aren't filtering any fluid. You're not passing urine, you're keeping all that fluid in and um that enters the pleural space and you get uh that enters the lung interstitium when you get pulmonary edema and hyperkalemia. Because as you know, one of the processes that the kidney performs, one of the things it does is it gets rid of um hydrogen and potassium. And if it's not able to perform its function, the potassium accumulates and you get hyperkalemia. So um very rarely will, well, not rarely, but it's common to um be become aware of acute kidney injury because of these um secondary things rather than um the decreased urine output um in terms of the aio, so the causes of acute kidney injury, um they can be prerenal, they can be renal or they can be postrenal. So, um prerenal causes due to a lack of perfusion. So, a lack of blood supply to the kidney and I've listed um things which can cause that there. So whether it's systemic vasodilation, renal vaso uh vasoconstriction, decreased cardiac output or decreased vascular volume, um renal causes. So they can be, so these are intrinsically involved diseases which affect the kidney. So that can either be glomerular disease, that can be uh interstitial disease or that can be a vasculitic disease. A vasculitis, um a small vessel vasculitis usually that affects the kidney and impairs the glomerular abi uh glomerulus ability to perform its filter and function, um postrenal. So, obstruction to urine outflow, uh so it can be intrinsic uh obstruction. So, nephrolithiasis, uh so um kidney stones and extrinsic compression. So, if you have a neoplasm or a tumor, that's um compressing the ureters from the outside, that can also cause um uh urinary outflow obstruction. Um any sort of bladder cancers uh obstruct um the ureters and the ureteral uh ureteric uh junction. And then um in terms of how we manage acute kidney injury, um it's very much about rehydration. Um if it's secondary to uh dehydration, so, decreased vascular volume, you want to rehydrate the person, uh you wanna monitor their fluid balance to know their urine output. You want to treat any underlying cause. So is there sepsis causing vasodilation causing achy I is there hyperkalaemia that you need to treat is the pulmonary edema which I mentioned earlier that you need to treat. Um then this is a very useful pneumonic stop the da drugs. So stop any diuretics. Um So, antihypertensives such as ace inhibitors, ARB S and um imino glycoside, antibiotics, Metformin and nsaids, um you can also relieve the obstruction, that's the cause. Um and then ensure appropriate dosing of drugs. So by that, I mean, drugs that the patients on now because they have a reduced kidney function. If there are drugs which are cleared by the kidneys, their doses need to be appropriately adjusted um usually decreasing the dose and consider whether this person may require um renal replacement therapy, dialysis or admission to ICU. And I would say that these are the main things that you need to know about acute kidney injury. Um I wouldn't make it more complicated than this. Um I would just know the prerenal renal and postrenal causes. Um And then if you have an understanding of those, it may be easier to solve questions regarding AKI. Um Yeah, then uh this slide is um sorry if you can't read my handwriting, I think you get a copy of these slides you consume in. Um but this is just rash the uh renin angiotensin aldosterone system. Um And it's just an image which describes how it works and, and how the glomerulus. So a glomerulus is a unit, a filtering unit in within the kidney, um how it's affected by these things um on this system. So, in terms of the glomerulus, I don't know if you can see this but um Nsaids and ace inhibitors which are drugs which I mentioned in the previous slides, um they can affect the tone. So the extent to which the afferent and efferent arterioles which connect to and from the glomerulus, how um open they are. And if you um if you can see if you see there, if you use both, you're affecting the uh glomerulus ability to filter. Um And that's why those drugs need to be stopped because if you have a decreased flow of blood into the glomerulus already due to AK I if on top of that, you add the effect of nsaids and ace inhibitors, you're reducing that kidneys ability that the perfusion of that kidney further. Um just a brief word on glomerular disorder. So, um so glomerulonephritis, um and nephrotic disease, nephrotic syndrome, you hear those words and there is a lot of different types um and they tend to overlap. Um and the way I divide it and the way um I suggest you guys think about it is that there are diseases which cause primarily protein urea. So, um protein excretion from the kidney and then there are diseases which primarily cause hematuria. So, um bleeding loss of blood from the kidney, um nephritis. So, any disease which primarily causes loss of blood from the kidney can progress to cause sclerosis, scarring and then that can cause loss of protein. So that means that uh protein urea. So the loss of protein can be a complication of any renal disease, regardless of whether it was primarily uh nephritic or nephrotic. And these two triangles at the bottom, they just show that um I move on to the next slide. Uh Let's just keep a slide that any disease, you know, all of these diseases will cause a loss of proteins. As you can see the ones to the left such as minimal change disease and um focal segmental glomerulosclerosis for example, they cause more protein loss and they cause little to no blood loss. Um other diseases such as good pastures disease. So, anti GBM disorder disease, they cause primarily loss of blood and um loss and some protein loss. Because a as you can see, um all of these diseases, the diseases have an underlying nephrosis. So, loss of um um protein and um some of them, not all of them and to varying degrees will cause a loss of blood as well from your kidney. And in terms of the signs and symptoms of the glomerular diseases, primarily nephrotic syndromes. Um So ones which cause mostly protein loss can be, these can be primary um or they can be secondary. Um they cause a significant loss of protein, more than 3 g in the urine within 24 hours. Um and they cause an oncotic edema. So, if you remember oncotic edema is caused by a loss of protein in the blood, um that causes fluid not to be kept inside the blood and it moves outside the vessels. Um and that causes edema. So people with um uh nephrotic syndrome will have swelling of the legs, they will have pulmonary edema, they might have um puffiness of the around the eyes and the hands. Um and because you're losing so much protein, the liver reacts and it produces more proteins and it produces more um lipids causing hypercholesterolemia could um produces more clotting factors. Um And that causes hypercoagulability. This is also due to the loss of antithrombin. So, that's a specific protein involved in the clotting cascade via the kidney. Um uh So, in terms of other things, it does, it causes hypertension. Ok. So, um and a risk of infection due to the loss of immunoglobulins in the urine as well. Um and the EGFR, so the glomerular filtration, glomerular filtration rate is preserved as filtration can continue through the defective membrane. So, in nephrotic syndrome, you have to really go deep into it. You have pics and these podocytes aren't working right? And that causes protein to leak through them. Ok. So the EGFR of the kidney is still able to perform its filtration, but it's through a defective membrane. On the other hand, in nephro in Nephritic syndromes, um which can, as it mentions here, be a symptom of a systemic vasculitis such as um HSP or granulomatosis with polyangiitis, which used to be called Wegner's disease. Um Those primarily are uh their main symptoms, hematuria or loss of blood. Uh There is also loss of protein as I mentioned earlier, but it's not as profound. So it's usually less than 3 g in 24 hours. You have um hydrostatic edema. So you all the protein is still there, all the fluids still inside the vessels. But because you have, your kidneys aren't able to filter as much, the fluid can get squeezed out um of the of the um of the vessels because there's just overload of fluid. Um And that also causes hypertension and the EGFR falls in immediately because um in Nephritic syndrome, you have the podocytes um and they're damaged and the kidney can't filter. Ok. Um So instead of having a preserved membrane and it's leaking, you just have a completely damaged membrane and the kidney can filter. Ok. Um And then this is going back to the slide and um essentially protein loss from the kidney can underlie any sort of pathology, glomerular pathology. Whereas loss of blood has present in some bananas. Um and the treatment in nephritis, what you do is you control the BP and you inhibit ras by using ace inhibitors or angiotensin receptor blockers. Um in terms of specific therapies, um these are dependent on the histological diagnosis. If you have to do a biopsy, um you have to examine the biopsy on uh um using histology and then um that way you can target therapy. Um and these are usually immunosuppressive treatments in terms of nephrotic syndrome, you're trying to treat the symptoms. So you're trying to reduce the edema. So you reduce the fluid and uh salt intake of the patient, you and you can prescribe loop diuretics such as furosemide, um treat the underlying cause. So do a biopsy and to decide the appropriate treatment um which can be, for example, steroids in um in MCD and then produce protein urea. So, um inhibit RAF again, using ace inhibitors or arbs and then treat the complications. So, whether that's thromboprophylaxis, antibiotic, prophylaxis and the use of statins because we mentioned that they can cause hypercoagulability. Um increase susceptibility to infection cause you're losing immunoglobulins and hypercholesterolemia. So, using a statin can reduce the num the amount of lipids moving on um acute interstitial nephritis. Um this is um an acute inflammation of the tubules and interstit of the kidney. Um It can present with an acute kidney injury. It's one of the renal causes of acute kidney injury and hypertension. It can present with eosinophilia. So, um you have a production of eosinophils um in response to inflammation causing the inflammation. Um and the Sinop count can be raised and then if you do a urine dipstick, it will show evidence of an immune reaction. So there will be increased white cells on the dipstick without the evidence of active infection. So, um as you remember, in urinary tract infection, you'll have increased white cells, uh presence of nitrates. Um and those are the two things which you need to diagnose uh urinary tract infection. But in this, what you have is a sterile pyura. So, pyura, so, pyogenic urine. So it's urine which contains b uh contains white cells but it is not um it's it's sterile. So there is no um nitrates, there is no evidence of bacteria inside the urine. Ok? And this just happens because there is a hypersensitivity reaction due to drugs usually penicillins and nsaids. Ok. So it's uh the body's hypersensitivity reaction um to um to um drugs. Um and the way you do it is you treat the underlying cause. So, remove the causative agents and you can also give steroids. They can also reduce uh reduce the inflammation. Um and this is reversible, uh acute interstitial nephritis. A reversible condition doesn't cause persisting renal damage if identified soon enough. Um Another one is acute tubular necrosis. So these two things. So um interstitial nephritis and then tubular necrosis. There, I always found them difficult to distinguish. Sometimes they have similar names. So, in necrosis, you have death of the tubular epithelial cells. Uh this is the most common cause of acute kidney injury. Ok. And it's diagnosed by seeing muddy brown casts on urine microscopy if you have you muddy brown casts on urine microscopy, that means you the the diagnosis is acute tubular necrosis, ok? And this is due to the death of the renal tissue and the cells within the kidney. Um and it can cause also an increased white cell count but will also cause significant blood. So, um you'll have a muddy brown test and an increased white cell count, ok? Um you'll have an increase in urinary sodium and a decrease in urine osmolality, which means that the tubules are unable to concentrate urine or hold on to sodium. So, one of the functions of the kidney is as part of the rash system is to retain sodium and water. Ok? To expand the intravascular volume. If the kidney is unable to perform that function, you have an increased loss of sodium from the kidney, from the kidney uh in the urine and you have a decreased urine osmolality because you have more water in that urine. Ok. So you have more sodium but it's more diluted because you have more water. So the kidney is essentially not able to perform its function and of retaining sodium and water. And the result is the opposite. Ok. Um And the causes are prolonged type of perfusion causing ischemia and toxins which uh kill tubular epithelial cells. So, if you have prolonged type of perfusion, you'll have AKI and um also acute tubular necrosis. Ok. Um And the hyperperfusion can be due to shock. So, shock is any sort of decrease in intravascular blood volume um due to sepsis and due to um dehydration. So, in sepsis, you know, you have systemic vasodilation and dehydration. You're just not taking in as much water as you should be decreased intravascular volume, hypoperfusion AKI acu tubular necrosis, um toxins such as contrast dye gentamicin is a big one. Um That's a very uh commonly asked complication of gentamicin is what can cause. And the answer is a cutar necrosis and it's uh renal to nephrotoxic and then nsaids as well. So, nsaids as you can see on most of these slides are culprits of a lot of these diseases um affecting the kidney and if you go back to the sliding at the start, it's due to the effect it has on the glomerulus and um the afferent arterial, ok, within the glomerulus. Um, in terms of management, it's supportive. Um, you give IV fluids and you stop nephrotoxic medications. Ok. Um, the kidneys are able to regenerate as well. Ok. Um ok. So, in terms of the other uh uh diseases, so we have renal tubular acidosis and there's four types of renal tubular acidosis. Um However, the third type is a mix of the first two. So it's 12 and four. Essentially that we're gonna be discussing. Now, this is when you can, if you like I did, if you spend too much time on this, it can go, you can get really granular and you can start really, really deeping it and thinking about it too much. Um But essentially in type one renal tubular acidosis, um the location of the pathology is the distal tubule. So that's the first fact you should remember. Ok. What causes it is that you have a dysfunction of the um proton potassium atpa use active transporter. Ok. Um And what that means is that the kidney is unable to excrete, put uh hydrogen back into the urine. Ok. As you know, um hydrogen ions are responsible for uh the acidity of fluids. So, um investigations if you're unable to excrete hydrogen ions back into the urine the urine will become more alkalotic, ok, or more alkaline. Uh So that's an increase in urinary ph. And the opposite will be true in the body. So the serum ph will then decrease or become more acidic and you'll also have a decrease in the serum potassium. So, uh from the diagram, as you can see, normally the hydrogen goes into the urine, the potassium goes back into the DCT. So the distal convul to tubule that can happen, potassium stays in the urine is lost uh and um hydrogen stays inside the body and the serum PH decreases. OK. Type two. This, this diagram gets a bit more complicated, but essentially the location is the proximal tubule again. OK. What happens is that there's an enzyme within the kidney called the car carbonic anhydrase. And it doesn't work as well. And if that doesn't work as well, essentially what happens is you don't produce enough bicarbonate. OK. Um This bicarbonate then stays in the urine. It's highlighted purple here. And what that means is you and you also know that bicarbonate causes um an alkaline. It has um it's an alkaline um ion. So it causes um an increased urinary ph and the opposite is true inside the body. So you have a decreased. So uh serum Ph and you have a decreased serum potassium. And this is because in order to balance the negative charge of the bicarbonate, uh the potassium would usually stay along with it Ok. So it stays in the urine. So um the bicarbonate stays in the urine. So you have an increased urinary ph potassium stays in the urine. Um So you have a di increased uh urinary potassium and a decreased serum potassium. Ok. And the management much as it is for type one is oral bicarbonate. Ok. Um And then in type four, what happens is the pathology is in the collecting duct. Um there is reduced aldosterone. If you go back to rats, um aldosterone stimulates the kidney. And what it does is it causes sodium and water retention and loss of um potassium and hydrogen. So, if you don't have that stimulation from aldosterone, the opposite happens, you start to lose sodium and water. Ok? So you have decreased sodium, absorb reabsorption and you start to retain less potassium and hydrogen. Ok. So you have um it retain more potassium hydrogen. So you have decreased potassium hydrogen excretion. So the result is um um a decreased urinary ph, OK? Cause you lose less hydrogen iron than your urine. A decreased, sorry. The result is um OK. And then the result of that is that um the retention of potassium inside the body and the retention of the hydrogen ions inside the body causes um a reduced production of ammonia inside the kidney and you have, and it's highlighted green here. So if you have no ammonia, ammonia is alkaline. Um what happens is if you have less of that in the urine, this urine is gonna become more acidic. Ok? And so you have a decrease in urinary ph and you have a decrease in serum ph and an increase in serum potassium. Ok. Um So you're not producing ammonia, the urine becomes more acidic. Ok? You're retaining potassium and you're retaining hydrogen. So the serum becomes more acidic and you get increase in serum potassium and the treatment is treating the underlying cause and fludrocortisone. Fludrocortisone is an exogenous uh mineralocorticoid which can perform a function of um aldosterone. Ok. I have a note here because this is in some exam questions. Um hyporeninemic hypoaldosteronism, it's seen in diabetes and it causes type four renal tubular acidosis. Ok. So if you see diabetes and you have these sort of symptoms and the results of the investigations, you should think of type four renal tubular acidosis. Ok. Um Moving on to chronic kidney disease. Um I think this is the final topic. Yes. And then I have some questions. So, um chronic kidney disease is a reduction in kidney function. Ok. And this tends to be progressive. So it's not an acute disturbance in kidney function. This is the case in aci this is a chronic progressive and it tends to also be irreversible, decrease, decline in kidney function. So it's described as a GF eg fr of greater than 60 protein urea. Ok. Or an eeg G fr less than 60. Ok. You have this thing called the A score. And this assesses the degree of protein urea and is based on the albumin to creatinine ratio. Ok? So essentially the albumin to creatinine ratio, as you know the creatinine, the rate at which creatinine is cleared from the body is constant. So if you use that as a background against which you can measure the amount of protein that's being lost in urine, you can say, ok, so for this amount of creatinine lost, we have this amount of protein lost. And if that number is very high, so you have a high, high value of protein lost for a constant creatinine loss, you can say, OK, this is abnormal. Ok. And why you use the ACR is because uh creatinine clearance essentially standardizes the concentration of urine. So if somebody had really, really concentrated urine, you wouldn't know if the protein lost in that urine is high or low, you need something to measure that against. Ok. Um And a note here is that the G fr, so the filtration rate can decline by 50% before the creatinine begins rising. Ok. So if you get a result that has an increased creatinine clearance, you know, the kidney's function could have decreased by um much more than that before you get that result. Ok. Um And the thing about CKD is it's usually asymptomatic. It's diagnosed on routine testing. There are a number of signs that the patient can present with such as it, itchiness of the skin loss of appetite, nausea, edema, muscle cramps, peripheral neuropathy, pallor and hypertension. All of these symptoms essentially relate to the functions of the kidney. Ok. So itchiness of the skin because you have an increase in number in amount of urea and uric acid that your body is producing and it's not getting lost by the kidney um nausea because you're keeping your body's keeping in toxins that it can get rid of when you become sick. Um edema because you have fluid overload, fluid overload. Um uh peripheral neuropathy, pal hypertension, muscle cramps. Again, symptoms caused by uh the kidneys, inability to get rid of toxins. Ok? Um Risk factors for chronic kidney disease include being of old age, um hypertension which slowly reduces the number of functioning nephrons inside the kidney. It destroys the glomerulus, um diabetes. Um So you'll be aware of diabetic uh nephropathy. Um and that can cause CKD smoking as well. And an interesting one is inherited lower nephron numbers. So people who have an inherited lower number of functioning units within the kidney, um they're more predisposed to developing chronic kidney disease because their kidneys will just run out of steam earlier. Um in terms of management, um you have to measure the EGFR um three months apart, ok, twice three months apart and um measure the albumin's creatinine ratio. Ok? Um Use ultrasound, there's a history of adult uh of autosomal dominant polycystic kidney disease. Um and usually in chronic kidney disease, uh the kidneys will be small. However, if the cause is adult, um A DPC KD, the um kidneys will be large. Ok. Um because they're cystic um in terms of the sequelae. So some of the problems which people with chronic kidney disease encounter are anemia of CKD. So the kidney is damaged, they can produce epo or erythropoietin. And what happens is you have a decreased production of red cells and if you have a decreased production of red cells, you develop anemia. Ok. Um As you know, so um in terms of managing that you give them oral or infused iron and you correct the iron first before we offer exogenous epo to inject. Ok. Um uh an IPO exogenous epo is actually a performance enhancing drug as well and then renal bone disease. So, um there's two things that kind of feed into renal bone disease. So, the first thing is that uh damaged kidney or um uh can't basically can't reduce, can't get rid of phosphate. Um And the second thing is it can activate Vitamin D So what happens is that the retained phosphate, it binds to calcium. And because of the lack of activation of Vitamin D you have decreased absorption of calcium from the gi tract. Ok. So you have phosphate which is bound to calcium causing a decrease in calcium. And you have lack of absorption of calcium from the gi tract causing a decrease in calcium. Ok. When that happens, the parathyroid glands which sit behind the thyroid gland. Um what they do is they increase the production of pth so, parathyroid hormone. Ok. Um And that causes bone resorption. So essentially, it causes the calcium, it causes you guys know this increased osteoclast activity and bone um mass gets lost, which causes osteomalacia, osteoporosis. And that's all in an attempt to increase the num uh the amount of calcium. Ok. Um In terms of the management, you give Vitamin D and recommend a low phosphate diet and you can also use bisphosphonates, ok. Uh which inhibit the osteoclast activity. Another very common complication, very commonly asked in exams is hypertension. Um and that's due to a dysfunctional um al angiotensin aldosterone system. Ok. So essentially the kidney is, it's just uh it doesn't play a role in ras anymore as well. So what you do is you offer an ace inhibitor and you offer an ace inhibitor to anybody with diabetes and a cr greater than three hypertension and acr greater than 30 to all patients with CKD and an ACR greater than 70. OK. Um And I know this is one slide that summarizes, essentially summarizes all chronic kidney disease. But I mean, this is pretty much what you need to know anything else that stems from this. Um is, you know, you could answer probably using all this information. OK. And with that said, I think I have a few questions on on the next. Oh no, I have one more thing to mention. Ok. So um drugs in chronic kidney disease. So ace inhibitors. So uh this is just a quick description that probably that can help you understand why we give ace inhibitors. So, in a hyper filtrated kidney. Ok. So in a kidney that's filtering too much and it's causing proteinura. So um a kidney where the pressure inside the glomerulus is so much that you're losing protein. Um What do you want to uh what happens is uh you have an increased efferent tone. So the vessel that's leaving the glomerulus is tighter relative to the vessel that's providing blood to the glomerulus. So it's creating an increase in pressure across the glomerulus. OK? And it causes protein loss. So, if you give an ace inhibitor, what happens is the ace in the um angiotensin which causes this constriction of the efferent arteriole is inhibited by the ace inhibitor. OK. And the efferent pressure increases uh decreases. Ok. And that causes a lower pressure across the glomerulus. Ok. So the protein isn't squeezed out the glomerulus as much. OK. And that reduces micro and macroalbuminuria. So, protein urea. Ok. Um Another thing is SGL T two inhibitors. So patients with um D causing protein loss, um plus or minus diabe uh diabetes. So, I know that SGL T two inhibitors are usually used in the treatment of diabetes, but any patients with CKD causing protein loss may benefit from treatment with an SGLT two inhibitor. OK. Um And that's that. So those are the main things. Um And then I have a few questions. I think there's four or five questions maybe. Um which you can answer, you could put answers in the chat or you can just answer them yourself. I don't really mind. Um The first question is about a 76 year old woman with hypertension, she's taking amLODIPine um, 10 mg daily, um, and a 24 hour BP meas measurement shows um hypertension 100 and 68/90. Ok. You have your investigations there and your albumin to creatinine ratio. So the question is which class of antihypertensive should be added? Ace inhibitor, alpha blocker, beta blocker loop diuretic or thiazide like diuretic. You can put answers in the chat or um, just answer yourself. It's up to you guys. I'll just give you a minute. OK? I'm gonna show dance for there. Yeah. So, so sign in the chat ace inhibitors. Yep. So that's the right answer. Yep. Ace inhibitor. So going back to the slides, uh I just did, uh, I tried my best to explain um, what you would add. Um, if somebody has um um a loss of potassium, a loss of uh uh protein in the kidneys and hypertension. So, hypertension and anybody with an albumin creatinine ratio, um, greater than um, you greater than 30. Yes. And this person has 50 requires an ace inhibitor. Uh next question, uh 78 year old woman is admitted to the surgical unit was suspected of vesical colic fistula. She has a history of hypertension type two diabetes and angina taking amLODIPine Metformin, glycoside, simvastatin bisoprolol. Her serum creatinine is 100 and 20 the consultant surgeon request a CT scan of abdomen with contrast, which medication should be stopped before her ct scan. AmLODIPine bisoprolol, gliclazide, Metformin or simvastatin. just give you a, give you a second on that. Ok. So I'll just go into the answer. So um the answer is Metformin. OK. So you'll know that um if a person is experiencing AKI, what you wanna do is you wanna stop the dam drugs. Ok. So diuretics, ace inhibitors, Arbs, aminoglycoside, Metformin and Nsaids. So um the answer there is Metformin. You'd stop that in a person with a uh rising or raised creatinine level. Ok. When they're about to get contrast which can further affect um or exacerbate AKI. Ok. On this person, she probably has um um if she has a vesical colic fistula, she could be suffering from dehydration. She maybe has underlying chronic kidney disease. We just want, you would stop the Metformin if you're giving her something that can cause a further decline in kidney function. Um Next question is 55 year old man. He's rescued from a collapsed building where he's been trapped for 12 hours without water. Ok. So it's a clue. Um His temperature is 35.6. Pulse rate is 100 BP, 90/60 90/42. So again, JVP is not visible at the abdomen is non tender. Um, your investigations are there, um which is the most likely cause of this biochemical picture. Bladder outflow, obstruction, direct renal trauma, hypovolemia, rhabdomyolysis or sepsis. I'll give you a circumstance for that too. Yeah, we have two answers there. Two different answers. Anybody else that could just move on? OK. Another one, rhabdomyolysis. Anybody else? I think this is a good question. OK. So um the answer is hypo bleeding. OK. So uh rhabdomyolysis, that's honestly, I think I would answer that too if I first saw this question. Um But the, the thing is that um you're getting from, from the vignette, there are a few things. OK. So um the person's been trapped for 12 hours without water, OK? Um Pulse rate is 100 and BP is 90 to 42. So they're kind of on the brink if not already experiencing an element of shock. OK. So you know that they're hypovolemic, OK. JVP is not visible and the abdomen is not tender. So you are now, so the JVP is not visible enough. So you, you're not. So uh essentially the amount of blood uh inside the body is not, is not high enough for there to be a visible JVP. OK. So, hemoglobin is 100 and 68 So it's unlikely that they're bleeding. OK? But um you have an increased sodium level, OK? So an increased sodium concentration, an increased potassium concentration, an increased urea and the creatinine. OK. So the thing is that um in dehydration, which is the answer probably here and then hypovolemia, the urea and creatinine rise will um not be proportional. OK? Uh or will be proportional. And um you also have a raised creatinine kinase, which is right, which would point you towards rhabdomyolysis. Ok? But um in rhabdomyolysis, the creatinine kinase would be in the thousands. Ok? It wouldn't be 100 and 40. It'd be way, way, way higher than that. Ok. So the answer is hyperemia. Yup. And then I think this is the last question. 61 year old man has two months history of ankle swelling. He has hypertension um and a 30 year history of sero negative polyarthritis. His medication includes ramipril, sulfaSALAzine, hydrochloroquine, um sulfate and diclofenac. His BP is 100 and 56. Over 90. He has pitting edema to mid thigh and signs of chronic deforming polyarthropathy in his hands, but no joint tenderness. His optic Funai show silver wiring and a v nipping urinalysis protein four plus plus no other abnormalities. The investigations are there. Um And which is the most appropriate initial treatment? Would it be Candesartan furosemide, indapamide, prednisoLONE or prednisoLONE and cyclophosphamide. So you're trying to figure out what's going on. Um What exactly is um happening and then trying to figure out what's the most appropriate initial treatment in this case. Let me give you a few seconds here. OK. So uh the answer is furosemide. So from the sides, um you may remember that in treatment of nephrotic syndrome, um one of the things you wanna do is you want to treat edema. This is a description of nephrotic syndrome. So they have hypertension, he has pic edema um and the fact that he has a chronic deforming uh po polyarthropathy. So, you remember that nephrotic syndrome can be caused, it can be either primary or can be secondary um certain conditions which cause arthritis. Um um autoimmune conditions can also cause nephrotic syndrome. Ok. So this person po potentially has a um secondary nephrotic syndrome. Ok? Um And you can also tell from the low albumin level, OK? Their albumin is 21. So they're losing protein in the kidneys via the kidneys. Um uh and that's causing their edema. Ok. And that's an oncotic edema. And what you want to do is you wanna give them furosemide and that will offload uh the fluid, the fluid overload that they're experiencing. Ok. Um The answers to all these questions, you can find the information in the slides. Um I think Bianca just said that you guys will get the slides. Um That's the end of the presentation. I hope it was OK. Um And I think there is a feedback form for you guys to fill in. Um But thank you very much guys. Thank you. And so yeah, I just put the feedback form in the chart. So if you can um just leave us some feedback, that'll be appreciated. So, yeah, pretty good slide. Thank you so much. Thank you. Thanks. Thank you, Bianca. Bye.