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So if you'd like to start uh for everyone's information, this is Chris Steven Marks presenting on acute kidney injury. Thank you very much. Indeed, I Liam for everybody for joining today. Good to see so many of you uh online and I know that things have been difficult both in Ukraine and Sudan. It gives us great pleasure to teach as part of the crisis, Rescue Foundation Medical School. UK. So I'm Steven Mart, I'm Professor of pediatric nephrology and transplantation at University College London, Great or Street Institute of Child Health and the Great Ormond Street Hospital for Children NHS Foundation Trust. And today I'm going to be concentrating on acute kidney injury. So what I hope to make what could be a dry subject quite interesting is to talk about some of the functions of the kidney, try and make it quite case based with a little bit of a discussion and a quiz talk about some definitions, incident etiopathogenesis, some of the clinical features to look out for in history, examination investigations and what the treatment and kind of bringing it all together. Thank you for so many of you joining today and for putting in the chat just where you are um currently but also which your medical school you're in. At what medical school? That's very grateful. So, the kidneys are amazing at removing waste and foreign materials at the least cost and useful materials and energy by regulating our homeostasis of both the body's water and electrolytes as well as acid base balance. And interestingly, kidneys are able to do this over a wide range of water, salt and protein dietary intakes and degrees of activity. So one way of assessing this historically in the past is to be take a group of medical students, you have them a little bit dehydrated by not giving them enough to drink and then doing vigorous exercise, sometimes running into a marathon after having a large protein load. So big steak intake beforehand and if that was the case, does m do you know um what you would detect abnormality in the bloods? So what first thing might be see in the blood test? Either you can put a hand up or um if you want to write in the chat. So is that is an increase in, yeah, it increase in uh protein or urea. Yeah. So yeah, so also put um that the urea being increased and that's exactly right. So normally what people say is the creatinine, but of course, the creatinine doesn't go up until um fairly laterally when you actually are in established acute kidney injury. And we changed the terminology really from acute renal failure to acute kidney injury to talk about the prevention of developing um kidney disease. And also because actually both adults and Children as patients don't like the word failure. So we've gone away from acute renal failure and chronic renal failure now to acute kidney injury and the injury being before you get a degree of renal dysfunction and the creatinine going up and chronic renal failure, chronic kidney disease. But the other thing some people say is what about your electrolytes? You can have a high remic dehydration or even an hypo dehydration. But in fact, naturally, um that happens so very often you're able to maintain normal sodium levels. And the way to think about the kidneys is really to think about what happens if they don't work and thinking about using a dialysis machine. And the two main issues that they do is they pull the fluid away. So that's called ultrafiltration. Um So basically getting rid of um the water, which normally happens through our urine production, but also the waste products, which also happen in urine normally if they're not able to be removed as well. Obviously, there are other body functions such as the production of erythropoietin by the kidneys as well. So let's put this all into perspective of the case. A 15 year old, a Caribbean boy, he's got a one week history of abdominal leg and facial swelling. He's increasingly short of breath and he and his siblings have had a few viral upper respiratory tract infections with sore throats over the last few months and they've had no rash, but a reduced oral intake over the last 24 hours with uria. So on examination, he's unwell. He's got a weight on the 25th percentile height on the second cent with a capability to be full time of two seconds. He's got palpable peripheral pulses, a prominent apex beat. He's 15 years of age and hypertensive with a BP of 15, 2/94 millimeters of mercury and he's tacked nee with lung crepitations in all areas and generalized edema and ascites. So initial investigations show a fairly normal full blood count. Uh hemoglobin of 1 20 white cell count of 12.3. A normal platelet count of 325 times 10 to the power of nine per liter. And that's negative sickle screen. He's got abnormal serum electrolytes. He's hyponatremic with a low sodium of 1 30 millimoles per liter. Hyperkalemic with an elevated potassium of 7.2 millimoles per liter associated with acidosis with a bicarbonate or TCO two of 14 millimoles per liter and evidence of renal dysfunction with an elevated urea and plasma creatinine of 24.8 millimoles per liter and 258 micromoles per liter respectively, he's got a low total calcium of 1.8 millimeters per liter. And uh as people were putting in the chat um about albumin levels. He's also got a hyper at 24 g per liter. And obviously, the filter is that because of dilution or is it because of actual protein loss? And is it due to protein losses in the gut? And, but without a history of diarrhea, the most likely is in the urine. And so having evidence of protein urea or any evidence of liver dysfunction. But in fact, his bilirubin is normal and so is his alt, he's got a positive uh urine dipstick for proteinuria with four plus and hematuria of two plus. Um but a normal heart on chest x-ray with no evidence um of infection, but there is evidence of infiltration with pulmonary edema and he's got two big echo kidneys on renal ultrasound. So, what I want you to contemplate and you can add to the chat um and we'll go through the end of the lecture, what you think is wrong with him? But which two of the following, the best descriptions of his clinical condition, do you think he has acute kidney injury? Does he have acute kidney injury on top of chronic kidney disease? Has he got chronic kidney disease or endstage kidney disease? Is he nephritic or nephrotic? Does he have neither of those? Does he have Nephritic syndrome? But without nephrotic syndrome, does he have nephrotic syndrome? But without nephritic syndrome or does he have both evidence of nephritic and nephrotic? The seats are originally for acute kidney injury coming up. So, thank you for that. What about evidence of nephritic or nephrotic syndrome? One of them, both of them or neither of them? Ok. And then also if you'd like to consider what the most likely diagnosis is. Sorry, I just got some people saying both nephritic and nephrotic syndrome. What's the most likely? Yeah. So what's a dad saying? The most likely diagnosis is a post infectious glomar nephritis, which is c So what's the most likely diagnosis? Hemolytic uremic syndrome? A minimal change nephrotic syndrome. B, postinfectious glomar nephritis, C renal venous thrombosis D and sickle nephropathy. E Yeah. So comments being we don't know how much proteinuria is but you do know that there's four plus on dipstick and a lower albumin level. Um But we've had votes for minimal change nephrotic syndrome and also post infectious and glom nephritis. So let's um talk a little bit about some of the definitions of acute kidney injury. Does MD A have an idea, want to put their hand up or tell us what they think acute kidney injury is. See, some people still trying to log in is that it's a, it's a, it's a sudden failure, to be honest with the not a gradual increase in uh uh but not a gradual increase in the symptoms. It's a suddenly like within 12 days of uh show showing of the symptoms and failure of the kidney functions. Yeah. Thank you very much. And also in the chart, there's a rapid of kidney function. Yes, sir. Yeah, sorry, a sudden loss of kidney function in less than three months, um characterized by azotemia. Ok. And we'll talk a little bit about azotemia as well. Also the people who are joining. Thank you for putting in the chat where you graduated or which medical school you're at. And um thank you for joining. Yeah. So the the features that we want to get with acute kidney injury is thinking about to being sudden decline in renal function. And as you said, accompanied by the retention of nitrogenous waste with a disturbance of water and electrolyte imbalance. But the important thing not only be about the sudden decline um in the renal function and the glomeru filtration rate, but it's potentially reversible. So that is the main thing to think about. So the sudden decline in GFR or glomerular filtration, which is potentially reversible, but it may not be a change in the urine output. You may or may not have a reduction with all the. So what is meant by the terminology, a urea? So do you have an idea? It's less than 100 mL of urine? Yeah. So literally, of course, anuria means no urine, but that's not true. But we generally define that you can have um what we call bladder sweat, which is really the active transitional epithelial layer of the bladder being secretory. So when we say anuria, we really define it as a urine output less than about one mil per kilogram per day or in an adult, we say around 75 mils. So in other words, you can be in the situation where a child is in Ric, but they produce some urine because it's this bladder sweat. So they've got the feeling that they need to pass the urine and it's very often it can be globular. It's not clear yellow urine that you're used to. But basically a secretion which is active from the transition epithelial there. And then we get on to the technology of oliguria. So by oliguria is where we have a reduction in the urine output and really is defined by the minimum amount is excrete the daily solute output of around 500 mo per day in an adult. But um we're really in a situation where we talk about this being around half a mil per kilogram per hour or less than one mil per kilogram per hour in neonate. But remember, the non oliguric states may happen up to 50% of Children with acute renal failure and you may have a normal or increased urine output if there's evidence of tubular dysfunction, secondary to aminoglycoside toxicity, resolving acute tubular necrosis or if there's an intermittent or a partial uteral obstruction. Now, someone mentioned earlier azotemia and that really is an important aspect because basically it means you've got an elevated urea, which is what you said. So it's an abnormally high accumulation of nitrogenous waste in the blood. It can reflect obviously acute kidney injury, but it can also reflect chronic kidney disease. It can also happen if there are other conditions such as a high protein diet, if there's glucocorticoids. But we can also see if there's inadequate um calories. So does MD know what we mean by the team, the term uremia. So is a team, it tends to be more of an American term. We generally talk about Uremia in the United Kingdom and in other countries. So what I mean by uremia is really the symptom complex which reflects that elevated urea level. So the symptom complex that you get where you're feeling tired, you can have a discoloration of the skin which really reflects the kidney dysfunction when they fail to regulate the body composition. So we talked a little bit about Nephritic syndrome and nephrotic syndrome in that case. So really to think about what is it? That's the difference. Now, some patients may have features of Nephritic Syndrome. Without nephrotic syndrome, you can also have nephrotic syndrome without Nephritic syndrome, you can have a mixture of the two. So when we talk about Nephritic syndrome, we very often mean microscopic hematuria. And very often if you've got a glimer nephritis, which is a histopathological diagnosis from taking a kidney biopsy, what we call percutaneous renal biopsy. In a patient who may have clinical features of a Nephritic syndrome with microscopic hematuria, that might be Coca Cola color urine with proteinuria, a reduction in the urine output. So, oliguria resulting in salt and fluid water retention and overload, which potentially will give you high BP. And that is what we call with those four features of hematuria, proteinuria, oli and hypertension as part of potentially an acute kidney injury or being a clinical nephritic syndrome. Now, nephrotic syndrome, if you imagine the kidneys are like a S SIB and if the S SI holes get too big, then the protein molecules will leak into the urinary space, therefore, resulting in loss of protein in the urine. So, proteinuria and that ongoing huge loss will result in a low albumin level. And we usually use the threshold for proteinuria of a gram per meter squared per day. And we usually use the features of hyper being less than 25 g per liter and a result of that loin level, the body tries to compensate by edema. So, third spacing of fluids associated with um hyperlipidemia. So if we look at patients that have a Nephritic syndrome, the most common cause that we would see is what we call a postinfectious gloms. Some people will say post streptococcal liver and nephritis. But remember other infections can actually cause it as well if you've got a nephrotic syndrome. But without a Nephritic syndrome, then that most likely in somebody who's never had nephrotic syndrome before, is most likely going to be a minimal change in nephrotic syndrome. But we have few features of both. And you've got a mixed nephrotic nephrotic picture. Then actually, then do you know what the most common cause? So if you've got features of Nephritic syndrome, so the hematuria, now a nephrotic range proteinuria with hypia, you've got uria edema and hypertension. So you've got features of both nephritic and nephrotic syndrome. Well, actually, the cause is most likely still going to be a postinfectious glomar nephritis, like you see with Nephritic Syndrome itself. So I trained around the world and when I worked in Newcastle, but also in North America, we used to have in the in emergency and the availability of having a microscope. So we would spin down the urine ourselves. And as we spun down the urine, you then look at the sample and potentially you would see this which is a red blood cell cast. And here you can see this on face contrast microscopy. So actually when the patient comes in and you see evidence of this, then to me that actually means that you've got evidence of the glom nephritis a that did you want to ask a question for your hand? Uh Yes, that this cost uh it is uh does this suppose a tubular problem or it's uh just a normal glomeru nephritis problem? So it's usually because of glomerular bleeding. So basically, you're getting clumps of the red blood cells coming down and passing into the urinary space usually when you've got um leakage. So you actually see these clumps and that red blood cell count is really patho mic of having a glomerulonephritis or some. It doesn't tell you why you've got the inflammation of the kidneys, but it tells you that something is going on inflammatory with them. So, let's talk about the incidence of acute kidney injury. Well, it's less common in Children than in adults and really has remarkably reduced in the developing world due to the advent of one thing. Does anybody know what that is? Well, it's actually the rotavirus vaccine. So being able to vaccinate Children, especially in Africa against rotavirus has really dramatically reduced the number of infections and that acute dehydration that leads on to an acute kidney injury. Usually what we call a pre renal failure. It's really important, but it really depends where you look at your baseline. So acute kidney injury is often associated with the major disease process, especially in tertiary referral units. But you must be worried that those that have got evidence of poor growth. If there's been a longstanding history of polyuria, polydipsia or evidence of renal osteodystrophy, you must consider whether you've got evidence of acute kidney injury on top of chronic kidney disease or acute and chronic renal failure. So, for acute kidney injury, it's important to consider prerenal renal and post renal causes. So here you can see the kidney, we're really talking about prerenal being before the kidney. So this is where you've either got decreased true intravascular volume or you've got evidence of circulatory failure. And by prerenal acute kidney injury, we're talking about the reduced true intravascular volume due to dehydration or gastrointestinal losses, salt wasting or diabetes, insipidus, third, space losses of sepsis and nephrotic syndrome and evidence of circulatory failure with either congestive cardiac failure or pericarditis or cardiac tamponade. When we talk about renal, we're really meaning intrinsic renal disease. So you can have prerenal where you're dehydrated. And then this proceeds to acute tubular necrosis and that can really either be toxin base. So, thinking of a hypoxic seem injury to the kidneys. Um drug induced nephrotoxicity are a toxin mediated phenomenon as well. We do see this also in tumor lysis syndrome with the breakdown of cells usually associated with um a tumor and potentially treatment. So for example, a B cell lymphoma being treated with riTUXimab, which is a BCE depletion agent and basically reducing hugely. Um and the break up of the tumor mass resulting in urate crystals, basically blocking the tubules of the kidney, resulting in this kidney injury, an intrinsic nephritis. So it can be drug induced or idiopathic. So, thinking about for example, sarcoidosis, but more commonly with drugs when we think about nonsteroidal anti inflammatory drugs, which is why I would always recommend if you either your own Children or Children that you look after that if they're unwell and they've got a fever is maximize the dose of paracetamol and adds in a nonsteroidal anti-inflammatory only if you're giving it regularly up to the maximum dose glomar nephritis, as we said is an important cause of acute kidney injury. And we talked about post infectious, there can be other types. So, membrane glomar and some of those are akin to C three or complement C three glomerulopathy. We've got lupus nephritis, HSP, nephritis or what we call iga vasculitis, nephritis. Um having an anchor positive vasculitis or anti GBM positive or an idiopathic rapidly progressive glom nephritis. We also see with nephrology, um what we call ethic hs so sugar and toxin, um positive um diarrhea, associated hemolytic uremic syndrome. But also we can see hemolytic uremic syndrome due to other drugs and post bone marrow transplant. Also, you can get progression of your acute kidney injury with acute tubular necrosis going on to cortical necrosis. And of course, if that's involving both kidneys, then you can result in having the evidence of overall renal dysfunction. There can also be a clot in the renal artery or vein and especially neonatal or what we call perinatal renal venous thrombosis. So it might not be the main vein, but it might start in the peripheral acute vessels and go in to the main vessels, we also have infection, especially if there's evidence of sepsis or plantar nephritis. And then of course, if you've got bilateral obstruction, either a bilateral ureteric obstruction or if you've got obstruction in solitary ki kidney or perhaps more distantly urethral obstruction and that can impact on both kidneys. But whatever the reason is, whether you have an obstruction by debris. Um as we said, or nephropathy, if there's been damage to the tubular epithelium or renal ischemia, we know from gentamicin and heavy metal animal studies with the reduction in glomerular capillary permeability, which also happens in ischemia that will result in acute kidney injury. Whereas if there's a high intra tubular hydrostatic pressure or a leak of infiltrate into the peritubular circulation from tubular epithelial damage resulting in an imbalance of waist excretion. But with normal GFR, that can result in acute kidney injury as well. So what are the, some of the key points to consider um when you're taking a history? Well, for me, it's really important to have an idea about the fluid status over the last 24 hours, how much has come in. So, thinking about what the total fluid volume intake is, um but also what the output is. So, actually, if you've got a fever, then you'd expect the requirement to have more um fluids. If you've got increased losses from diarrhea and vomiting, then you require more input. Obviously, if you've got a massive hemorrhage or burns, then you require more fluids as well. But also thinking about if there's any evidence of symptomatology from urinary symptoms for the flu or the polydipsia taking a good past medical and drug history, especially including an adolescent recreational drugs in this young adult, but also going back and getting a good antenatal history was a normal antenatal scans. Did they manage to do a third trimester? Ultrasound? Because if that's normal, the most likely thing is your normal kidneys, this might not be evident from just the quick 20 week ultrasound, which um is the, is used to look for abnormalities but very often we only pick up gross dilatation or hydroureter nephrosis. It's also important um to think about uh previous urinary tract infections. If there's been other tests, if there's been any evidence of rickets growth, failure, failure to thrive organic failure or any surgery. And in looking up to these patients, we take a full family history looking for any evidence of renal problems. So not just asking is MD in the family, got any kidney problems but specifically asking for high BP and dialysis and transplantation in any family members. Moving on to examination and looking at the state of the patient, their hydration, their observations having information of what their last weight was. But with serial plots of the weight hikes and head c looking at um their overall um clinical status is really important and their peripheral perfusion evidence of the JVP edema or the core peripheral temperature is as well as important as their other observations. Slots of waist height and head circumference will show if there's been any change or reduction in the sents and any signs of cardiac failure or multisystem disease with peri prop arthritis, rash or have evidence of or lesions. So, specifically looking for palpable kidneys or bladder and any abdominal masses. So, investigations will eventually be targeted but initially potentially treat for any inflammation with elevated sr and crp evidence of anemia, thrombocytopenia, thrombocytosis. Any evidence of hemolysis or schistocytes on the blood film, looking to see what the coagulation screening cross matches Um and also checking um your electrolytes but also renal function with your creatinine, checking on the calcium, magnesium phosphate and alkaline phosphatase and albumin as well as liver function test bone profile. I never be scared to do a blood culture and c reactive protein in the patient in whom there is a history of suspicion of fever and temperature. So initial investigations may in fact come back showing you um that there's evidence of chronic kidney disease with a low ized calcium, a high PT parathyroid hormone level and a low ferritin. And that might be really important in management. You might want to look at the reticulocyte count of the coons test to see if there's any evidence of hemolysis as well as an E coli, the comp C three and C four, as well as the cree nephritic factor and any evidence especially of inflammation with immunoglobulins, including IGA A. So teter and anti DNA beam antinuclear antibody double stranded DNA quantifying how much DNA there is became extractable nuclear antigens the anchor and the anticardiolipin antibodies as well as an autoimmune profile and the anti glomerular basement membrane antibody. Oh The one thing I would really stress is the importance of getting one drop of urine to be able to do urine analysis. And hopefully not just after you've done the fu but if you do get some something overall ratio, if there's evidence of proteinuria, if you think there might be an infection and looking for my culture sensitivity and considering the excretion of sodium depending on the intake and what the like for you to follow up with the patient. So if you look at urine electrolytes, acute kidney injury on patients who are not on diuretics, then you'll see that the sodium is low with an elevated urea urine plasma to creatinine urea and creatinine ratios, which would be commensurate with uh low sediment that we'd see in prerenal acute kidney injury. Whereas the urea level, your protein urea, sorry, the urine to plasma urea or creatinine levels um are important and they will be elevated in pre renal acute kidney injury or low in renal acute kidney injury when you're most likely going to see urinary sediment. So I wouldn't routinely do a chest x-ray on patients. But if there was any concern about their breathing infection, and it's also worth doing an ECG especially in the case of tachycardia. Also considering doing an echocardiography and an urgent renal ultrasound to really principally exclude obstruction that will also pick up larger kidneys of an acute process of small kidneys or chronic renal failure, considering doing a percutaneous renal biopsy or an x-ray of the left his left wrist and hand. If you're worried about chronic kidney disease and the frequency of doing blood tests is going to be determined by the clinical picture. But if you've got a rapidly progressive glomar nephritis may be repeating the bloods every 3 to 4 hours. Whereas if the numbers are fairly stable and every six hours, we'll probably suffice. We want to do a bone profile, liver function test at least once a day with the full blood count during dip state and urine electrolytes unless you're already on diuretics and a renal ultrasound scan, especially if the initial images suggest for that it's indicated. So going on to assess the fluid balance. So looking clinically for patients dehydrated and tachycardic with full peripheries, prolonged cap refill time with dry mucus membranes and sunken eyes. You may consider doing a flu challenge 10 to 20 mils per kilogram of normal saline over an hour. We normally suggest 10 mils per kilogram and then have a reassessment, especially knowing what the urine output is of that child. We give a further challenge if the patient was euvolemic, but if there was no response, if they were euvolemic, then we would give furosemide um after the flu challenge. And if they have signs of clinically fluid overload with tachycardiac rhythm, elevated jugular venous pressure, edema hypertension, then we'd give fu if fluid overload is severe and consider dialysis if they don't respond. So, the important thing is to remember, it's a multidisciplinary team, not just doctors but the nurses looking after the patient, the pharmacist are recalculating the drug doses, the dieticians really to make sure we've got a high calorie diet, the play therapist and social worker to really assist with the psychosocial team and the looking after managing of this patient. So we'll do potentially further fluid boluses of crystalloid colloid with furosemide as indicated by the clinical state. And we'll try and do at least a daily weight if not twice daily, accurate input output, recording at least four hour BP and four hour monitoring of the peripheral core temperature gradients and food management. We would basically be giving the food po and then holding back, potentially giving FRM. And we would cut down to sensible losses especially if they're OIC and giving 400 mils per meter square per day with replacement of the urine output of the UIC. We restricting to about 50 to 75% of normal if they're overloaded. And we'd modify that to the pure restriction of dialysis of urine output established in the poly urine recovery phase. You got to be careful because if you're replacing the and sensible losses for the last 24 hours, then you may actually set a fluid target being a much better way than especially if the renal function is continuing to improve because you may be chasing your tail, so to speak, by giving too much fluid if you're replacing the fluid loss over the last hour. So let's um have a consideration how you would manage um hyperkalemia. Um So if you've got an elevated potassium, thinking about putting them on a cardiac monitor, giving them salbutamol if they're acidotic bicarbonate and they're not salt water overloaded. But considering um giving fluide potentially calcium reum to stabilize the heart. We recently, we've used their code to good effect. Uh but also in the rare instances, I've done this over a decade, um probably about a dozen times of having to get an insulin injections infusion and really trying to try to treat the um um blood sugar level and the um insulin infusion at the same time, if you've got a low sodium, then that might be secondary to fluid overload. So, again, you'd want to fluid restricting, potentially consider kidney replacement therapy. I very rarely would actually go ahead with the hypertonic saline. But if you got evidence of hypernatremia secondary to sodium retention, so an elevated sodium level, then again, we'd consider FFU and if the patients on a ric proceeding to dialysis, if they got a little calcium and then giving calcium supplements, when, if you need an activated vitamin D is also beneficial and the ongoing fluid management would be to cut down the fluids. So we would be thinking of here um is giving insensible losses of 400 mils per meter square per day. And that would be um um done with the replacement of your out put and we give all the out if they were or cut back. If their food overloaded, we replace the I with intensive BSS for 24 hours. It said the targets, the renal function continues to improve. So let's um consider um ongoing management of these patients. So if you got a high, there we go. If you've got um a high phosphate, then you're going to restrict your dietary phosphate intake, potentially give a phosphate binder. If you're acidotic, depending on your fluid status, you may want to give sodium bicarbonate. And if you've got elevated BP, you're wanting to know whether that's due to fluid overload or alteration in the vascular tone. So you might want to give diuretics initially to get rid of the salt and water and some medical management and some dialysis of the failure to respond to diuretics or pulmonary edema and evidence of Licia. So some of the nutritional aspects of acute kidney injury, we know that it's associated with a cata bolic state of malnutrition can develop um and delayed recovery. So we've got to ensure that we get good nutrition. So we would have a dietician involved very often if they're hyperkalemic and you've undertaken the usual cardiac monitor, salbutamol bicarbonate, furosemide, calcium Rezum or ch insulin dextrose infusion, you may then go on to wanting to restrict their um potassium intake as well with the dietician maybe put them on a low phosphate feed as well. And we would want to aim for at least the maintenance calorie intake and protein intake of around 0.6 g per kilogram. We start an nutrition peoria or vi a naso gastric tube to minimize catabolism uremia. We try not to give TPN if possible, But for the purposes of looking at the drug doses, it's good to have your own local formulary. Having a look to see what drugs you may want to change with the drug dosages with acute kidney injury. Many drugs require a decreased dose or a prolonged dosage interval, renal failure. And you've got to know uh what nephrotoxic drugs to avoid. So what are the indications for kidney replacement therapy? Well, usually if your potassium is very high. So above 6.5 and not responding to medical management if you've got severe fluid overload and hypertension with pulmonary edema and they're all resistant to diuretics. If you've got a high urea, which is unable to come down, usually about 40 mils per liter or 30 of minutes if there's evidence of multisystem failure, liver failure, um cerebral dysfunction or a potentially an anticipation of a prolonged or such as he uremic syndrome. So, what modality would you choose for your kidney replacement therapy? Well, peritoneal dialysis is very easy to set up. Can be carried out by experienced and trained ward nurses and it's relatively easy to do and can be continued. As long as you've got a tube going into the abdomen called a tin of catheter. But with that tube, there's a risk of infection. So, peritonitis, there's a risk of leakage and drainage problems as well. Hemodialysis is the goal. So, gold standard solute clearance, but it requires a patient to be hemodynamically stable. You can't be having a patient who's hypotensive and it might be quite difficult to get vascular access if you're intravascularly dry, so many patients acutely will go into intensive care for continue ven venous hemofiltration or diet filtration where you can get a good ultra filtration to remove the fluids is gentler than you hemodialysis, which would be a kind of a 45 hour treatment that you would get maybe every other day. So about three times, four times, potentially a week CV H in the intensive care is also good for solu interference and you can put on a dialyser. So C DH DF he filtration, remember you require some form of continuous anticoagulation and remember it might still be difficult to get that. How common is acute kidney injury? Well, it really depends on what your definition is. If it's just a rise in creatinine, then that's gonna be different according to a patient who requires kidney replacement therapy with per or hemodialysis. Also, the outcomes can be very different. Some it's just that you're able to survive off dialysis, which means you may have chronic kidney disease. And in others, it may be that patient didn't survive, but it's very much dependent on the center reporting the quality of the basic care. But knowing that prevention is better than cure, especially the tumor lysis syndrome. And especially if you're looking at units where already they've got a very low kidney function. A premature infant can have an estimated glomerular filtration rate, less than 10% of normal or 10 mils per minute for 1.73 m squared. And that's variation depending on what patients you've got in and what your definition is used mean that's why the mortality is reported, I think from 10 to 60%. So let's go back to the patient. A 15 year old, a Carrie boy, he had abdominal leg and facial swelling, family history of upper respiratory tract infections. He's got no rash but it's become ur he's unwell full time for two seconds. He's got palpal peripheral pulses, prominent apex feet, hypertension with tachy with lung crepitations in all areas. He's got generalized edema Andie. So it sounds like his total body was overload. But despite that, his hemoglobin is not too bad. He's got evidence of hyponatremia hyperkalemia. He's got a low calcium, a lower album, but a normal phosphate and liver function test. He's got four plus a pro uria two plus of hematuria, pulmonary edema on his chest x-ray and tu e right kidneys and ultrasound. So, if we go back to that question, which two of the following and the best descriptions of this clinical condition, is it acute kidney injury, acute on chronic kidney injury? Is it chronic kidney disease? Is it end stage kidney disease? Is he neither nephritic nor nephrotic? Is he nephritic but not nephrotic? Is he nephrotic but not nephritic or is he nephritic and a nephrotic? So please add to your answers above. I think the majority were seen previously acute kidney injury and you were unsure about nephrotic nephrotic. But now everybody I think is putting a ane acute and option e as will need the OK, maybe, maybe, maybe. But this is my, no worries, no worries. And a lot of people are going for A and H which is evidence of nephritic and nephrotic syndrome. And I think that is the correct answer. And so if I just go back and show you, so remember he's got four plus of proteinuria with a low albumin and he's got evidence of edema, generalized edema. So that would give him nephrotic syndrome. He's got microscopic hematuria, he's got proteinuria, he's got oli uria with retention or fluid and he's hypertensive. So I think he's got, eh, so he's got evidence of acute renal failure with nephritic and nephrotic syndrome. What is his corrected calcium? So if you remember his total calcium is 1.8 and his albumin is 24 So you can put in the chart if you, which range is this corrected calcium for A, for 1.7 to 1.8 B for 1.8 to 1.9 C 1.9 to 2 D 2 to 2.1 and E 2.1 to 2.2. So I think the answer is E 2.11 to 2.2. So what you need to do to get corrected calcium is you take the total calcium and you add 40 minus the patient's albumin because you're correcting for the hypoalbuminemia and you correct with the factor of 0.025. So for this case, his corrected calcium was 1.8 plus 40 minuses albumin which was 24 40 minus 24 is 16, multiply. It by the correction factor of 0.025. That's the same as doing four by four by 0.0250 0.025 times 0.45 times by four is 0.1 0.1 times four, is 0.4 add the 0.4 to the 1.8 and you get a result of 2.2 which of the following would not be part of an effective management plan for his hyperkalemia. Again, you can put the answers in. Is it a calcium carbonate? B calcium gluconate C calcium res sodium decode monitor E zide F insulin and dextrose G salbutamol and sodium bicarbonate. So answer so far including furosemide. Remember zide can get rid of the potassium. Remember, calcium Rezum. So we yeah. So calcium and sodium I think will bind with the sodium in the guts. Calcium gluconate can be used for stabilization of the myocardium when you've got a hyperkalemia. So just a reminder of managing hyperkalemia with a cardia monitor salbutamol sodium bicarbonate. Fru calcium sodium, we do use zirconium now and occasionally an insulin dextrose infusion. But for hyperphosphatemia, we would think about phosphate binders and that would include calcium carbonate. So that's with an elevated phosphate would be calcium carbonate. So it is not a management plan for a high potassium. How would you treat his hypertension? Would you give 4.5% albumin? He's got a low albumin. Would you give 20% albumin go through? Would you just give, would you get intravenous labetalol? Would you give a low salt diet, oral amLODIPine, atenolol, enalapril, furosemide, nifedipine. What do you think we've got intravenous furosemide as a result. What about giving albumin with furosemide? He's got album. I'm sorry, I managed to trick you by saying that. So I wouldn't give intravenous 20% of in this case because he's already got deteriorating kidney function. And if you give the say again, why not oral uh orally should be given? Well, I think if this patient's got pulmonary edema, then very often they're breathing a bit faster. The absorption of oral medicines is poor So you want you to give intravenous to try and offset the amount of fluid that you can as you possibly can. So that would be the reason. So in this case, it would just be wanting to give intravenous for those of you. Despite his initial fluid and medical management, he stops producing any urine for 48 hours as creatinine continues to rise and it doubles further to 512 and you're only allowed to one investigation. Would you do A N an doubled DNA ant basement membrane antibody, an antistreptolysin ter and an, an, an autoimmune screen, a blood film C three C four and autoantibody screen immunoglobulin levels or a renal biopsy. So choose your letter E to eight from that list. My answer is actually I which would be all of the above, but I've not given you that choice. You're only allowed to make one decision. It's um a Thursday night, you're only allowed one test. What test result are you going to get back the following day? Potentially? Which is going to change your understanding of what the condition is and the management. Yup, I've had h which is percutaneous renal biopsy. And of course, that's looking for evidence of a cosy glomar nephritis because over the weekend, you might want to immunosuppress even if it was a post infectious glomar nephritis and consider giving intravenous me for prednisoLONE. And I completely agree. Um I would do a renal biopsy, GB M antibodies being said as well as the S 14 ants. B Yes, you're right. It could still be a post infectious gloms could be good pastures. It's gonna take a while for those results to get back. And really what you want to see is, do you have a necrotizing vasculitis? Do you have evidence of intercapillary proliferation? Do you have evidence of a glom nephritis that you're going to want to treat? And what's the most likely diagnosis? Is it? A hemolytic uremic syndrome? B, minimal change in nephrotic syndrome, C A post infectious nephritis, D renal venous thrombosis or ele nephropathy. Yup. So most people see a post infectious gloms, which I think is right, so well done. So the take home messages as monitoring changes in clinical status is paramount looking at observations and blood and urine test results. The most crucial element to management is fluid balance. We should check if patients have clinically acute kidney injury and chronic kidney disease. I've left some uh references for you and in the handout as well. I'm very happy to answer any questions. Thank you for your attention. If you just please note as well on the chat and if you go there is evidence of filling in the feedback form and if you feed that and then that counts towards your attendance mark. So everything gets recorded uh that you have a question. Happy to answer any questions. Uh Yes, it was uh regarding question number D that you put on the side. It was I think regarding uh solution for calcium carbonate. Will you show that a second? So talking about um question number, question number D this one C which was looking for the management plan for hyperkalemia. So an elevated potassium. Are you still there? Is that? No, no after when I after this, so the treatment of hypertension? Yes. What's your question? I just wanted to know just, just want to wanted to know the end. Yeah. So basically, to me, the question is not really what's the hypertension? It's what is the cause of the hypertension. And in this case, of course, it could be renal mediated and hormone mediated. But the most likely is because of also salt and water retention. So to get rid of the salt and water, you need to give intravenous furosemide. He's got pulmonary edema. You want it to act fast otherwise he's going to end up requiring intubation, ventilation and going to an intensive care unit. So that's why I think intravenous furosemide. Thank you for your kind comments in the chat. Really glad that so many of you were able to join. As I said, if you um fill out the evaluation forms by just clicking in the link. Also, there's some people who um you've tried to type in your names and it's not come up 100% clear. So there's one with three dots and also zoom user if you could just please uh make sure you put in the chat, your names so that we're able to um include you. I'm really grateful that so many of you were able to join today and for your involvement and asking questions on the chat. So thank you very much. Or some of you are writing in now and somebody's asking why don't you give Albumin? Because if you got that incipient state of pulmonary edema and you've got acute kidney injury, which where you're becoming oligo auric. And in this case, it was aneurys. If you give a 20% albumin, that Albumin will pull in the lungs and the only place to get rid of it is through the kidney. So if you can't actually get your diuretic to work, then you're going to be in the situation. But that's um what the major problem is going to be. So you're just gonna precipitate requiring intubation and ventilation beforehand. So get ru to try and get as rid of as much fluid as you possibly can. If there are no other questions, then I'd just like to take this opportunity to. Thank you very much, Professor Marks for presenting today. And yeah, just one last call, if anyone to do that feedback form and then we can end the call and you can get on with your days. Thank you. I know it's been a long day of lecture. So thank you for paying attention and staying to the end, really appreciate it and have a good day. Thank you all for your um feedback, but also your interaction during and our thoughts are with you. Wherever you are can see people really all over the world and from the UK um Saudi Arabia, we've got Sudan India. Um Our thoughts are with you, Bahrain. Really hope that things improve over there and thank you for your attention and we hope the world becomes a better place soon. Take care.