CRF Acute kidney injury Stephen Marks
Summary
This on-demand teaching session will cover acute kidney injury and its clinical features. Professor Stephen Marts from the Great Ormond Street Institute of Child Health will guide participants through an understanding of the kidney, discuss patient participation and examination, and explore common causes and treatments. Through a case-study approach, learn the definitions of acute kidney injury and its impact on body composition, and the issues of proteinuria, nephritic/nephrotic syndrome, and common causes such as post infectious glomerulonephritis. Engage in an interactive quiz and get an understanding of how to diagnose acute kidney injury in a medical setting.
Learning objectives
Learning Objectives:
- Describe the functions of the kidney.
- Explain the clinical features of acute kidney injury.
- Distinguish between nephritic, nephrotic and mixed nephritic/nephrotic syndromes.
- Recognize abnormalities in electrolyte and nitrogenous waste products in the blood.
- Interpret and correct total calcium levels using serum albumin levels.
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You didn't see me? Okay. And can you? Yes, yes. Yes, we put you. Can I just check if you can see one screen or two screens, one screen? Excellent. So shall we make a start? Yes, please. So, um welcome everybody and nice to return to you. My name's uh Professor Stephen Marts um from University College London, Great Ormond Street Institute of Child Health. I'm in charge of the kidney transplant program here at Great Ormond Street, but also director of our clinical research facility. And I'm going to be taking you through acute kidney injury today. So, what we will do is look at the functions of the kidney, uh we'll begin by having some audience participation. So uh looking at uh different aspects of the kidney and we'll start with the quiz. Well, then look at some definitions, look at the incident CTU pathogenesis of acute kidney injury and some of the clinical features to look out for as well as the treatment and bringing it all together. So the kidney is a wonderful organ and in the fact that it's able to remove waste and foreign materials at the least cost in the useful materials and energy by regulating homeostasis. So that's the body's water electrolyte levels and asset based balance. But not only is it able to do that normally, if you take a group and in the past, it's been medical students, uh hopefully with ethical approval where you don't give them very much to drink, you give them a large protein intake and they have undergo an excess um exercise regime usually by undertaking a marathon. Um What is the first thing that you would notice if you took your blood test, what abnormalities would would you would you notice you want to just put your hand up or just a mute and speak? So many people think it might be the sodium level. So do they get undergo hyperglycemic dehydration? But actually with normal kidneys of the start, you're able to regulate what about abnormal crackin because of dehydration getting acute kidney injury? Well, indeed know that's neither what you do see is um and I see somebody is put in the chat hike raton. But what you do see actually is an elevated urea level as the first abnormality because the kidneys are able to regulate the SOMA states is over a wide range of water salt and protein intakes and degree of muscular activity. And what it does, it allows the cells to act on the blood and ultra filtration and otherwise assist in the bodies from. Uh So let's start with the case to try and illustrate this So this is a 15 year old Africa Caribbean boy, he's got a one week history of abdominal leg and facial swelling, who's increasingly short of breath. He and his siblings have had a few viral infections with sore throat over the last three winter months and he's had no rash but reduced oral intake over the last 24 hours with some oliguria. So an examination, he's unwell. His weight's on the 25th percentile height on the second center. He's got a capillary refill time of two seconds with particle peripheral pulses. He's got a prominent apex, speak with BP. 15, 2/94 millimeters of mercury. He's tackled need with lung reputations in all areas that generalized edema and societies initial investigations um sure that he's not anemic. His hemoglobin is 1 20 white cell count to 12.3 with normal platelet count at 325. His sickle is negative because he was Africa rabin. He's hypo know trimix. So a low sodium of 1 30 millimoles per liter, hyperkalemic at 7.2 millimoles per liter. And with his hyperkalemia celebrated potassium. He's acidotic with the law bicarbonate level of 14 millimoles per liter and an evidence of renal dysfunction with an elevated urea of 24.8 millimoles per liter. Anaplasma crab in the 258 micromoles per liter. And you can see that he is hypocalcemic, but that's the total calcium and one always has to correct the total calcium and there's a, a degree of hypoalbuminemia. So with a low albumin. So if you take 40 minus your serum albumin, which is 24 in this case, and that is 16, you multiply that by correction factor of zero point 025. And that says the same as four times four times 0.25 or four times 0.1, which is 0.4, you at that 0.4 onto the calcium of 1.8, which is your tosca calcium and 1.8 plus 0.4 gives you a corrected calcium of 2.2, which is normal. So, in other words, although the total calcium is low, the albumin level being low and reflecting the amount of bound calcium, it's actually normalized when you corrected. He's got a normal false fate level of 1.6 million moles per liter and is the L P L T Billy Ruben. As you can see, he's got four plus of protein urea with two plus of the material urine dipstick testing. He's got normal heart size on chest X ray, a reality signs of pulmonary edema otherwise. And an ultrasound, he's got two big bright kidneys. So the questions I want you to consider is which to the polling best described as clinical condition. Does he have acute kidney injury? Is the acute kidney injury? On top of chronic kidney disease is a chronic renal failure. What we now call chronic kidney disease? Does he have end stage renal failure on the stage kidney disease? Is he neither nephritic non nephrotic or does he have nephritic but not nephrotic syndrome, nephrotic but not nephritic syndrome or does he have both nephritic and nephrotic syndrome? What do you think is the most likely diagnosis? Is it humanistic uremic syndrome? Does he have a minimal change, nephrotic syndrome? Does he have a post infectious glomerulonephritis, renal venous thrombosis or sickle nephrography? So, do you want to put down in the Baltic? What you think the answers are? So which to the following describes clinical condition. A B C D E F G N H that we just discussed. So if you just put me in a box one, sorry. A yeah, one A you come to an acute kidney injury. Lectures. That's good. Making sure you know why it's not acute kidney injury on top of chronic kidney disease. Does he have Nephritic Syndrome? Nor nephrotic or nephritic non nephrotic or is it both? Yep. So we've got votes for acute kidney injury and nephrotic nephrotic syndrome. And then what do you think is the most likely diagnosis? Post infectious glomerulonephritis is coming up. So, hemolytic uremic syndrome, minimal change nephrotic syndrome for B C's post infectious glomerulonephritis during a venous thrombosis and the cycles nephropathy. We've got quickly, could be minimal change nephrotic syndrome or could it be post infectious? Okay. Well done. We'll talk a little bit about it and see if you bring it together at the end. So here you can see um two kidneys, you're looking beautiful. Um I think the animation basically just showed you there that the kidney stone, for example, could obstruct at the at the top here at the Pelvis ureteric junction or within the ureter at the bottom of the physical ureteric junction, from fact in the urethra and remember if you've got a contralateral kidney which is fine, without any evidence of stones, you will have a normal kidney function. So let's consider what the definitions are for acute kidney injury. Well, acute kidney injury is really the sudden decrease in the renal function, which is due to a decline in the glomerular filtration rate, which is potentially reversible. It's reversibility which is important and given your acute um it can happen with or without oliguria. So in other words, you may have a reduction in urine output, but that might not be necessarily true. And when you get the reduction the kidney function, this is accompanied by retention of nitrogenous waste and a disturbance of water and electrolyte imbalance. Some patient's can have um an urea and by an urea literally means no urine. But in fact, that's not necessarily true because there's a active transitional epithelial a or within the bladder and that transition ophelia, they're actually produces some fluid. So, in fact, in an adult, you can have this production up to about 75 mils per day, which looks and candid by urine. Although it tends to be a little bit more gunky and people generally call that kind of bladder sweat. So it's important to note that, you know, we've got patient's that have had bilateral native nephrectomy. So, the kidneys are right and have been called to the dialysis unit when they're producing urine and it's obviously not urine. It's the fact that they've got this active transitional material there. Of course, unless they've got transplant kidney, they could have oliguria which is a reduced urine output. So that's less than 300 miles per meter square per day, half a million per kilogram per hour and older Children and 1 mg per kilogram per hour and mean it and it really is the minimal in mind necessary to excrete the daily soldier type put which in an adult is around $500 moles per day. Beware as a nonoliguric state can happen in up to about half of Children with acute kidney injury. And a normal or increased urine output can occur if you could tubular dysfunction due to aminoglycoside toxicity, resolving, acute tubular necrosis or intermittent a partial ureteral obstruction. So, azotemia is one of the terminology that you might see in your textbooks, very often comes from America, which is the abnormal high accumulation of nitrogenous waste products in the blood. Basically means an elevated urea content in the blood and this can reflect acute or chronic. So irreversible kidney dysfunction but can occur in other nonrenal causes. So, if you've got a very high protein diet, for example, you're giving steroids and adequate calories or you know, very sick patients' and in terms of care, and that's more the terminology in America. Whereas in the UK, we use the uremia to really describe the whole symptom complex reflecting organ dysfunction that occurs when the kidneys fail to regulate the body composition. So ask him the questions about Nephritic nephrotic syndrome. So, Nephritic syndrome is when you have um some microscopic hematuria and very really microscopic, tend to be coca cola colored urine with protein urea but generally not nephrotic range and can be associated with fluid and salt retention. And that can result in um acute kidney injury, which is oliguric with hypertension because of the salt and fluid overload. Nephrotic syndrome is really where we start describing nephrotic range proteinuria. So the kidney is like a sale of the save holes, get bigger, the protein molecules leak into the urinary space. And if it happens at an increasing amount of about a gram meter square per day, then people use the terminology nephrotic range proteinuria and that more massive proteinuria results in the leaking of protein into urinary space. So that the blood level evolvement drops, hypoammonemia before 20 below 25 g per liter. And to try and to calibrate the oncotic pressure, you get peripheral edema and it's very often associated with hyperlipidemia as well. The commonest cause of having a nephritic syndrome is really a post infectious glomerulonephritis. Whereas the commonest cause of the nephrotic syndrome is minimal change nephrotic syndrome. But if you've got features of both mixed nephritic and nephrotic syndrome, then like nephritic syndrome, it's most commonly a post infectious glomerulonephritis. Now I trained in a couple of places in Newcastle and also in Toronto, Canada's, we're used to actually in the emergency um did stick the urine but also spin it and separate it out in a centrifuge in accident emergency department, a lot of work, but actually very easy to do and actually gives you a good results. So that if you see this red blood cell cast and you've spun the urine, then you know that you've got a glomerulonephritis. So by reassuring diagnosis, if you have acute kidney injury, how common is it? Well, it's less common in Children than in adults and frequently secondary to a prerenal acute kidney injury, which we'll talk a little bit about in the moment and very often in the world due to gastroenteritis or sepsis. So with the advent of rotavirus vaccination, it really hasn't had an impact. And the number of Children with gastroenteritis resulting in acute kidney injury, but acute kidney injury is often associated with other major disease processes. So for example, Children in tertiary referral units, for example, they may be getting cardiac surgery and it's not uncommon for to see acute kidney injury. On top of chronic kidney disease, which is suggested by poor rule. A history of Polidori in politics. See and evidence of renal and osteo district. And these can be Children that were potentially Anthony Italy diagnosed and Mr full upper patient's that we didn't know, knew nothing about previously. So let us consider the forms of acute kidney injury being prerenal before anything getting to the kidneys, intrinsic to the kidneys themselves and post renal. So, for example, obstruction and when we talk about pre renal failure, really talking about decreased through intravascular volume, which is really due to dehydration or gastrointestinal losses, salt wasting or diabetes, insipidus or third space losses of sepsis and nephrotic syndrome. And the circulatory failure can be associated with congestive cardiac failure, pericarditis or a cardiac tampon ad, if it's intrinsic renal disease, then acute tubular necrosis should be considered. So, an x emmick hypoxic injury, which can be drug induced or toxin mediated. And in fact, we very often see this in uric acid nephropathy previously do two tumor lysis syndrome. But with the advent, all respiratory is that's been much reduced in pediatric oncology. We sometimes see a drug induced or an idiopathic interstitial nephritis. Remember you only need one and doors or by Ibuprofen to have an idiosyncratic response and a tubulin system arthritis. But we also have glomerulonephritis and post infectious glomerulonephritis would be the communist a member know proliferative or Mizan geo capillary, glomerulonephritis or many of the ones now associated or a like uh C three glomerulopathy, lupus nephritis or he notion on purpura nephritis or what we now call IgE vasculitis, nephritis, nephritis of chronic infection. And Cassel stated vasculitis uh Goodpasture syndrome, anti corona basement membrane positive lemur nephritis and idiopathic uh rapidly progressive glomerulonephritis. We sometimes see intrinsic renal disease with vascular lesion. So, hemolytic uremic syndrome, severe a toxin, producing drug inducing bone marrow transplant, nephropathy, eric article necrosis, uh thrombosis sepsis and pilon arthritis. And when we talk about post renal, we're talking about obstructive uropathy. And as I said, uh obstruction and sultry, kidney urethra obstruction or a bilateral your it eric obstruction, but no matter what your underlying pathogenesis is to what because is. And we know this from various animal models using gentamicin and heavy metal, which increases and the renal dysfunction by a decrease in the kill marla capillary permeability or by having a rat model where you obstruct and the ureters and you look at the debris and cast causing a high intra tubular hydrostatic pressure, which also reduces and the camera filtration rate. Or if you look at your bill, epithelial damage and the leak of poultry into the purchase of the circulation, which also causes imbalance of waste expression. But on a relatively normal glomerular filtration rate will eventually be turkey kidney eventually as well in the ski mia uh for any problem, which also causes a decrease in the femoral a capillary permeability so clinically, the important things to it really take home or to think about the presenting complaint. So think about what happened on the preceding 24 hours. What are the fluids in and what are the fluids out by fluids in? What's the intake been? And obviously, if you've just taken 500 mills and you had a huge vomit, you may have actually vomited the whole fluid volume that you've just taken in. So it's always good, especially in babies to talk about wet nappies. But think about how many times they've gone to the toilet too to make sure eight in an older child and whether it's reduced volume, thinking if they've got additional losses. So if for every degree centigrade, the fever is elevated, you've got increased requirements and you've got because you've had increased losses, especially if you've got diarrhea and vomiting and in other situations with huge fluid loss such as burns. But thinking about if you've got polyuria, polydipsia, it's really important to get an idea about if there's any previous urinary symptoms, what the flow could be an element of chronic kidney disease. And of course, in trauma or where there's any evidence of hemorrhage, huge blood loss can result in high pop in the mail. It's important to ask fully about drug history. So this is prescribed, non prescribed, as I said, antibiotics, but also can be nonsteroidal anti inflammatory drugs, but also recreational drug use, especially in adolescence, taking a detailed neonatal history, antenatal scams, and also purse natal imaging thinking about previous urinary tract infections. If there was any test evidence or investigations for rickets or failure to thrive but generalized, considering the growth. So not just looking at what the weight and height is, but looking at the progress during the normal health checks. But also Children. For example, we've got multi organ system involvement, organ failure, previous surgery and especially if there's any family history of kidney problems, high BP, the requirement for kidney replacement therapy and transplantation, examining the patient is really important. So looking at the overall status but actually going back and reassessing, has there been a difference in the peripheral profusion if there's a prolonged capillary, refill time of three seconds, if you give a flu Pulis, does that normalize how things change? But thinking about measuring the temperature, the heart rate, regular systolic BP and if it's elevated or even though you might be wanting to repeat it every five minutes, getting an idea if there's a difference in the corporate oral temperature, we talked about the Anthropocene metric measurements with the way tightened, especially in younger Children, the head circumference, but looking at changes over time as well, looking for the state of hydration and an older child may be looking at the jugular venous pressure as well as examining in all kids for evidence of peripheral edema, making sure you exclude cardiac failure and multisystem disease, especially for vasculitis with evidence of a rash, arthropathy, arthritis or oral lesion's and especially examining for palpable kidneys or bladder masses. Investigations going to be tailored to what you think of the underlying problems. But a baseline, full blood count, blood film and potentially if you've got Patiki Eye looking for hemolysis is yes, are if you're considering and vasculitis or inflammatory autoimmune condition, coagulation screen and cross match if you're thinking about doing a biopsy, serum electrolytes. So thinking about uh and sodium potassium but also checking bicarbonate. The real function with urea crack in in glucose, calcium phosphate and alkaline phosphate ease as one profile as well as uh albumin as part of liver function test. Uh And if there's sex is not only you're going to check the coagulation screen, but you're also going to look for the blood culture as well as the c reactive protein. If there's a consideration of chronic kidney disease, then looking at the ionized calcium as well as the parathyroid hormone and ferritin. And so you might get hypocalcemia with secretary hyperparathyroidism and um a low ferritin with our in deficiency anemia um or even a normal chronic and Amenia of chronic kidney disease. But seeing if there's a reticulocyte count and if it's a comes positive humility uremic syndrome, if it's an accu color injury, then there might be a mess take and s pressure coli infection causing humanistic uremic syndrome. And if you worry there may be elements of complement activation, especially if you've got post infectious glomerulonephritis with the low complement C three C over. And if there's a low complement, see three, excluding A C three. Nephritic factor has been part of the C three glomerulopathy. Cm, immunoglobulins can be helpful if you have an elevated IGA because that may show a lotion and purple or what we call an iga vasculitis nephritis. But remember that having a normal immunoglobulin, a level does not exclude this. If you're concerned if I post infectious glomerulonephritis, where you may have a low complement C three level, but a normal compliment, see four level but an elevated antistreptolysin ot to an anti DNA is B which you would want to see change in convalescence. If you're worried about, for example, systemic lupus erythematosus, the lupus. It writer seeing if there's any evidence of presence of anti nuclear antibody as well as double stranded D N A quantifying that as well as extractable nuclear antigen, any any potentially an anchor or anticardiolipin antibodies, if you called lupus, a generalized lots immune profile but never forgetting an anti glomerular basement membrane antibody. If you're worried about GPM disease, if you get any urine, then think about urine dipstick and take the urine from my costly culture and sensitivity. If you've got any urine, having a look and see what the electrolytes are and checking the fractional exclusion of sodium by having the urine sodium over the plasma sodium and multiplying that by the plasma cracked, it will be the urine cracked and, and that can be really helpful, that fraction discretion of sodium because it might give you an indication if it's prerenal and when it's low, as you can see here or renal and be aware. Because when you want to look at your new electrolytes and acute kidney injury, it's important, try not to do them when they're on diuretics, try to do and before you commence diuretics if possible. But also just remember that if you've just given a diuretic and you have and have elevated urine sodium, it could be by the diuretics and may in fact not discern between premium immunal other investigations will be as clinically um suggested. Um E C G chest X ray would only be, for example, as in this case with pommery edema being worried um management with that with urgent intravenous frusemide echocardiography. If you're worried about longstanding, potentially a ventricular hypertrophy, an urgent doctor with a large time would be helpful to exclude an obstruction. So if you've got hydra, no froze is or even hydroureteronephrosis, but it will also pick up right kidneys of an acute process or small kidneys of chronic kidney disease. Always remembering to do approached industry know biopsy and the X ray of the left wrist and hand, looking at the bone age is important as well. So I said we need to go back and reassess the patient's the same is true with investigations. You need to go back and frequently determine um the repeat serum electrolytes. Now, you may be doing a nice tap every hour because you've got hyperkalemia that you're actively managing, or you may be able to just do the bloods every 40 hours depending on the degree of dysfunction. And it's going to be determined by the clinical picture. You will want to be checking about calcium. So for example, if you got a patient who's hypocalcemic and they're acidotic, then you'll need to create the calcium and give intravenous calcium and calcium gluconate. Especially if the hyperkalemic for cardio protection, you may want to keep on giving and calcium prior to giving your bicarbonate. Because if you do give sodium bicarbonate intravenously, you may precipitously drop your calcium, you further and provoke uh seizure activity, undergoing daily poor blood cope and in your analysis whenever you can and also you're on the electrolytes. And sometimes you may want to repeat the ultrasound depending on the initial result. It's important to think about the hydration status and where you want to be with this patient. So especially protect Kardec if they've got cu peripheries or bloke ability refill type, if there are dry mucous membranes, some can eyes with the law, urinary sodium less than 10 millimoles per liter in older Children or 20 millimoles per liter in units. And the same is true with the national exclusion of sodium, less than 1% which would be up to 2.5% Munitz. If the are dehydrated nego peaches, I suggested that we would give a fluid bonus of 10 to 20 mils per kilogram of flu challenge of normal saline over an hour. If they, you believe it and you don't have any signs of hunger edema, then I'd give a flu challenge anyway, a 10, 20 miles per kilogram. So normally we say in APLS practice and teaching of 20 miles per kilogram. Although this is coming down to 10 mils per kilogram. This is what we do within nephrology. You give 10 mils per kilogram and you quickly reassess and you can give the 20 mil per kilogram bullets after that. If you, you believe maker, you've given a flu challenge and there's no response, then you can give up to 5 mg per kilogram due to concerns about a toxicity. I would normally give 2 mg per kilogram of intravenous frusemide. And if no response, give another 2 million g per kilogram, frusemide and then consider if there is a little bit of response but no massive putting on a frusemide infusion. If they're clinically overloaded, tachycardic with the gallop rhythm and elevated jugular venous pressure with evidence of a Dhiman hypertension, then I'd consider intravenous frusemide in 2 mg per kilogram. If the fluid overload is severe, followed by another 2 mg per kilogram and then have frusemide infusion or analysis if there's no response to the frusemide. Remember this is a multidisciplinary team approach. So, not only with doctors and nurses, but also pharmacists and dietician, a member of a psych social team with the play therapists and specialists, the social worker and the psychosocial team. We want to get further fluid policies of crystalloid, a colloid with or without frusemide is indicated by the clinical state of hydration, urine output. We want to do daily or twice daily weights with accurate input output, recording at least four hour BP monitoring of the peripheral core temperature brady um and are ongoing fluid management. Well, the simplest would be to give insensible losses which is fragile mils per meter square per day or 30 mils per kilogram per day and replace the urine output, giving 100% urine output if the patient is euvolemic, but restricting to up to 75% urine output if they remain clinically overloaded, and we would modify depending on their dialysis or urine outputs. And just see how the response remembering that in the pollen uric recovery place, you need to replace your with insensible loss is for 24 hours. But then you might be best to set a flu target if the renal function continues to improve. So let's start with some of the features. Does anybody know how we would manage? Um hyper clivia. Anybody want to shout out or put in the chat, how you're going to treat an elevated potassium level? We can give some beautiful nebulizer too. Yes. So giving some beautiful nebulizer as uh to try and offset the start is a temporary relief but is worthwhile and then also infusion of uh insulin and uh glucose. Yeah. So, I mean, I've given insulin dextrose infusions over, you know, over a dozen times over the last 20 years and even I trend not to use it sometimes it's just to get the numbers a bit better so the kids can go to theater and get dialysis access cord yet. Sorry, good calcium gluconate infusion as a cardio protection. Yep. So cardio protection of calcium a zillion and next and lift the hyper hypertension. Hyper Yes, calcium gluconate. Yeah. And uh if the hyperkalemia is so high, patient needs to go for dialysis. Yep. If they're acidotic and the BP is okay, you might want to give bicarbonate it. You want to put everybody on a cardiac monitor, potentially giving frusemide intravenously might offset some of the potassium. If you get some fluid over, we've got the recording that we can use nowadays as well. And as you said, in slims extra. So I think you got it. All right. And they're bad said important to put on a cardiac monitoring. If they've got evidence of hyponatremia, then that's usually due to fluid overload. So we're gonna fluid restrict uh renal replacement therapy and potentially give hypertonic ceiling. But to be honest, I very rarely have doing doing that. And actually it's usually the fluid overload as opposed to the total body sodium being low hypernatremia is usually due to sodium retention and very often that will be all set by frusemide or even Dallas is if they're oliguric and if they're hypocalcemic, then that very often is multifactorial will require one alpha hydroxycholecalciferol and calcium supplementation. If they've got high phosphate, then actually dietary phosphate restriction is important. But if they're not eating, you can't really do very much. Dallas has only removed a bit of phosphate but you can use phosphate binders with their eating acidosis. Remember I said if you got hypercalcemia, correct the calcium first or try and get it up. But if you're acidotic, giving sodium bicarbonate but watch what the BP is beforehand and hypertension maybe secondary to fluid overload or alterations, vascular tones. We may need diuretics. Otherwise medical management. Dallas is if you don't respond to diuretics or calm redeem anolik Yuri persist, working very closely with the multidisciplinary team and getting the dieticians involved because acute kidney injury is associated with catatonic state. And malnutrition can develop very, very quickly. It delays the recovery of acute kidney injury. And there's anecdotal evidence that good nutrition actually improves the long term outcome of our patient's dietetic review. For all Children with the kidney injury. You, we need to consider a low potassium know phosphate diet and we aim for at least medicines, calorie and taking protein intake of 0.6 g per kilo. We need to start nutritional feeds earlier if you're nasogastric tube to try and minimize catabolism and uh uremia, especially if they're not clinically well. And we try and avoid total parental nutrition wherever we can working closely with the pharmacist is really important between the drug. Does it just the kick in the injury and for the purposes of correcting drug doses according to the G F R, who'd assume a G F R of 20 miles per minute from 1.73 m squared, many drugs required, decrease the doses are a plum dosage in of interval or make sure the two. So always check your formularies at the British National Formulary for Children. Be an F C is excellent resource as well as your pharmacist and try and avoid nephrotoxic drugs as you can. When would we consider um kidney replacement therapy? What kind of things would you think called? Any ideas for the audience? Either put your hand up or add something to the chat? When would we consider kidney replacement therapy with dialysis? How does that uh there is a consistent him, a tricky area. He material consistent. Yeah, so I wouldn't, I wouldn't say that a patient needs Dallas is just because of having macroscopic you materia. Remember if you're putting a line in it's a vascular space and so you might be in a situation where you could actually make things worse. The career to name is uh by, yeah, people always say the crowning but remember the crown in is really just a biomarker of your kidney function. If you're craning is 4000 or 8000, I agree the chances of getting it down to normal when you're treated, if there's an element of acute kidney injury and chronic kidney disease, but it's actually not going to cause you any harm. What numbers do cause you harm, what results cause you harm increased protein. So again, having protein, your issue, right, that if you've got ongoing protein urea. So the kidneys like to say the syphilis get bigger. If there's protein going to urinary space, that will damage the kidney over time, irrespective of um you know, the degree that you've got of um if the more protein urea you've got obviously the worse it gets. But we don't know if the protein urea is necessarily coming from active inflammation or chronic damage. But having protein urea itself will actually worsen and the overall kidney longer term. So we try and minimize protein urea where we can, I was thinking more about potassium. You can have a cardiac arrest with a potassium of of 10, 11 millimoles per liter, which I've seen having a very high urea level. So above 40 millimoles per liter. In fact, some people even say 30 millimoles per liter in units. But I've actually seen me in eight, recovered with from acute kidney injury with real levels of 60 millimoles per liter that never had kidney replacement therapy. Potassium level usually above 6.5 minimal petito but actually nominates an infants actually do relatively well even in the face of hyperkalemia. If you have a multi system failure, or you think you're going to have a prolonged oliguria, then that also is part of the way of diagnosing as you can see here. So what are the choices of Dallas is mortality that we can have very often if the patient is in intensive care, you may have continue being a venous chemo filtration or diet filtration. But generally, if there are no intubated and ventilated, we reconsider peritoneal dialysis where we can or even hemodialysis, which requires at least four hours and three times a week when you're on maintenance, hemodialysis. So paratenon, Dallas is very easy to set up. It can be carried out by the ward nurse is it's quite easy and um and to use and user friendly, but it may be continued indefinitely with the tank of capital. Though surgeons very often say that after about five years of using your peritoneum, the chances of getting extended by another five are lower. The problems are that you with peritoneal dialysis, you can get peritonitis as the leakage and drainage problems which again can be troublesome. Remember, hemodialysis is the gold standard. So you're clearing but you really need to be hemodynamically stable and you need good vascular access. So Hickman line won't do it. You need a permanent permanent human dialysis catheter which is a cuffed line and that is called a permacath up or you need a temporary noncuffed line such as vast camp. And we generally, historically, we'll keep them in for 7 to 10 days. Although I know we do keep them in longer nowadays. CVH is, gives you good ultra filtration, gentler therapy with tall you clues clearance, which may be even be improved with the dialyzer. But you really require continuous anti coagulation or citrate and vascular access maybe the field. So how do patient's do? Well, there are various prognosis because it depends what your baseline population is. What, how, what degree of it you can injury you're going to have. Is it the how low do you get the E G F R? What's the rise relative rise in plasma crackin is the patient's requiring dialysis therapy? What's the outcome is the death or how patient's do off Dallas is it varies from center to center. The quality of basic care? Remember that prevention is better than cure. Patient's included will also vary. So if you go a very small um level three neonatal unit that takes 22 weekers, then of course, you're going to have more acute kidney injury than potentially older Children. If you've got uh neonatal surgical unit, then again, you're going to get all of those comorbidities. A cardiac intensive care unit where they're doing cardiac surgery where many patient's will have insertion of a personal Dallas of catheter. The theme of the operation expecting that the new requires some Dallas of therapy. And again, the mortality were really very up to about 60% of Children. And it depends if you include HIV or surgical patient's as well. So let's go back to the case presentation. It was a 15 year old boy. Remember the abdominal leg and facial swelling, shortness of bread. He was unwell weight on the 25th percentile. Is that due to a Dema fight on the second central? Is he small? Where does told her his parents um he's hypertensive but he's got to generalize the demons societies and monk reputation. So it sounds like he's fluid overloaded and you can see he's got some weird email on his chest X ray with two big old bright kidneys. So I think there's a lot going on from this that you can see is a cute, we then talk about the calcium levels. Are you going to treat the hypertension? And what investigations? So watch tube the following in the best descriptions of the clinical conditions. I think you got this right of the A and H. So that's acute kidney injury and nephritic and nephrotic syndrome. What range is his corrected calcium? If you remember, we said that his total calcium was 1.8 with an argument of 24 and therefore his calcium, his calcium corrected is going to be between 2.11 and 2.2. And remember we take 40 minus the patient's argument, which is 24 that's 16, you multiply 16 by 0.25. That's the same as four times 0.1, which is the same as 0.4. You add it on to the 1.8 and you get 2.2. So that's 40 minus the patient's argument. You multiply that totally by 400.25. And you've got that you're corrected calcium when you added to your total calcium. And in this case, it's 2.2, which of the following would not be part of the effective management plan for hyperkalemia is a calcium carbonate. Be calcium gluconate. See, calcium rizzo knee, um D cardiac monitor. E frusemide, Ethan's index jewel's infusion detail. Beautiful and age sodium bicarb krusa might. Well, who is my, just get rid of niacin? They all are needed. So, the what doesn't treat hyperkalemia? Cardiac monitor doesn't treat? Yeah, but as part of the management plan I put. So you would want them in a cardiac monitor, isn't it? That would be part of the effective management? You've had sodium bicarbonate. Well, if you're acidotic and hypokalemia, then it will promote movement of potassium and reduce the potassium that you measure in the blood calcium carbonate would be. Yeah. So the answer is a calcium carbonate because that's to treat hyperphosphatemia. Are you going to treat hypertension? Is it intravenous? 4.5% albumin or would you give 20% albumin with frusemide intravenous frusemide, intravenous, labetalol, a low salt diet or amLODIPine, atenolol, enalapril, frusemide, or Nifedipine. It could be another proof. So, if this is an acute presentation, remember his, his BP was 1 50. He's got evidence of fluid overload. I wouldn't be giving an East inhibitor to reduce the, the blood supply to the, uh, the salt. Yeah. You'd want to lose salt diet. But it sounds pretty sick. But he's probably not eating quite yet. Frusemide. So aggressive diuretics. Yeah. So, I think intravenous frusemide, would you want? So you've got oral fruits in my divine. You've got d you've got c being intravenous frusemide or 20% argument with Frusemide because he's got a little argument which one you would do the b because it's acute situation to the intravenous. So emergency then should be aggressive. Yeah. So I would agree that it would be intravenous cruise of mind and you're going to give that with or without the 20% albumin. Maybe we tell women. So, actually I would pick pressure. You would. But remember he's already close to my, sorry. Yeah. Bruise on my album naturally would get, yeah. So I wouldn't give the 20% album refuge in because remember he could be becoming an uric, he's already oliguric. And actually, if you give 20% argument, it will pull an intravascular state. And if he's already go early signs of Palmer edema, especially on the chest X ray, then you might precipitate him having an arrest or the requirement of intubation, ventilation and going to intensive care. So I think the answer is seen and I would just give intravenous freeze um eyes. So despite your fluid management, medical management, he becomes an uric, as we said, for 40 hours as possible, craning continues to increase to 1512. And what one investigation would you do to help make the diagnosis to be? See? No, I think answer is probably all of the above, isn't it? We want to know. I want to know immunology, but you're right. If you think it's supposed infectious, then the conference C three C four and an anti structuralist. The name anti DNA is be teacher would be good if it was. This patient was and uric and the creatinine was now 1000 on Friday morning. What would you be wanting to do? You would be the Yeah. So the question is which one of these results would change your management? You write that if you'd probably want immune suppression. If you thought it was lupus or anti glomerular basement membrane antibody, you'd be thinking about plasma exchange to remove these antibodies. But actually, what you want to see is her active and the inflammation is, and if you've got a crescentic lamanna nephritis as part of your rapidly progressive lemur nephritis with the kremlin increasing the percutaneous, you know, biopsy, you get the result potentially at the end of the day to see how much degree of activity? So I think the one answer would be renal biopsy. And then what's the most likely diagnosis is a humility Remix syndrome is a minimal change. Nephrotic syndrome. Is there a post infectious glomerulonephritis, renal venous thrombosis or a sickle nephrography A B C D or E posting pictures, pictures. Yeah, I think still with all of that. Yeah, a few coming up, see in the chat as well as saying it's I agree it would be most likely a posting pictures system are nephritis. So the take home messages are monitoring changes in clinical status is paramount need to observe the patient, take regular blood in urine test. And the most crucial element to management is a fluid balance and electrolyte management. And that's part of general pediatrics and important is to check if you think clinically this could be acute kidney injury on chronic kidney disease as opposed to just acute kidney injury itself. I can use some reading material there as well that you can have. I'm happy to answer any questions and thank you for your audience participation. Just remember if you go onto the chat, if you click on the feedback form, you can put information on the feedback and then we will send you a certificate with your details. Thank you for doing the feedback. All those great to hear if anybody's got any questions and I'm very happy to help as well. Would the minimal change disease not happens because of infections because that uh so minimal change disease, very often happens when you've got a pure nephrotic syndrome. And by that, we mean, remember that nephrotic range proteinuria together as a result of that protein loss of the urine, your blood levels go down. You get changed the oncotic pressure in the development of a team mail very often associated with hyperlipidemia. When you start getting microscopic hematuria, you just should wonder is this a mixed nephritic nephrotic picture? But remember 25% of minimal change, idiopathic nephrotic syndrome will also have microscopic hematuria if you're in a situation where you've got high BP, again, that could be features of a Nephritic syndrome. But just remember that again, about 25% more after you give steroids and for nephrotic syndrome will have hypertension as well. So I think they're important differentials to keep in your mind, but to have a pure minimal change and that degree of renal dysfunction, a cramp going to 512 is unusual. Of course, you can have new presentations of focal and segmented glomerulosclerosis. But again, that happens much less. Okay. Thank you. Any other questions? Very happy to answer. Well, thank you very much for joining. I know that it's um still difficult times in Ukraine we're thinking of, you know, some of you have put um where you are around the world. And so thank you for that and I hope that things get better in Ukraine. Um We hope for peace eventually and I know that it's really affected you also really very happy to, to be part of the CRF Ukraine Medical School UK Elective program. Thank you for joining today and uh enjoy the rest of your Taney. I just had a question come up about is pt are better than a cr measurements in Children. So this is talking about urine, um laboratory findings. So the most important thing is to try and do an early morning urine dipstick. So that's the first urine of the day dipstick it. And if this protein areas sending it to the laboratory for either an albumin or a protein to creatinine ratio, the question is is either than better. Well, remember uh protein to creatinine ratio. Remember, tubular and glomerular protein urea. Whereas an argument to creatinine ratio tells us more about glamour earlier protein urea, which of course is much more relevant. However, I would say it is more than likely that you will only get one result in wherever you are. I personally prefer, you're an argument to cramping ratio. My institution, I can get both but I can get the urine protein to creatinine ratio back that day. Whereas arguments cramping ratios, the only run the assay twice a week. Okay. So thank you for your questions and thank you for your interest and have a good day. Season. Bye bye. Thank you very much. Have a good day. All the time.