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Thank you very much, indeed. And good afternoon and welcome, everybody. My name is Steven Marks and professor of pediatric nephrology and transplantation at University College, London Retirement Street Institute of Child Health and I lead the kidney transplant program here at Great Ormond Street Hospital and the NIH are Great Ormond Street Hospital Clinical Research Facility. It gives me great pleasure to speak to you today for the Crisis Rescue Foundation, Ukraine Medical School, UK, on acute kidney injury. Um, our thoughts are with everybody in the Ukraine and those that are displaced just now and with the current situation understand that not many people can attend live. I will be having an interactive session, but I will not be enforcing. Ahem, anybody. So if you are interested or want to participate, then please, just a mute if you're able to and answer any of the questions. So I'm going to start talking a little bit about what the functions of the kidney are. Talk a little bit about a specific case to kind of highlight acute kidney injury and think about some questions and lead onto some definitions. Thinking about etiopathogenesis ISS and incidents of acute kidney injury some of the clinical features in general pediatric management, looking at history, examination investigations, thinking about the overall treatment of these patient's and bringing this all together. So the kidneys are important. Organs that remove waste and foreign materials at the least cost and useful materials and energy. And they regulate homeostasis so the body's water, electrolyte levels and acid base balance over a wide range of water, salt and protein, dietary intakes and degrees of muscular activity. We know this because we actually are in the situation of where there's been some studies where they take a group of medical students. They are relatively dehydrated by not giving you enough fluid. They give them a high protein load with increased, uh, um, input or steak, for example, and then they get them to do vigorous exercise and makin to running a marathon. And in fact, even in those circumstances, if you check blood tests at the end of it, there's actually very little change. But does MD know what you would see as the first change in a blood test of somebody under those circumstances? Well, very often people think it's probably you might be getting hyperglycemic, dehydration and your sodium level goes up, but that usually doesn't happen. Initially, some people think, Well, maybe you're in acute kidney injury. Your creatinine is elevated, but in fact it's the real level, which you notice that first becomes elevated and the way to think about the kidneys and the way that they deal with the clinical situations. They allow cells to act on blood and and ultra filtration of fluid. So when you think about us making a dialysis machine, the two things they do is they remove fluid. So that's the ultra filtration and the undergo dialysis or removing the waste products. But of course, they're not able to remove all the measurable and immeasurable waste products that we have. So the first is to consider a case of a 15 year old Africa Caribbean boy. He had a one week history of abdominal, leg and facial swelling. He had increased shortness of breath, and he and his siblings that had a few viral infections with sore throat over the last three winter months. He didn't have a rash, but he had reduced oral intake over the last 24 hours with Oliguria, an examination. He's waited on the 25th percentile height is on the second center aisle. He's got a capillary refill time of two seconds with powerful peripheral pulses. A prominent apex beat a BP 15 2/94 millimeters of Mercury. He's technique with lung crepitations, and he's got generalized Dema and societies. So does them. Do you have any ideas or summary that they would like to make of this clinical case? What are the features in the history and the examination, which you think are pertinent? Are there any symptoms and signs that worry you? Um, maybe, maybe something Some infection just, uh, just occurs kidney. And there is a problem. So yeah, so you're right. I think probably the most likely diagnosis would be a post infectious glomerulonephritis. And we use the term post infectious glomerulonephritis, probably wrongly, because by Glomerulonephritis, you're almost describing histo pathologically what you see. But of course, you rarely end up having to do it. Percutaneously know biopsies on these Children, so there's fake features there that may make you consider Nephrotic syndrome because he's got abdominal, leg and facial swelling. He's increased shortness of breath so he might have total body water fluid overload, and you can see that in Generalized Dhiman, a society's is evident on clinical examination. Sometimes you may be in the situation that the fluid is in the wrong place, but they're intravascular dehydrated, yet they've got total body water excess. But in this case, he's got warm peripheral, uh, peripheral pulses. He's got palpable pulses. He's got a query full time of two seconds, and he seems to be hyperdynamic with a prominent apex beat. But the tachypnea with lung crepitations in all areas sounds like he might be in recipient Pommery edema as well. Now, in a kid such as this, it's important to think about what they're fluid status is like. And the two things to say is that his weight is on the 25th Center on the height of the second center, and that may be entirely normal. Or maybe that he's actually got total fluid overload. He's very edematous from the history and from the examination with generalized demonise. I it ease, and actually his dry weight is much less so. Maybe, in fact, his dry weight is on the second central anyway, like his height. The other thing is the BP we all know that hypo attention. So a low BP can be a terminal sign of shock, but in this case you're in the situation. There's clinical scenario where actually, BP may not be helpful. So maybe there's too much salt and too much fluid on board and salt retention resulting in hypertension. But also, could it be something going on within the kidney, such as a glomerulonephritis and hormone mediated Rinnan mediated hypertension as well? The other aspect to consider is, could this be acute kidney injury, where you've come to a lecture, an acute kidney injury? So that's likely but just always have in the back of your mind the differential diagnosis of chronic kidney disease because many chronic kidney disease cases and Children are undiagnosed, and it's not until they present with an acute inter current infection that precipitates an acute kidney injury on top of the chronic kidney disease. That you're able to make the diagnosis is that they've had a longstanding irreversible kidney failure or chronic kidney disease. So if there was any more history such as, for example, this 15 year old boy has he progressively been drinking more and more fluid over the last few months. If he was drinking five liters, seven liters a day, of course it could be habitual polydipsia. It could be what we used to go psychogenic polydipsia. But could it actually be a chronic kidney disease if he's starting to get up at the night to go to the toilet? So he's got nocturia with increased intake of fluids overnight to try and replenish his fluids and rehydrate so all of those aspects are very important. But it sounds like there's very much an acute history with reduced oral intake over the last 24 hours and the period of oliguria. So what about the investigations were here? You can see a hemoglobin of 12 g per deciliter, 100 and 20 g per liter, a white cell count of 12.3 platelets of 3 to 5. So not particular anemic sickle screen was negative. You can see here his electrolytes have shown a lower sodium so hyponatremia and elevated potassium level, or hyperkalemia. There is evidence of acidosis is with the bicarbonate, or T CO2 level of 14 millimoles per liter, and there's evidence of renal dysfunction with an elevated urea of nearly 25 millimoles per liter and a plasma crotan elevated at 258 micromoles per liter. Interestingly, his total calcium is lower, 1.8 millimoles per liter. But actually his corrected calcium may be normal because if you correct his calcium for the hip pop, um, anemia. So in these cases, it's important to know. How do you correct a total calcium into a corrected calcium for the high pop anemia And where I work in London, we don't actually get a corrected calcium with the biochemistry results, and the best way is to take 40. You subtract the patient's albumin level. You multiply that overall number by 0.25, and then you add it to the total calcium to give you the corrected calcium, the phosphates not particularly high that you would see in chronic kidney disease when one would expect hyperphosphatemia, an elevated serum phosphate level. And there's nothing concerning in the alkaline phosphatase lt or Billy Ruben. But urine dipstick testing. You can see he's got four plus of protein urea and two plus a P material, and you remember my clinical description was potentially upon read. Um, and that was evident in chest X ray, although he had a normal heart size. And when you undertake a renal ultrasound and you see two big echo bright kidneys, there's no evidence of hydronephrosis. There's no evidence of polycystic kidney disease. Then there's very likely an acute phenomenon going on, because if you had chronic kidney disease, you'd expect to see small, shrunken kidneys. So the question is to consider what are the two following best descriptions for his clinical condition. Does he have acute renal failure? What we call acute kidney injury. Does he have acute kidney injury on top of his chronic renal failure? Chronic kidney disease? Does he have chronic kidney disease or end stage kidney disease? Is he nephrotic, or does he not have any signs of it nephritis or nephrotic syndrome? Is he nephritic but not nephrotic? Is he nephrotic but not nephritic? Or does he have both? So what are the features that you would look for to make those diagnosis? What is the overall most likely diagnosis, which we've already discussed? Could it be a humility your emmick syndrome? A minimal change? Nephrotic syndrome, a post infectious glomerulonephritis? Could there be evidence of renal venous thrombosis or sickle nephropathy. And then we get to the consideration about what are the definitions of some terminology. So acute renal failure is now called acute kidney injury. But you can have acute and uric kidney injury or acute oliguric. What do we mean by these terms? What's the difference between Azotemia and Uremia? And what do you mean by nephrotic nephrotic syndromes? So acute kidney injury is a sudden decrease in the renal function, accompanied by the retention of nitrogenous waste products, resulting in a sudden decline in glomerular filtration rate, which is potentially reversible. And you may or may not have reduced your night put or oliguria, but you can have this disturbance of water and alleged light and balance. And when we talk about annually, although it literally means new urine, that's not entirely true because it's defined as urine output, which is less than one mil per kilogram per day. Or you can have up to 75 mils of urine per day in an adult, and that is due to the act of Secretary labor of the bladder epithelial labor, and it's due to what we call bladder sweat. So I've been called when I was training to the hemodialysis unit to say that Children who had undergone bilateral native nephrectomy is that the kidneys have been removed. It was remarkable they were on hemodialysis, but they were beginning to produce some urine. But it's not urine. It's this bladder sweat. So what is all Ligurian? Well, that's when your night put is below 300 mils per meter square per day or 3000.5 mils per kilogram per hour. Although it can be up to one mil per kilogram per hour in the in, its and oliguric is the minimum might necessary to excrete the daily. So you type 02, 500 millions more per day in an adult. But remember, you can have nonoliguric state and up to 50% of Children with acute kidney injury, and you could have a normal or increased urine output. So even polyuria when there's evidence of tubular dysfunction. Secondary to aminoglycoside toxicity. Resolving acute tubular necrosis, an intermittent to partial ureteral obstruction. One of the confusing terminal Jesus versus is a tenia and jury mia, and this can be seen in American and British textbooks. Americans very often talk about a CT. Mia's the abnormally high accumulation of nitrogenous waste products in the blood, and you see this by an elevated urea level. It can reflect acute or chronic renal dysfunction, but it actually can occur in other reasons. So if you give patient's intravenous methylprednisolone, then that high dose of cortical steroids can result in elevated urea level, as you can also have, as I explained, with high protein diet with an adequate calories, medications such as tetracycline or patient's who've undergone surgery, trauma, infections of burns. Whereas in the UK as opposed to azotemia, we really talk about uremia, which is the symptom complex, which reflects organ dysfunction that occurs when the kidneys fail to regulate body composition. So I talked a little bit about nephritic and Nephrotic syndrome. So what is the difference? Well, Nephritic syndrome is when you have microscopic hematuria so dipstick positive for hematuria, you might see red cells when you're microscopy. It's usually associated with protein urea, but doesn't have to be as massive protein, urea, albumin, urea as you would see in Nephrotic syndrome. And it's usually associated with an acute oliguric kidney injury with fluid overload and hypertension, Nephrotic syndrome is more having nephrotic range proteinuria, which is at least a gram per meter square per day of protein loss you're now going to creatinine ratio is usually about 2 50 mg from minimal or overall protein urea, 40 mg from meter squared per hour. And that continual loss of protein results in lower albumin levels in the blood stream and hyperglobulinemia. So an albumin level very less than 25 g per liter, and we'd be associated with the Dema and Hyperlipidemia. So the commonest cause of a nephritic syndrome is a post infectious glomerulonephritis, or sometimes even a post streptococcal. But we see other infections, which can cause it for nephrotic syndrome. The commonest causes a minimal change, disease or minimal change in a frantic syndrome. And if you've got features of nephritic and nephrotic syndrome, then that's most likely due to post infectious glomerulonephritis. So here you can see a red blood cell cast. So this is when you take a urine sample either in the ambulatory care unit or you take it in your act in emergency unit. You spin it down and you actually see these red cell casts, and with that, you could be quite confident the patient's got glomerulonephritis. So what is the incidence of acute kidney injury? Well, it's less common in Children than an adult, but it is frequently secondary to pre renal failure associated with the gastro enteritis. Recep since and we've definitely seen a reduction in cases internationally and globally due to having the ability of a rotavirus vaccine reducing rota virus induced viral gastroenteritis with fluid and water loss and electrolyte loss in the stools usually associated with vomiting and diarrhea. But Accu killer injury is often associated with a major disease process, so it can be seen in tertiary referral units. And I mentioned features of acute kidney injury on top of chronic kidney disease, which may be suggested by pro growth history of polyuria polydipsia, or evidence of renal osteodystrophy. So when we think of acute kidney injury, we usually think of the pre Reno Reno lamp Post renal components. Prerenal is very often when you've not got enough fluid getting to the kidneys, so decreased to intravascular volume, usually due to dehydration, gastrointestinal losses with a viral gastroenteritis with diarrhea and vomiting, although can occur in salt wasting or diabetes. Insipidus and third space losses of sepsis and Nephrotic syndrome. But it can indeed happen with pump failure, congestive cardiac failure, evidence of pericarditis or a cardiac tamponade. And we start seeing this intrinsic renal disease if you potentially got evidence of acute tubular necrosis, either is a hypoxic ischemic injury, drug induced or toxin mediated, and this is usually associated with uric acid nephropathy and tumor lysis syndrome. But of course, we're able to give her a spirit case too many Children nowadays and obviate this development. There can be a drug induced interstitial nephritis or idiopathic, and you only need to actually have one doors of many medicine cations, including non steroidals anti inflammatory drugs, to have, uh, interstitial nephritis, which can develop. So it's really difficult to predict. And I would always advise giving paracetamol regularly for patient's with fever, especially if they've gotten into current illness. Before giving nonsteroidal anti inflammatory drugs, we talked a little bit about post infectious glomerulonephritis, but it could be a member know proliferative glomerulonephritis or CT glomerulopathy Lupus nephritis. I gave vasculitis or his lotion and purple nephritis, or nephritis associated with chronic infection Anca Associated Vasculitis, Goodpasture Syndrome with anti GBM antibody presence and an idiopathic rapidly progressive glomerulonephritis when the crackling is basically doubling every day. Other causes within the kidney would include hemolytic uremic syndrome, which may be drug induced after bone marrow. Transplantation may be due to cortical necrosis, so you've had an initial hypovolemic insult and then secondary to that. You then get a cortical necrosis on top. There may be evidence of renal artery stenosis, a renal venous since from bosses and in fact, any infection, especially causing sepsis and pilot nephritis. But mostly if there is obstruction in a soldier kidney or bilateral your it terry construction of bilateral urethral obstruction as part of an obstructive uropathy. So let's think about the pathogenesis and developing acute kidney injury well, very often you may end up having a decreasing glomerular capillary permeability. Do two studies that we've done undertaking gentamicin and heavy metal animal studies. But we know by obstructing and the tubules with debris and cast, you get high inter tubular hydrostatic pressure, which results in reduced glomerular filtration rate and any cause of today. Epithelial damage results in a leak of the infiltrate into the para tribulus circulation and an imbalance of waste excretion with normal glomerular filtration rate but any a ski maker vascular problem can result in decreased Think of millennial placement and the Camarillo capillary permeability, resulting in acute kidney injury. So looking individual patient's, it's important to get a full history thinking about how hypovolemic may they be. What's their fluid intake for the day? And it's really good to get over a 24 hour period. What's their intake? What's in normally and what's the urine output? If you've obviously got additional fever or losses from diarrhea, vomiting or burns or any bleeding, then obviously you're going to have to give more fluids as a result, to try and replenish those Ms fluids, but looking to see if there are any urinary symptoms, what the urinary flow is if there's evidence of politics or hemorrhage. But there may be something in the history and a clue within the drug history and always important to think of the neonatal history. The past medical history scanned, um, neonatal history. If there's any ultrasound performed in the infant up to now, looking to see if there's a previous you know, tract infections and tests and looking to see of evidence evidence or failed to thrive, organic failure or any surgery. Having other family history may point you in the right direction. So if someone else in the family's required dialysis and transplantation or has had high BP, required renal replacement therapy with dialysis and transplantation, then that would be important to know. And with one's clinical evaluation and assessments about going to see the patient looking at the general state just now, looking at their routine observations the temperature, their heart rate, systolic BP, respiratory rate and doing a series of plots of weight, heights and head circumference is but also noting, when you think the patient was dehydrated and thinking about what you find in the peripheral profusion, JVP or any evidence of a Dema. If there's any evidence of cardiac failure or multi system disease, it's important to see if there's any rash or three apathy, arthritis or oral lesion's. And especially if you pop a the kidney and you can feel them or any additional bladder's or masses. And what investigations, while trying to have a look at the blood, excluding humility, your emmick syndrome by looking at full blood count blood film Esr Checking on the coagulation screen, excluding the cross match and serum electrolytes and looking to see if there's any evidence of infection with the blood culture and C reactive protein, it's important to get a feeling if the patient's hypocalcemic and checking and Einars calcium is the evidence of secondary hyperparathyroidism within elevated BTH. Knowing if the bone marrow is going to make more cells by looking at the particular site count have an understanding of what's going on with the Coombs test. If you've got a high index of suspicion of humility remix syndrome, then understanding the V Tech and Equalize Urology, the complement C D. C four and the C three nephritic factor and interestingly, on many of these occasions, the immunoglobulin level A will be normal. They 13 anti DNA is be will be helpful if there is evidence of a post infectious glomerulonephritis in a in a double stranded d n a quantifiable d n a e n a anchor anti neutrophil cytoplasmic antibodies and anticardiolipin antibody with autoimmune profile anti glomerular basement membrane antibodies as important as well, but I would invariably always say, If you get one drop of urine, just try and have a look. See if you can do a urine dipstick. If there's enough sample, send it for our electrolytes and your micro See culture and sensitivity. And look to see the fractional execution of sodium, which is the urinary sodium over the potassium sodium in the recipient, and you take the donor's plasma Kratt in in, uh, and divide by the urinary creatinine to have a look to see if there's any difference. So how can you tell you're in the electrolytes and acute kidney injury, so you shouldn't do that? Look at the urine electrolytes per se if you've just given diuretics to the patient, but very often. If you've got a prerenal acute kidney injury, you'd expect the urinary sodium to be low and the urine, urea, the urea urine, plasma urea ratio and the urine plasma creatinine ratio to be elevated. Whereas if there was intrinsic renal disease, then you'd expect to hire urinary sodium with a low urine, urea, urine, plasma ratio of urea and creatinine, and there'd be evidence of a sediment on dipstick. Other investigations to include will include a cardiovascular assessment with an E C G. We would only really do a chest X ray if there were signs you're worried about pulmonary Dema developing an echocardiogram, especially if you had hypertension. Or you're worried about longstanding hypertension to check on the cardiac function. If there's any evidence of left ventricular hypertrophy, and it's really important to do a Doppler ultrasound of the kidneys having a look to see if there's any obstructive element if you've got hydroureter nor froze is. But if you've got large, bright kidneys, then you can be confident. There's probably an acute process, as opposed to small kidneys, which you might see of chronic kidney disease but also thinking of doing a biopsy of the kidney, especially if you've got rapidly progressive Lamar nephritis. And the creatinine is doubling every day to see if there's evidence of a crescentic glomerulonephritis to give cortical steroids, even if you have a post infectious glomerulonephritis. And it may be important to look to see if there's evidence of rickets from chronic kidney disease, but also to see the bone age should by undertaking an extra of the left wrist in the hand. So by going back and reassessing patient's is important. It's also important to see how things change with blood tests, and sometimes if you've got abnormal lecture lights, which we'll talk about in a minute. It's really important to frequently measure them, and we can now do I stats or do capillary bloods as well. But remember, if you're getting finger prick and you're squeezing, you get humanized potassium's and they're going to be elevated. So sometimes it's really important to do good. Venous sampling Having a look to check If the calcium and phosphate levels have changed at the argument, levels have changed. Having a look to see the full blood count and the urine dipstick every day If there's any urine to be had and testing for urinary electrolytes and maybe if there was an intervention because of an abnormal renal ultrasound, it may be important to go back and look at this again. So where would you be in the fluid status management? Well, if a patient appears to be clinically dehydrated by being tackled cardiac with ku peripheries, a prolonged capillary full time with dry mucous membranes, sunken eyes and low urinary sodium, a fractional discretion of sodium. Then we would give a fluid challenge of 10 to 20 miles per kilogram. So normally, starting with 10 mils per kilogram, you give it have a look at the response and then potentially, if they are okay and not getting fluid overloaded, you could consider giving another temper kilo. If they're euvolemic, then also, I would consider at that point a flu challenge up to 20 mils per kilo with normal saline over an hour and again to Allah quarts of temples per kilo. And consider frusemide up to 5 mg a kilo if there's no urine response. But when they're overloaded and their tachycardic with the gallop rhythm elevated jugular venous pressure with the Dhiman hypertension, I would go straight to giving furosemide 5 mg per kilogram. If there is fluid overloaded severe when you're considering dialysis, if there's no response to the freezer, might therapy? I just wanted to emphasize importance of a multidisciplinary team and working closely between doctors, nurses, getting your pharmacist and dieticians involved. And sometimes in fact, even your play therapists and social workers and supporting families with an acute presentation. Because it can be quite difficult. And for a kid who was entirely normal and well going to school and then all of a sudden they've got an acute kidney injury going on in the required mission to hospital with psychosocial team involvement. And if you have any Axion, then it's important to go bad and have a reassessment of the patient. Considering further fluid bonuses of crystalloid, a colloid giving frusemide is indicated by the clinical state and monitoring the patient with at least twice daily weights having accurate input and output recording, seeing what the BP is every four hours even more regularly for hypertensive, for a hypertensive and for early monitoring to see whether it's got evidence of a peripheral core temperature gradient. But it's really important to have ongoing fluid management. And if you're in the situation that the patient is in producing any urine, you may want to cut back to giving urine. Replacement with insensible loss is at 400 mils per meter square per day, or 30 miles per kilogram per day. And we would give all the urine if the patient is euvolemic and you can do this by seeing what was the urine output in the previous, uh, where you're going to give this on top of the insensible losses. But if they're getting more and more fluid overloaded, you might want to maximize the amount of urine replacement you give, or at least restrict, to between 50 and 75% of the urine output of the previous hour. And it may be important to modify to fluid restriction if you're on dialysis or the urine output is in fact been established. But remember, if you go patient's that are recovering for the acute kidney injury, especially if they've had Christie Reace revolves, you put a capture and you've relieve the obstruction. You might become poly uric, and it's important to replace the urine output with insensible. Loss is for 24 hours, but then setting a flu target. The renal function continues to improve, so I just wanted to consider how you might manage some electrolyte abnormalities. Does M. Do you have any ideas how you manage a high potassium level or hyperkalemia? Well, the first thing to do would be to repeat the blood test, and then I start send it to the laboratory, trying to a venous sample to make sure it wasn't humanized, that it's a true potassium level and reflection of the body potassium. And if it remained high, you'd want to put on some egg leads, start some cardiac monitoring getting a nurse to get some sub you toble nebulizer to try and reverse, but we can medically think about giving some bicarbonate sodium bicarbonate. If there's evidence of Essid doses giving some frusemide calcium, resolve the, um, for example, maybe use to temporize the situation and also thinking about insulin. Dextrose infusions. If the patient has that low sodium level, or hyponatremia, which may be secondary to fluid overload, then we can fluid. Restrict and consider giving hypertonic saline. But I rarely give this. Nowadays, it only treats a number, whereas if you're hypernatremia and it's due to sodium retention, you wanted to give frusemide analysis of oliguric. Having a low calcium can be multifactorial and considering one off our hydroxy calciferol and calcium supplementation is important. Hyperphosphatemia is also important thinking about dietary phosphate restriction. Phosphate binders, acidosis with sodium bicarbonate therapy and also hypertension, secondary to fluid overload alternatives in the vascular tone, you may want to give diuretics medical management. Dallas is if they're failing to respond to diuretics or if they have Pommery Dhiman Remembering. If you're in the situation that you've got a low calcium so hypocalcaemia and your acidotic, it's really important to keep on giving calcium because when you give bicarbonate, it will lower the level further. So if you do have a patient that's got a low calcium and a low bicarbonate, keep on giving calcium. And because you may be in the situation that if you're giving more and more bicarbonate, then your costume level may drop precipitously and you might get a hypercalcemic seizure. It's important to consider the nutritional aspects of acute kidney injury, which is associated with the Cata Bolic State and malnutrition can develop rapidly. Malnutrition delays, acute kidney injury recovery. And there's anecdotal evidence the good nutrition improves outcome, and you need to undertake a dietetic review for all Children with a key I to prescribe a low potassium low phosphate feed and make sure you've got enough protein. We try and do things centrally, so we try not to give TPN unless we have to. And the issue is that some adolescents, especially don't want to have a nasogastric tube. But sometimes it's easier to do that and less likely to have electrolyte disturbances than if you're giving intravenous total parenteral nutrition. I always have a look and see where the drug dosages are and think about correcting for your acute kidney injury. So if you've got a G f R, which is low 20 miles per minute for 1.73 m squared, you may want to change the doors. Try and avoid nephrotoxic agents if you can, and look to see the drugs that you do need to have, whether you need to decrease the dose is or have a prolonged dosage interval. So when would we consider? We know replacement therapy and patient's going on to Dallas is well, if you've got a high potassium level above 6.5 millimoles per liter or the patient severely fluid overloaded upon read email, which is resistant to diuretics or a very high urea level above 40 millimoles per liter can be above 30 minutes. But I've seen mean it's even with urea levels of 16 mhm. And if there's evidence of a multi system failure, um, so you've got liver failure as well as kidney failure. You anticipate prolonged oliguria, such as a political remix syndrome, and we consider Dallas is normally we would start with peritoneal dialysis, which can be easy to set up. It can be card out by the ward nurse is. It's very easy to use and maybe continued indefinitely with 10 cop catheters, although there is a risk of peritonitis, leakage and drainage problems, although hemodialysis the gold standard. So new clearance You require a patient to be hemodynamically stable for a 4 to 6 hour session, but normally we would just start with a short spin of two hours. But remember, a vascular access may be difficult in these patient's, many of whom maybe an intensive care where they could undertake continue venovenous human filtration or humid I'll filtration, which gives you good ultra filtration. And so your clearance maybe improve with the dialyzer and all those. A gentler therapy invariably requires continuous anti coagulation. And so giving heparin considering sentry anti coagulation or vascular access again, maybe a problem in the intensive care setting. So how do patient's do? Well? There are various reports is there's various definition, depending on how you look at acute kidney injury. Some, it's just requirement of kidney replacement therapy with Dallas is some. It's a doubling in the crack in. In some, it's about the outcome. Looking at death versus going back to chronic kidney disease, off dialysis or having full recovery of the renal function. So it does depend on your individual center because obviously, if you're a large neonatal center, you've got a cardiac unit, then the reporting is going to based on a different baseline population. But remember, prevention is always better than cure, and you need to think about whether you're even going to go down. Include your premature neonate. It's so based on all of this, the mortality rates of the literature been between 10 to 60% but also include babies who've got multi system involvement surgical patient's hypoxic ischemic encephalopathy. So if you go back to our case of the 15 year old Africa Caribbean boy, we can see that he's become Edematous. He's been unwell, not drinking as much. His weight's gone up, he's hypertensive, He's taking me with long reputations, and he's got palm redeem on his chest X ray with two big echo bright kidneys of acute kidney injury, with something going on intrinsically with the kidney with four plus of protein urine hematuria with abnormal um, electrolytes with hyponatremia hyperkalemia at 1 37.2, respectively, Acidotic with bicarbonate 14 urea of 25 cracking of 258. So what do we think is the best description of his clinical situation? Is it acute kidney injury? Acute on chronic. Is it chronic kidney disease? End stage renal failure. Is he? Neither nephritic non nephrotic is he nephritic? But not nephrotic nephrotic but not nephritic. Or is he both Nephritic and Protic? You can put your hands. Or maybe maybe the first is like ecotrin anal failure. Yeah, I think. Or it can be injury. And the second one? I'm not sure, but maybe maybe it's like nephrotic syndrome. Yep. So let me go through the questions, then with your answers. So I think there's acute kidney injury in the patient. I think there's nephritic and Nephrotic syndrome because if you saw you had four plus of protein urea, but he dropped his albumin level, but he had elevated BP. Remember? Hematuria protein urea kicking the injury with fluid overload. That's the Nephritic syndrome and the glomerulonephritis. And then Nephrotic syndrome is nephrotic range proteinuria with a high pop anemia and the Dema. So I think he's got features of acute kidney injury nephritic and nephrotic syndrome. So do you remember what range his calcium is, if you remember from the description that I gave, so I think it's 2.11 to 2.2. And remember what I told you as you take the patient's corrected calcium by calculating that if you take the total calcium, you take 40 minus the patient's argument and you multiply it by a factor of 0.25 double. Some sources use correction factors, so in this patient, 40 minuses albumin was 24. That gives you 16 16 multiplied by The conversion factor of 0.25 is 16 times 0.25 is 0.4. You add it onto the total calcium of 1.8 and you get a corrected calcium of 2.2. Which of the following would not be part of his effective management for his hyperkalemia? So he's got a high potassium level. Would you give calcium carbonate calcium gluconate, calcium rizzo knee um, cardiac monitor frusemide Insulin dextrose. So beautiful or sodium bicarbonate? Which would you not do as part of his management for hypochelemia again? You can put your hands up, or you can put your answers in the chat. But that's right. Calcium carbonate is used for high phosphate levels, or hyperphosphatemia as a phosphate binder. If you're eating and taking phosphate in at the same time, how would you treat his high BP? In this case, would you give an intravenous 4.5% albumin infusion or 20% Albion infusion with frusemide? Would you just give intravenous or oral frusemide intravenous labetalol or a low salt diet? Or would you use oral agents such as Amlodipine, Atenolol and Allah Pro furosemide or nifedipine again? You can put your hands up, or you can put your answers in the chat so you're right that the patient does have a low albumin level. But the question is, would you give 20% argument to a patient who is fluid, overloaded and become oligo and uric? Well, the answer is no, because if you give 20% of women and it's going to pool an intravascular space and it's going to go into the lungs and precipitate worsening Pommery edema because the frusemide may not act if the tubules are all stuffed with your eight and therefore not allowing the work of the frusemide to happen. So because of the Palmer edema, I would give intravenous frusemide to this case, which would reduce the salt and water overload in this case and try and reduce his BP. So I think a question such as this is, How would you treat his high BP? It really means water is the cause of the high BP and how would you treat it? And I think it's salt and water retention in this case, which would respond to intravenous Firouz amount despite initial fluid, the medical management he becomes an uric for 40 hours, and his plasma crown in increases to 512 is basically a Friday morning. Your laboratories are all about to close, but what what investigation would you do to help make the diagnosis? Well, if the creatinine is increasing and you've got rapidly progressive glomerulonephritis, it's true you want to exclude Lupus nephritis of systemic Lupus erythematosus Goodpasture syndrome with anti glomerular basement membrane antibody antistreptolysin on anti Gainey's be of a post infectious glomerulonephritis, or an autoimmune screen or blood film to exclude humility, uremic syndrome or C three, C four and auto antibody levels to think about doing a screen to exclude a connective tissue disorder Looking your immunoglobulin levels. If IGA was elevated, it might suggest an IGA nephropathy. But to be honest, if you're in the situation that the creatinine is increasing and it's a Friday morning, you're wanting to do a kidney biopsy to see what's happening inside. And what's the most likely diagnosis is a humility cure. Emmick syndrome, a minimal change, nephrotic syndrome, a post infectious glomerulonephritis arena, venous thrombosis or a sickle nephropathy. And again, if you put your answers in the chat or put your hand up. And I agree with you that this is most likely a post infectious glomerulonephritis. So the take home messages are monitoring. Changes in clinical status is paramount. Have a look at the observations. How do they change? Go back and look at the blood and urine test. But the most crucial element to management is a fluid balance, and check if the patient is clinically has acute on chronic renal failure. I've put some references in here, but I'm of course, I'm happy to answer any questions, but thank you for your attention. Thank you for joining us, and I hope the situation improves in Ukraine. Thank you very much. Um, thank you very much, Professor. If anyone has any last minute questions you'd like to ask, um, please go ahead. Um, otherwise, please feel fill in the feedback form that I post in the chat. Um, it's very important for us to keep going with the medical school. Um, and we hope to see you in lectures on Thursday. There is. There is some questions which are coming in. Um, there's one in the chant. So Fatima's asked, How do we differentiate between Nephrotic syndrome and the free tick syndrome? So as I showed you the slide, it's important to look at the individual patient. But there may be features, as was in this case of Nephritic syndrome and Nephrotic syndrome. But when we say in the fridge stick syndrome, that's when you've got microscopic hematuria. Although you can have microscopic hematuria together with protein urea, but doesn't have to be nephrotic range, so you may just have one plus or two plus, and usually the patient's have acute kidney injury with salt and water retention. They've become hypertensive, and they're oliguric as a result, so nephritic syndrome being hematuria protein, urea or Ligurian hypertension Nephrotic syndrome is is when, If you imagine, the kidney is like a sieve, sieve falls get too big. The protein molecules leak into the urinary space, so you get a nephrotic range proteinuria, which is usually above a gram per meter squared per day. The level of protein in the blood goes down as to the level of albumin to less than 25 g per liter and the patient's of evidence of edema. And that's usually associated with hyperlipidemia. Fatima also asked, Can Children have both syndrome? So yes, as in this case, this patient had a post infectious glomerulonephritis. And you remember I said, that's the most common cause of a nephritic syndrome alone but also can cause a mixed nephritic and nephrotic syndrome? Ahmed asked in the chat about When will the patient need a kidney transplant? So there'll be a further lecture that I'm going to do on chronic kidney disease and transplantation, and I'll be doing that lecture to try and educate, as you say, so that we understand a little bit more about chronic kidney disease, which is irreversible kidney failure, and I'll be giving that lecture two weeks time today at exactly the same time. But invariably, if you've got irreversible kidney failure, we would want to do a pre emptive living related kidney transplantation first and hopefully Obviating the need for dialysis. And then there's a question in the chat about what antibiotics are the most effective in treating pylon arthritis. So it's a very good question, and I always recommend people have a look at their local data to see what microbes and organisms are more likely causing your new tract infections and what your local sensitivity panels are. As you're aware, we're in the situation that we're getting much more resistant organisms around the world, so using antibiotics wisely. But obviously, if you've got a patient with a significant Pilon arthritis, then we would want to institute therapy with intravenous antibiotics, especially if there's evidence of sepsis. We undergo sepsis, fixed protocol where we look for different signs and make sure that we get antibiotics quickly into patient's that present unwell with an overwhelming infection. We would try and get a urine culture where we could, but of course, if the patient was systemically unwell, we would wait to get a sample, although of course you could take a super pubic sample. Potentially, we would use broad spectrum antibiotics. Some places would just start in general pediatrics with intravenous kept track zone. We invariably would go because patient's having been treated previously with other antibiotics. We would think about giving intravenous, which takes about Anami case. But look and see what your local organisms are and taking it from there. Any other questions as we come up to just about an hour? Well, thank you very much indeed. Everyone for your feedback, for all your questions for your involvement and really great to be able to continue to teach you all. I know some of your disperse some of your Ukraine, but I thought so with you, wherever you are. And let's hope for future piece thinking of you and thank you for joining. Don't forget to give your feedback. If you go into the chat now, you just clink and you'll get the link. And if you do that, that's really important for us to keep our medical school going for us to know that you've attended, and this applies to those that are watching this, um, live and those who are going to watch it recorded with streaming. Thank you very much. Have a good day and hope to see you very, very soon. Bye bye. Thank you very much.