Computer generated transcript

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

Additions that we have. Hello, my name is uh Steven Marks and uh welcome to the talk today on chronic kidney disease and transplantation. I'm professor of pediatric nephrology and transplantation at University College London and the clinical lead for kidney transplantation at Great Ormond Street Hospital for Children. I'm going to talk you through a case presentation today. A little bit about the functions of the kidney as well as uh normal age related uh renal function. Um a little bit of a background on abnormal kidney function and considering um acute kidney injury. Um but focusing mainly on chronic kidney disease, common presentations that we see of acute kidney injury on top of chronic kidney disease and end stage kidney disease management. That's when patients require kidney replacement therapy with dialysis and and or transplantation. And I'm gonna focus a little bit about newborns because uh their kidney failure is a little bit different in potentially in the etiology. So you have a premature male infant, he's born at 34 plus six weeks gestation, but a good birth weight of 3.35 kg. His mother had normal initial antenatal ultrasounds at six and 12 weeks having had previous pregnancies. But at 20 weeks, gestation, there was a diagnosis of right sided hydronephrosis. But the feeling that the other kidney, the left kidney was a little bit bright and obviously bilateral kidney and abnormalities are of concern. And this is as you can see um the bright kidney that you can see in the fetal medicine um units and they were referred, having the scan at 21 weeks to gestation. As time progressed, this um fetus developed bilateral hydronephrosis and the kidneys became more echogenic and there was reduction in the like or volume. And um it was initial um induction of labor at 34 weeks. And typically we see an element of distress syndrome. There was no new method but this neonate required ventilation for five days. It was a neonatal intensive care unit for eight days. Uh insertion of catheter um required drainage of both kidneys with uh bilateral nephrostomy for a couple of weeks. And the crown rose to 288 micromoles per liter, which we'll talk about is very abnormal kidney function for an adult, never mind. Um for a neonate. And during the interventions received one blood transfusion. This you can see is the micturating cysto urethrogram. So, this is where instillation of dye through urethral catheter. And you can see this very abnormal um bladder which is uh very irregular, will have a trabeculated wall. And this here is a segment which is the dilated posterior urethra. So this is actually posterior urethral valve. So, an obstructive uropathy associated with the kidneys not forming properly. So, bilateral renal dysplasia, but there was no evidence of other obstruction on these nephrostogram that we did, which is where we put dye in through these tubes which are directly draining um the kidneys. So this name underwent resection of the er valves when the creatinine came down. And um you can see here it's very common for us to go back um at least a month later to have a relook and check there's no residual valves. And I again, I brought this case up because actually what's going to happen to this child longer term. Um because actually, you've got abnormalities both in the development of the lungs with neonatal respiratory distress syndrome, with reduced lipo volume. And actually, you've got very abnormal kidney function. So, the important factor is whether you've actually got abnormalities in the development of both of the kidneys. So, what does the parenchym of the kidneys look like? Are these small kidneys which are dysplastic? Are they already cysts within the kidney? Do you have uh evidence of vesicoureteric reflux? Which of course, if this neonate ends up having recurrent febrile pyelonephritis, which can potentially with reflux or infected urine into the kidneys cause even more damage. And actually, the bladder may not be functioning normally. And what is normal bladder function? Um at a month of age may actually develop abnormal bladder function um later on and therefore impacting on the overall kidney function. But these recurrent episodes of being unwell urinary tract infections, episodes of hypotension and dehydration really may impact and actually the development of having um worsening um high BP or proteinuria may also impact on the longer term impact. So actually, this child actually was growing and developing. Normally, we have a baby clinic where uh we see these infants together um with dieticians. And you can see that this infant was able to grow, develop normal BP without proteinuria. And in fact, um had a requirement for sodium bicarbonate. So many of these kidneys will waste salt, so lose salt in the urine. So, um and may require sort of bicarbon supplementation. A bit of iron and actually prevention of uh urinary tract infections with trimethoprim prophylaxis. And you can see you're at 15 months of age at a a normal um G fr without um uh hypertension and proteinuria. So, a very good outcome in this infant which I think I portrayed at initial um slant looked like was going to run into more tricky problems. So the kidneys are able to remove waste and foreign materials at the least cost um but regulate the homeostasis. So, not only regulate the electrolytes and acid base, but to do this over a wide range of water salt and protein dietary intakes. And if you consider what we have in the sense of um dialysis machines. The two main impacts are actually um the dialysis itself. So removing those waste products, but actually removement of fluid, the ultra filtration. So we are in a situation where you will see that um some uh neonates and infants and laterally, elder Children may end up being polyuric, producing lots of urine, even though their kidney function may be uh very abnormal. And of course, the more urine you produce the better because that means that you're in a situation where you're allowed to take more fluid. And, but there are other aspects of the regulation of the homeostasis. Um and that's not just the acid base but also the kidneys producing erythropoietin. Um for example, which um is the backbones of actually then producing er red cells. So, in chronic kidney disease, very often we'll see a normal chronic noy anemia of chronic kidney disease. So what is it that this um presentation shows it really talks about the vulnerability to kidney failure. And that is really because actually, if I go through the premature and even mature um neonates um of good sizes have relatively low BP with an elevated renal vascular resistance and that low renal blood flow results in a low glomerular filtration rate and that really improves during the first year. So it is very difficult to predict in an individual um neonate what's going to happen. Although as time goes on and you can see that the kidney function is deteriorating and not improving. And that gives a, a worthwhile indication of what's going to happen in the future. So just to give you an idea is like, what do we mean? Well, very often um the data that we have um are looking at um BP measurements during the first few hours of life. And I put in the mean BP because very often if you have intra arterial catheters or an umbilical arterial line, and you're measuring central um aortic blood pressures, you very often will be looking at the means. But for me, it's really helpful to look at the systolic blood pressures as well as the diastolic BP. And you know that very often um when we're looking at the the overall blood pressures, it's kind of looking at uh that BP measurement according to the gestational age. So a 24 week and expecting um uh I mean BP of around 24 millimeters of mercury obviously increasing during and the gestation. So how do we look at the actual kidney function itself? Well, we talk very much about biomarkers and the plasma creatinine really is a biomarker. Um But in the first few days of life, the initial wise will reflect maternal creatinine. And it's only because the placental is doing the function of um um the removal of waste products from um the fetus that um we therefore have to be very careful of looking at the creatinine within the first few days. But normally by the seventh day, you get a good idea of what the neonatal plasma creatinine is itself. Hm, we use creatinine as a biomarker because it's released from the muscles. So obviously, if you are small for dates, um and also if you're faltering um growth, um so what we used to call failure to thrive, then you would expect a lower plasma creatinine. So that very often it may not even be flagged in the results. Because in um nes and infants and Children under the age of 18 years of age, when you get a plasma creatinine value, you don't actually get an estimated glomerular filtration rate that you, you get by um a patient in the United Kingdom who's over the age of 18, having a blood test anywhere from the GP practice to cottage and community hospitals to teaching and, and district general hospitals where you'll get at least A MDR D or an NPG FR, which will estimate your kidney function based on your sex and information about your uh ethnicity. And um very often and we'll take into parameters including for example, size. So when you get to the zero of creatinine, which will show is usually very low in the twenties, you really um will depend on what plasma creatinine your blood. So are depending on your pre development and your muscular build as uh adolescent. Um but really, we don't find huge changes in your kidney function until your kidney function is really halved. And that at that point that your plasma creatinine will increase. So, always be wary of that small thin child that you may have done bloods to check the kidney function. And when they actually show that the plasma creatinine is at the upper level of normal, that may be a very abnormal kidney function for that child. So, here is an indication of that kind of fetal and maternal plasma creatinine variation through the gestations. And you can see that um if you take the fetal serum creatinine and you divide it by the maternal serum creatinine, it is around by one but will vary. Um as you can see here anywhere from um about point 7-Up to about 1.6. And here you can see the changes reflecting in that plasma creatinine in premature neonates. Um starting from those with gestational ages under 27 weeks to those of 31 to 32 weeks. Um And you can see that usually by the time you get to um seven days, you're getting to that and a dear plasma creatinine. But as I said, your plasma creatinine will tend to um improve in as your G fr improves within the first few months in the first year. Mmm after birth. And this you can see here that even very abnormal plasma creatinines initially, which may reflect, for example, maternal chronic kidney disease or acute kidney injury will take some time to kind of normalize down. But you will see that normalization happening um within the first few weeks. And again, this shows you the uh improvement in plasma creatinine that you see over the first four weeks um which you see in term infants. Um but more acutely in the very, very low birth weight infants, especially those um under 1 kg of weight. So in adults, uh as I said, you get the G fr that um kidney function, which is a S 1.73 m squared. And basically, you should look at that as a percentage of kidney function. And here's a Cock Gaul equation that was previously used um which takes a, a factor, you take some aspects of such as the age, the weight in kilograms and the plasma creatinine to determine um what the creatinine clearance is in those per minute. Whereas in Children, we use a Schwartz or a modified Schwartz formula or KD FP, which very often uses a constant. We generally use 36.5. But you can see here anything from 30 up to adults of 66 to 2, which I think it overestimates. But generally we'll use 36.5. You multiply it by the height and centimeters and you divide it by the plasma creatinine, we can do formal measurements of uh kidney function. And uh for just now um when we do blood tests, we'll do a cyst statin and see and there's again, various formula which I can tell you about, but generally you want it to be under um, one. Um, the value I personally don't do the 51 chrome EDTA clearance. And we move to Iohexol in my institution. And again, it means taking various blood tests at, um, before injection of Iohexol and usually 12 and four hours afterwards. And actually, it's a day case admission and a lot of costs. And actually some of these newer methods such as the statin C are much better. And I wouldn't really do it until you've reached 12 months of age. Because actually, as I've said to you, even in um Children with chronic kidney disease, you would expect the kidney function to improve in the first year of life. And when we looked at patients with chronic kidney disease, we even see that that reduction in the GF um reduction in plasma creatinine and improvement in kidney function can happen up to um a medium um of 5 to 3.2 years as well. You can also do a time during collection looking for creatinine clearance itself. So here we are looking at the glomerular filtration rate in neonates. Again, this is mils per minute per 1.7 m squared. And if you look absolute percentage wise, which is the same as G fr you can see that a premature neonate will have a very, very low kidney function, which uh can be even in single digits compared to a term neonate who will have kidney function, which will improve over the first few weeks from 2040. Um up to about 50 mils per minute per 1.7 m squared by one month. And interestingly when we use the terminology of uh end stage kidney disease being less than 15% less than 15 mils per minute per 1.73 m squared. You can see this really applies to premature infants, um um uh term infants as well as neonates um and from birth. But actually, when we look at the um perspectives, as I said, you would expect them to have an improvement in their kidney function until the first year as you can see here. So let's talk a little bit about um the various forms. As I said, you may have an improvement in the kidney function. It may be acute kidney injury as opposed to chronic kidney disease, but there may be an element, for example, a placenta abruption or something tragic happens that causes for example, hypoxic encephalopathy. Um but it doesn't necessarily mean irrecoverable and damage to the kidneys and you may get kidney function improving. So you might not be in a situation of developing chronic kidney disease or endstage kidney disease, requiring kidney replacement therapy. We've generally gone away from using the terminology renal failure to kidney injury and kidney disease. So, acute kidney injury and chronic kidney disease and endstage kidney disease in modern medicine. And this is with a lot of patient public involvement um moving forward as you can see here. So when we talk about acute kidney injury, we mean a rapid reversible deterioration of the kidney function associated with an autogenous waste product accumulation. But if you actually prospectively look at a cohorts of babies, for example, in neonatal intensive care unit, it depends whether you've got a big maternity units or whether you're a tertiary or quaternary unit that gets uh severe um patients with and congenital heart disease that you do major operations. But it'll be up to about 10% of the babies will experience some form of acute kidney injury, other than that prerenal failure or so called vasomotor nephropathy is the most common type and happens up to about three quarters of all neonatal cases. So, in a neonatal, it's a special kind of circumstance. Normally, we say that when the kidney function is deteriorating and you've got an increase in um the plasma creatinine by, by 50 micromoles per liter per day. And we also think about those cases where you have a reduction in the urine output to less than 0.5 mils per kilogram per hour, um or even one mil per kilogram per hour in neonates. But what we know is that acute kidney injury is very often associated with asphyxia in um um neonates is very often no uric. So these infants will very often produce normal amounts of urine. So, when we talk about acute kidney injury, you'll remember the all descriptions of prerenal. So again, this idea of not getting enough fluids to the kidney renal being intrinsic kidney disease itself. And postrenal very often being an obstruction to the urine flow. And typically, if you have prerenal acute kidney injury, it's because you're not getting enough fluid there because of and dehydration or excessive losses such as vomiting or diarrhea or third space losses. As we very often see with sepsis or nephrotic syndrome or as I said with uh those babies with congenital heart disease, especially if they're in cardiac failure, that intrinsic kidney disease can very often be acute tubular necrosis. We see very often malignancies or interstitial nephritis or glomeru nephritis or vascular lesions. So commonly in the, it would be a renal uh venous thrombosis which can happen perinatally. So, antenatally as well as um before birth. But also we can see it's an episodes of um significant pyonephritis and sepsis. And then obviously, if you have one normal functioning kidney, then you should have normal kidney function. So to have an obstructive uropathy, it's either got to be um kind of bilateral ureteric obstruction or a urethral obstruction such as urethral valves or in a patient who's got a solitary functioning kidney, uh which is obstructed, for example, may have um renal agenesis of the other side or a multicystic dysplastic kidney, which is nonfunctioning. So here is really what we're thinking about. Um in so, thinking about prerenal failure, being hypoxic ischemic encephalopathy, dehydration, hypervolemia, hypertension and congestive cardiac failure, intrinsic to the kidneys. And so renal disease such as hypoplasia, dysplasia, very often they are salt wasters, as I said, as opposed to those with vascular disorders, acute tubular necrosis, nephrotoxic agents or pyelonephritis. And those, as I said, with post renal failure especially may be obstruction caused by diverticulum or ureterocele as well as those with a neurogenic or neuropathic bladder. And we need to think about uh the complications. We need to consider fluid, electrolyte and acid base imbalance, er convulsion sepsis, um evidence of renal vascular thrombosis and the clue to that might be the development of arterial hypertension. So, we may see these neonates presenting with acute on chronic kidney disease, um precipitated by infection or dehydration. Those that we antenatally know have abnormalities on ultrasound. But it may be that neonates discharge has got poor feeding comes in and it's all felt that maybe it's a bit of dehydration, you give fluids and it doesn't improve the kidney function and you may have the history that they really had really wet nappies and uh really trying to feed. So there may be polydipsia and polyuria and the failure to grow, grow normally. So, faltering growth with the development of uh uh renal dystrophy, hypertension and or proteinuria as well. So, I would suspect chronic kidney disease if you think the creatinine is abnormal, especially if there are features of chronic kidney disease such as anemia, um hyper high potassium levels, hyperkalemia, low calcium level or high phosphate such as um hypercalcemia, hyperphosphatemia and uh secondary hyperparathyroidism. So that low calcium, high phosphate, high pth H even with a high um a low 25 C vitamin D level, looking to see if there's bilateral renal anomalies on the antenatal scans and even postnatally if there are called renal defects that you may have undertaken an ultrasound because of urinary tract infections. I wasn't sure you get a good family history of chronic kidney disease. So specifically asking if anybody in the family has um high BP, proteinuria, chronic kidney disease and the answer to all of those questions may be no, but there may be a strong family history even of endstage kidney disease because many will think that a family member who's had dialysis, for example, but then has had a kidney transplantation may be cured of their kidney disease. So us actually asking specifically for family members with dialysis or transplantation. Also, um neonates infants that have ongoing um proteinuria, it's important to look into as well as after an episode of acute renal failure or acute kidney injury. So, historically, um when I was in North America, we looked at the data. So about a third of cases due to what we call congenital anomalies of the kidney and urinary tract um were usually obstructive neuropathy such as P era valves with renal dysplasia. A third being glomerular causes and a third being other very often cystic kidney disease and genetic problems. But really, as time has gone on this cat or structural malformations happening up to and about a half of cases, those with inflammatory conditions, about um a quarter of hereditary nephropathies about 1/5. And really when we look at the data that we now get from the UK Renal Registry, if you add the dysplasia, um with or without urinary reflux to those with obstructive uropathy, you get over a half, having congenital anomalies of the kidney and urinary tract and very often there may be syndromic cases. So this is uh um a picture of an uh who was born that was unable to be resuscitated. And you can see here, absence abdominal wall musculature syndrome or previously, it was really called uh prune belly syndrome associated with bilateral cryptorchidism. Um So, abnormalities in the genital urinary development as well as megaureter, bilateral significant ureters with kidneys that never really forms properly. And here really showing you that if you do an ultrasound, looking to see if there's a presence of cysts, if there um are, then if it's a big cyst and there's a cyst in the liver that might make you more think of an ultrasal recessive polycystic kidney disease. Um big kidneys that we can get an autosomal dominant polycystic kidney disease. Sometimes we can get renal elop heat and and so abnormalities with cystic kidney disease, for example, in and tuberous sclerosis. Um because the TS C um two gene obviously um go um at the same region if there's a mutation as the PKT, supposed cystic kidney disease. But we do see other rarer forms of glomerulocystic and kidney disease and what we call HNF one beta. So this is nuclear plan to one beta transcriptions, which can be associated with mature onset of diabetes in the young. But very often if there's small kidneys or small with cysts, that could be congenital anomalies of the kidney and urinary tract with dysplasia with or without reflux vascular insults. Um but remember all causes may result in small kidneys by the time you've got endstage kidney disease. So the size of the kidney may not give you the answer and we will definitely do genetic tests and ve a way putting a needle and doing a per intrarenal biopsy. If we think of patients call endstage kidney disease because the likelihood is that you get sclerosis, glomeruli, you wouldn't see anything to give the diagnosis and these small kidneys are more likely to bleed by undertaking a kidney biopsy. If you have normal sized kidneys, then it may um help you try and work out if there's inflammation in the kidneys or familiar nephropathies or nephrotic syndrome, which may be evident from the presence of significant proteinuria with um edema and um low albumin levels in the blood. But other cystic kidney diseases such as uh nephrons may also be evident. We may be in a situation that we've got obstruction, as I said, from posterior to valves of vis ureteric or pelvic ureteric function obstruction or neuropathic bladders or the development of nephrosis or renal calculi. So, what is the most frequent genetic cause for end stage kidney diseases in the first two decades of life? Well, whenever I ask this question, especially, um to even adult nephrologists, they will always say polycystic kidney disease. And actually, it doesn't, it's this condition called juvenile nephro theis that we're seeing an awful law. It's a recessive cystic kidney disease caused by genetic mutations in M PHP 1234. The number of genes are being identified is now into double figures. Very often can be positive in genetic tests in Children presenting in endstage kidney disease. So, what do we look about? Well, the gradations of a chronic kidney disease. So if you look at the glomerular filtration rate and so this is mils per minute per 1.73 m squared or even a a percentage of kidney um function, you will see that grade one or stage one. chronic kidney disease is when you have normal kidney function when the G fr is above 90%. So that may be when you've got renal parenchymal disease present. It may be in um older Children where um for example, they've got um type one diabetes they're at risk of developing kidney disease with micro, it's important to continue to monitor these patients with time if they go stage two chronic kidney disease, with between 60 90% of kidney function, usually it's silent. So there's no symptoms of chronic kidney disease, but they may develop biochemical abnormalities even at the lower end of the G FR. But it's not until your G FR dips to 60% and lower. So, between 3060 mils per minute per 1.73 m squared. When you have stage three or grade three chronic kidney disease, or you've got biochemical abnormalities and poor growth, for example, and poor appetite. We see very often clinically in our predialysis clinic. Those that start developing kidney function, which is between 50 30%. They may be getting more tired, more severe symptoms, not eating, attendance in school may go down, um really very sleepy, missing school, missing days of school, um difficult to treat anemia. But uremia may not be able to be as controlled as well as we want with um dietetic input and obviously adherence to both fluids and diet as well as to the medications is really important, especially in adolescent age group. And although we see end stage kidney diseases where um stage five chronic kidney disease, where the kidney function is less than 50 mills per minute per 1.73 m squared. Um this often is where kidney replacement therapy is required, but very often, especially in neonates and especially in the first few years of life with infants. As long as we're able to get you to grow, you don't have significant proteinuria or hypertension and we're able to control your acid base status, your urea levels and your metabolism, your chronic kidney disease. Uh bone mineral disease is well controlled the calcium phosphate secondary hyperthyroidism. Then you may not need to go on to requiring dialysis and transplantation. But you may be um have a gastrostomy and requiring regular visits to clinic every week to monitor or regulate your feed changes in your dietetic input and um your medication as well. But you may see older Children, especially those if there's recurrent infection presented with hyperemia, um fever, diarrhea, vomiting, additional losses which may be obvious two burns or hemorrhage or polydipsia um where they're actually quite polyuric as well. But looking to see especially uh if the child has taken any drugs and that's prescribed drugs, you only need one dose of a nonsteroidal antiinflammatory such as Ibuprofen to cause a tubular nephritis. Um But also looking to see if you've got any abnormalities um with other antibiotics being prescribed recently is really important to oversee as well. Also, we look at um the overall drug history, including recreational drug use, especially in adolescents and it's really important to question them um out of your short of the parents who may tell you um the truth which may be um part of why they've ended up with abnormal kidney function, but it's really important to go back and look at the neonatal medical and surgical history that we discussed as well as the family history, um which we talked about earlier and looking at the patient going back and examining them, seeing if there is an acute um or chronic presentation. And that might be helped by looking at s plots of the weight, height head circumference, looking at the mid parental, um um the target centile ranges as well may be important trying to understand where that child should be. But looking for acute issues such as hydration, cardiac failure, signs of multisystem disease or any obstruction that you might have evidence and doing investigations and seeing if there are features of chronic kidney disease with the time that we talked about. And if you have any drops of urine, do urine desity, see if there's intrinsic kidney disease. Is there evidence of proteinuria and hematuria. Do they have microalbuminuria, albuminuria, proteinuria, which you can measure in the laboratory with albumin or protein to creatinine ratio and then thinking about doing an ultrasound. So there's big bright echogenic kidneys may be helpful, as I said, in delineating that um of what the causes, especially if you've got cysts developing a very small chronic kidney disease. Um So very small kidneys, even for um an infant or child is really important. And the exclusion of hydroureter nephrosis and the prospect of obstruction, which of course may be required in acute scenario. Um Older Children, we would consider doing an X ray of the left wrist and hand. And considering if we don't think this congenital normal is the kidney and urinary tract, perhaps doing a percutaneous kidney pumps. And then it's essentially the monitoring of the kidney function, but going back and repeating this with time. So seeing what's happening, for example, on daily checking to see if there's a change in the hypocalcemia, the hyperphosphatemia, the low calcem, the low phosphate. So if there's evidence of dehydration. So, um you've got a patient who's tachycardic has co peripheries who don't give a refill time, then you want to give them a flu challenge. Could this be acute kidney injury on chronic kidney disease or is it just acute kidney injury and giving a flu challenge? Normally, if there's abnormal kidney function, we'd be conservative. And the change in a BLS guidelines to giving 10 mils per kilogram and reassessing before giving the 2nd 10 mils per kilogram up to the 20 mils per kilogram, which used to be the b that was recommended if they're evola again, assuming they're intravascular dry, but then giving flusemide if there's no response and making sure it's a slow infusion not to cause any oxicity. But if you are fluid overloaded with tachycardia gallop rhythm, elevated uh to venous pressure, evidence of edema and hypertension, then you may want to start with flusemide from the get go and then giving further fluid boluses of crystalloid or colloid and flusemide, um, or, um, um, looking on the clinical state and getting information such as what's the daily or even twice daily weights. Um, if they are rapidly changing, but getting a good input and output and if you're becoming oligoanuric, thinking about how much fluid that you're going to give and then cutting back, especially if you become polyuric and regularly measuring the BP at least every four hours initially. And seeing if they are developing um per peripheral perfusion and prolonged time and looking at the peripheral core temperature brilliant, we normally say the simplest is to give in sensible losses. Um And if er you're volemic, you can give 100% urine replacement. But if you're overloaded, maybe be restricting that to 50 to 75% of urine output. But obviously, depending on how much uh urinate pos coming on because um once they start producing and it may just be insensible losses in the polyuric recovery phase, you gotta be careful, you're not driving that polyurea. So again, you may want to cut back um to restricting to a certain percentage of giving a maximum um or replacement depending on the clinical status of the patient. So I'm just gonna talk about some of the aspects of how you manage hyperkalemia. For example, where you'd want to put the Monardi monitor, think about um initially giving them um um salbutamol nebulizer. Um if they're acetic, some sodium bicarbonate, if their fluid overloaded and have hyperkalemia and acute kidney injury and then giving flusemide to offload some of that fluid together with the hyperkalemia, as well as calcium or sodium resonium and insulin dextrose can be um used. Um We have um other drugs such as uh zirconium, which we can use nowadays, if they've got low sodium levels, that may be result of fluid overload. So, restricting the fluids and if they don't respond, considering kidney replacement therapy, if they're intensive care, it may be due to um their current multifactorial um injury and it may require continuous uh venovenous hemodiafiltration. Very rarely. Would that advocate hypertonic saline just to um replace um um the sodium that's lost? I think you need to look at the overall clinical status. But if the sodium level was high and it's due to sodium retention um as opposed to just um total body water reduction. Although there may be an element of the two considering flusemide and dialysis. If they becoming oliguric, a low calcium level may be multifactorial. Um and you may want to give calcium supplementation if they're no by mouth, um give them calcium infusions thinking about one of the hydroxycholecalciferol. Um If they're then taking um medications enter, if you've got a high phosphate, then the only things you can really do is if you're taking um food or diet or a feed as prescribed by your dietician. In which case, thinking about reduction in the phosphate intake, thinking about um that dietary restriction together with your um dietician and using phosphate binders together with the feet or the foods that the patient is taking. And if they've got acidosis and their BP will take it, then we would think about sorting bicarbon therapy to um change the acidosis. And if they've got hypertension that may be secondary to fluid overload or alterations in the vascular tone. So I think it's really important you work out what the cause of the high BP is. And if it is total fluid um body water overload and thinking about diuretics, increasing that diuretics. If they don't respond to medical management and thinking about dialysis, especially if they don't respond to diuretics or developing pulmonary edema or significant uria, always be aware that acute kidney injury is associated with a catabolic state. And malnutrition can develop rapidly and acute kidney injury recovery and anecdotal evidence that good nutrition can improve outcomes. So, we have a dietetic review of all neonates in order to Children with acute kidney injury, who need to be on a low potassium low phosphate diet. But getting at least their maintenance calorie intake and protein intake for the recommended um national nutrient intake according to the gestational age. And we would start nutritional feeds orally or via a gastric tube to minimize metabolism in uremia. After not on TPM for the purposes of correcting drug doses according to G Fr assuming the G FR is less than 20 MS per minute per 1.73 m square before recovery. But look and seeing what's happening to the G FR, if it changes, you're gonna have to change your dose and look it up the PNF for Children and change it according to the G fr, many drugs require decreased doses, a prolonged dosage interval. Um but consult your P and pharmacist for further advice and try and avoid non nephrotoxic drugs. The prognosis will vary um according to the different definitions of acute kidney injury and the outcome and the center reporting. Um but remember, prevention is better than cure. So when we're thinking of endstage kidney disease, this endstage renal failure management we used to think about really is for the rest of your life. So you either have a functioning um kidney transplant or you're requiring one form of dialysis. And if it's peritoneal dialysis, there will be peritoneal dialysis catheter and you'll be getting exchanges, it will be attached to a machine. So that's automatic peritoneal dialysis or um continue cycling, peritoneal dialysis, um which may be over a night lasting for about 1012, 14, even longer, maybe 16 hours depending on a very young infant that were having difficulty trying to alter volt and mainly that's done at home and we can train the parents to do that. Hemodialysis used to historically, just be in centers. So in the hospital, but we're not able to have that um given in um home as well with home hemodialysis training. And then we aim to give a preemptive kidney transplant just before you ever require dialysis. And although there are deceased donor options, especially on blocks, so that's where you use both kidneys of a infantile donor. Um And although we would consider trying to maximize transplantation with donation after brain death, um kidneys and heart beating donors, we do also take donation after circulatory death, kidneys as well. And although we aim for a preemptive living parental um kidney transplantation, so at least um with a three antigen match where it's all possible, which would be a biological father or a biological mother, we will indeed look at other family members and even consider worsening matching than that to consider proceeding with a living donor transplantation. But for example, if you had a six antigen uh mismatch, so that was no matching HLA A B or dr, then we would consider that that would be a higher immunological risk and we potentially could actually put them into the period exchange program or that's they called the National Kidney Sharing Scheme. So I can donate my kidney to my child and you can donate your kidney to your child. So we do um a swab, no swab can be two way or three way. So if I give you a practical example of a patient, if you've got a G fr um of about 70% in a child who presents at two years of age with an acute illness. You can see here at one year, follow up that kidney function after one year. So three years of age has dropped to 60%. So is trending towards 40% at two years and at three years is about 25%. This is when this patient is five years of age. And we start planning for live related kidney transplantation. But by 5.5 years, having had an intercurrent infection, um the GFR drops to less than 10 and um this is 2.5 year follow up and this child needs um acute dialysis but with four year follow up, uh six years of age having received a living uh maternal donor kidney transplantation of four years, you can see very good kidney function which after some acute rejection um and defect of complications, you can see there's worsening renal function um at 60% or 60 miles permanent of 1.73 m square. This is one year after transplantation and that's seven years of age. And you can see the same thing that deteriorating in kidney function. So now eight years of age with six years of follow up after two years, post transplant, such that, that worsens to 20% at seven years. And I actually, whilst we plan for the next kidney transplantation at three years after the first kidney transplant, you can see that this um child requires dialysis at eight years, follow up. So four years, post kidney transplant at 10 years of age with worsening kidney function. So if we look at the overall nine year follow up, um so five years after transplantation, when this child is 11 years of age, they um have received uh their second kidney transplant. But again, you see the vagaries and this starts reducing. So by 14 years of age, 12 years, follow up eight years after the 2nd and 3rd, after the first kidney, her kidney function is reducing until we think about transferring to um an adult nephrologist at 17 years of age with reasonable kidney function with a G fr above 50 M per minute per 1.72 square or 50%. So if we consider what we look at the circular model of end stage kidney disease management and these Children and who've got abnormal kidney function will require a lifetime either of dialysis and may have one or two or even more kidney transplants. So I think it's really important to monitor changes in clinical status and their serial observations of the urine test and the most crucial element to manage his fluid balance, but check if it's clinically acute on chronic kidney disease. So here's to consider um what is the estimated glomerular filtration rate. So if a is more than 90 mils per minute per 1.73 m squared. Uh B is 60 to 90 some people say 60 to 89 or 89.9999 recurring, you get the idea and that's B and C is between 30 to 60 mils per minute or 1.73 m squared. T is 15 to 30 mils per minute per 1.73 m squared. And E is less than 15 mils per minute per 1.73 m squared. And if we look at those parameters of percentage of kidney function or per minute per 1.73 m square, what do you think they are for? Stage one, stage two, stage three, stage four and stage five chronic kidney disease. And which of the following would not be part of an effective management plan for hyperkalemia. And the options are cost from carbonate. Some gluconate calcium resonium card monitor for and in and in fusion salbutamol resulting bicarbonate. So if we get you to put into the chat, so if you want to put in the answer to the first question, what is the estimated glomerular filtration rate of a patient with stage one chronic kidney disease? So if you just put it in the chart, what the, what do you think it is? That's the 90 A. Yeah, it's a bit of a misnomer because we call it chronic kidney disease. But actually the abnormal kidney function. Um um somebody to put less than 90 of course, it is greater than 90. Um, somebody else putting um different values. Yeah, the majority are a so stage one chronic kidney disease where the G FR is above 90 mils per minute per 1.73 m squared. Question two. What is stage two chronic kidney disease? What's the G fr? Yup. So few PM. Yep. So that's B 60 to 90 mills per minute per 1.72 m squared. Stage three, chronic kidney disease. Is it a greater than 90 b 60 to 90 C 30 to 60 D 15 to 30 e less than 15. Again, people put into the chat. Yup. So that's C 30 to 60 miles per minute for 1.73 m squared. Stage four chronic kidney disease. Is it greater than 9060 to 9030 to 6015 to 30 or e less than 15? Yup. More. Most of you putting 15 to 30 miles per minute. And what stage five chronic kidney disease? Greater than 9060 to 9030 to 60 15 to 30. 0, yeah. End stage, most people will be there. So less than 15 mils per minute per 1.73 m squared. And the last one, question six, which of the following would not be part of an effective um management plan for hyperkalemia. Is it a calcium carbonate? B, calcium gluconate C, calcium resonium dec cardiac monitor, Ezide F insulin and dextrose infusion glutol and H sodium bicarbonate to which of the following would not be part of an effective management plan for hyperkalemia. That's stump a few view. Yep. So insulin and dextrose infusion has been labeled there. Um I try and give it rarely but it does actually um put the potassium into the cells. So it can be a benefit especially in anuric patients to get them to theater for dialysis access. Um But so you can use um salbutamol um acutely sort of bicarbonate if there's acidosis and hyperkalemia, flusemide, if there are fluid overloaded, especially if they're producing um some urine, put them on a calcium, a cardiac monitor and give him calcium gluconate to stabilize the myocardium as well as calcium resonium. So the only one which is not um the management plan is a calcium carbonate because that's used for hyperphosphatemia. It's an elevated phosphate level, not an elevated potassium. So that's um my questions of my talk. As I said, um the gold standard is really to aim for a preemptive living related kidney transplantation where, where we can for our patients and their family are happy to answer any questions. Thank you very much. Thank you so much, Professor Mark. If anyone does have any questions, feel free to um yourself now and you can ask your question. So we do have one question in the chat box, professor and they were asking, what was the answer for the previous question. So when you say the previous question you mean um question six. So the agent which is not used to manage high potassium level was a which was calcium carbonate because calcium carbonate is a phosphate binder. So it binds with the phosphate that you take in your food. So the answer was that a because calcium carbonate is used to bind phosphate, not potassium. Yeah. And people asking about um hyperkalemia so very often if they come in and they've got an elevated potassium level. Yes. You want to give salbutamol nebulizers. Basically, it will stabilize you before you're giving all the additional treatments. But remember very often it's a hemolyzed sample. So make sure it's a venous free flowing sample as well. So get someone to go off and get uh salbutamol nebulizers already. But at the same time, um repeat the venous free flowing sample as well. Just to say as well. Just to if you look on the chart, you'll see that to get your certificate of um attendance. You need to also um click on the link to fill in the feedback form as well. Thank you so much, professor. We do have one more question. Um For question one, if the GFR is less than 90 wouldn't it be the line where the red flag is raised or would it be anything below 100 or 99? Yeah. So in the olden days, we used to say that having kidney function between 80 100% was normal, we now basically see anything between 90 100 and 20% because if you have significant proteinuria, um and your G fr is higher than 120 maybe that the kidneys are overcompensating what we call hyperfiltration and that will cause damage. Um We say you've got abnormal kidney function if you've got proteinuria, high BP and or microalbuminuria, for example, but for example, if we know that you've got abnormal kidneys on ultrasound, on both sides, you're at the risk of developing chronic kidney disease. So that's why the definition is above 90 MS per minute per 1.73 m squared. Um So you have normal kidney function when you've got stage one chronic kidney disease, it sounds funny, but that's the way we describe it because once you start having 89% kidney function or G fr of 89 MS per minute to 1.73 m squared, that's when you've gone into stage two. Well, thank you very much indeed for all your questions and for your attention today. And thank you for all the team. Thank you so much, Professor Marks. Thank you so much for enhancing our knowledge on like the very kidney diseases. I believe we found it extremely helpful in this particular hour. I personally found it quite helpful with regards to how the kidney might look on an ultrasound. Um and as well as managing the correct fluid balance based on the urine output. So once again, thank you so much on behalf of everyone that has also joined today. Um Professor M you are extremely helpful and if I can just ask everyone to just fill out the feedback form as soon as they can, and you will receive a certificate straight after our next lesson would be next week, Wednesday at 5 p.m. And that would be on pneumothorax and pleural effusion by Doctor Mackey Ching. And we look forward to seeing you in our next session. Thank you so much, everyone attending and thank you so much, Professor Mark. Thank you very much and thank you everybody for joining and taking the time tonight. Have a good evening. Bye-bye. Thank you very much to everybody. Thank you. Thank you.