Starting with a refresher on neonatal renal function, pediatric nephrologist Elizabeth Black, MD, offers a guide that covers the factors that can impair kidney health before, during and after birth; treatments that can prevent acute kidney injury in those at risk; the latest dialysis options (and how to modify them for the tiniest patients); and simple keys to follow-up that may lower the risk of chronic kidney disease in adulthood.
All right, well thank you so much for that introduction and I'm so happy to be here. Um I mean to try to get through all of these slides, It's a big topic. Um But I will go ahead and get started and feel free if you have questions, feel free to drop them in the chat or to just speak up. So um I'm gonna just a brief overview. We'll talk about fetal renal development. Um I'll define acute kidney injury. And neo neyts will identify some risk factors. We'll also talk about prevention and management of neonatal renal insufficiency and then long term consequences and follow up. So just a brief, I'm not gonna go into the prone Effros and the metadata froze and all of that if you remember those from embryology, but I'm just gonna talk briefly about feel real development, but I'm going to start us off with a question. So an infant born at 28 weeks. Gestation with necrotizing colitis is suspected of having a. K. I. Preterm infant susceptibility to make ai is related to the to the typical course of development for genesis. But what gestational ages, Neffa genesis complete, and I'll let you think about that for a second. Um And then we will and you can drop your answers in the chat or just think about it to yourself and we will answer this question as we go along. So um if you remember we have three fetal kidneys. Uh only one of them sticks around. That's the meta Knight froze. Um And it develops about 7 to 8 weeks. Gestation in humans. Um And by week nine we have our very first memory away forming uh And then and we start to have fetal urine between 11 and 12 weeks. Um and by as early as week 12 you can actually see the fetal bladder on ultrasound, it looks very tiny. Um bye week 18-20 units actually have a make derision cycle where they retain urine and actively void. Uh most effort genesis is completed by 32 weeks and we're done by 36 weeks so that 32 weeks uh number is an important one to remember because if you're born prior to if you get to 32 weeks gestation, you've got most of the Net Franz you would have gotten if you've made it if you've made it to term and prior to 32 weeks we do see decreased different mass. In preterm infants. Um In in ventura born before 36 weeks, we do know that they have some ongoing post natal Neffa genesis but it's definitely not normal. Um It's a shorter period than in term neon aids. Um And those net franz don't seem to be as functional. Uh We also know that those preterm infants have fewer neutrons. So we, in nephrology we call that having a decreased Effron mass. Um After posting italy there is a transition from fetal to infant life. So fetal G. F. R. Is quite low um and remains low immediately after birth. But after birth we have those blood flow changes. So we have blood pressure and increasing and an increase in real blood flow. R. G. F. Are also increases um due to an increase in surface area as those knee franz are better perf used. Um And we also have an increase in sort of different function moving from um sort of centrally to peripherally in the kidney. Uh and then and in um even in termini unaids, the tubular function remains immature. Okay, so like I mentioned, G. F. R. Is quite low actually immediately post natally. So at birth this is in term infants, your G. F. R. Is only about 10 to 15 mls per 1.73 m squared per minute. Um And by and we don't really see them reach their full sort of adult levels of renal function or filtration until 1 to 2 years of life By one week. The G. F. R. is about 40 in infants. And that's about when we see the creatinine normalize. So at birth, infant serum creatinine reflects maternal creating. And we expect that to be kind of a more normal infant or a more normal infant level by about a week of life. But that process is quite delayed in premature infants. So you can see there um in this table this is a uh an older study from 1999 where they looked at um this large group of preterm infants and they found that that maturation in G. F. R. was delayed even up to 52 days post natally. Um And that that delay was longer the more preterm you were. So that makes it a little bit tricky to define neonatal A. K. I. And I'll talk about why. So in neonatal there's a few different Ak I definitions the most widely used one is the modified KD go um criteria. Que digo stands for kidney disease improving global outcomes. Um It's a very large um uh working group that publishes all sorts of guidelines for nephrologist. Um And they define a. K. I. As put here. So they say that um we say stage zero or you know, no A. K. I. If that urine output is greater than 0.5 ml per kilo per hour and there's no change in serum creatinine or if the increase is less than 0.3 mg per deciliter. And then they sort of use that 0.5 is the mls per kilo per hour as their urine output cut off for stage one and two for stage three it drops to less than 0.3 or an area. Um And then they use the same uh sort of creating changes um as we see in other like adult forms of um or the adult definitions of a K. Ii. Where they say 1.5 to 1.9 fold increase or 2 to 3 times increase. Um And the one thing that they do is they do use that based on the lowest prior created in the past seven days because we know that the creatinine and infants is or in um urinates is not at steady state. So there are some significant problems with the K. Deco definition, even though it's sort of the most widely used one we have, like I mentioned, it is adapted from adult criteria so it may not be appropriate for tiny preterm infants. It's also kind of a lagging indicator. We know that creatinine doesn't change right away after injury. Um And that change in creatinine maybe less or delayed because such small little preterm infants have such low muscle mass. Is and we know creatine comes from muscle. Um The urine output cutoffs may also not be that useful because we see in units that they generally maintain urine output until they're a K. I. Is pretty darn bad. Um Like I mentioned um earlier we know that creating adverse is maternal create need. And while it's expected to normalize by one week in term infants that can take a lot longer in preterm infants. And the KD go criteria don't really tell us what to do when the CME create name does not decrease is expected. So if I have an in you know a preterm infant who is creating is about one at birth and we get 2.7 and it just stays there for weeks. I don't the KD group criteria doesn't tell me if that counts as an A. K. I. Or not, even though it probably there probably is some real insult that's occurring. Um So again we see this is just another from that same study. Um That the decrease in serum creatinine is also delayed in um preterm infants. So we would expect this is in millimeters per leader, which is a more international unit than the milligrams per deciliter we use here in the States. And so by seven days of life, we expect that to be kind of this 30 to 40 million moles per liter. That corresponds to about 0.3 mg per deciliter. And in um preterm infants, that process is pretty delayed. Okay, the other issue with que digo is that we were pretty sure those urine cut offs output cutoffs are too low. Um So there was a study in 2013 that looked at um mortality and A. K. I. Um and urine output in uh neonatal in the nicu. And they found that an increase in the odds of infant mortality. Um In infants who had a urine output of less than 1.5 millimeters per kilo per hour. Which is three times that the you know highest value that que digo uses. We also I think as pediatricians we usually consider that less than one millimeter millimeter per kilo per hour to be allegory A. So that 10.5 number. It's hard to know sort of where that came from. Um So the KD go the KD go is kind of what we have, but it may not be the best one. And there are efforts that have been ongoing to sort of revise and create new definitions of a K. I. N. G. O. Needs. Um I also mentioned that um creating may lag um behind injury or it may not change that much if it's uh if we're still looking at maternal creating. So there's a few other biomarkers that we can use in infants, but they also have their own limitations. So sis tendency is something that the pathologists really like. This is a marker of kidney function. It's actually produced by all nuclear ated cells. Um It's not dependent on muscle mass and the creating of 0.8 is normal in a two year old and a 10 year old and a 30 year old. So it's really not that dependent on body size. The issue with this tendency is we still don't really know, we can estimate. There's no good estimating equations for G. F. R. In the unions. Um In terms of estimating kidney function. Um The equations that we use are for Children a year and up. Um And we also we know that they naturally have lower G. F. R. So it can be hard to say like what exactly a normal G. F. R. Is for say a 32 weaker. Um Other biomarkers include neutrophils gelatinous associated lipo, Carlson or Engel. This one's getting a lot of attention. Um It is a marker of A. K. I. Alright acute kidney injury. So we look at urine en gal and an elevated urine en gal is very predictive of acute kidney injury. Um Not all centers are using it but Children's hospital Oakland can actually run it in the house. Um T. I. M. P. Two and I. G. F. B. Piece seven are both produced by tubular cells. And there have been studied in conjunction with each other to predict renal tubular injury. Um And then though again not available at most centers and then kidney injury molecule. One is another um urine marker of tubular injury that is currently experimental in being studied. So question two. We'll just put kind of what we talked about with the KD go criteria into practice. Um so you're seeing a male infant born at 28 weeks gestation who is now two weeks old and he weighs uh 1150 g. He has nec necrotizing colitis in his N. P. O. Currently receiving I. V. Nutrition at 100 and 20 mls per kilo per day. You're called to his bedside to evaluate decreased urine output to five million L over the past 10 hours previously. His urine output was appropriate. Um most recent labs should be u. n. of 26 and created of 1.2 Compared with 12 and 0.8 from the day before. You suspect a. K. I. Using the kidney disease improving global outcomes classification system with stage of A. K. I. Business and have so pause for a second. Um well you consider it, but they did put in the urine output has been .43 um per kilo for 10 hours. The creatinine is up by about 50%. Um and the b. U. N. has increased from 12 to 26 and feel free to put your answer in the chat. Yeah. So I see people saying be this would be considered stage two or sorry, stage one. Um Ak I buy que digo but I would be as an apologist. I would be a little bit more concerned about it because that urine output is so low and so it may um the KD go criteria may give us an idea of sort of what's going on but may not be totally appropriate for Neo needs. All right. So I'll address some talk about some risk factors for acute kidney injury and donates and it's really important I think to recognize the risk factors because ideally what we want to do is prevent a K. I. So I sort of think of the risk factors for acute kidney injury as broken into prenatal perinatal and postnatal sort of factors prenatally a lot of those um are sort of socioeconomic um or kind of go along with our social determinants of health. So mothers who have and and there are all sorts of things that are contributing to preterm birth and low birth weight infants. So we know chronic stress issues with nutrition if a patient is or if a um if the natal parents is to um is undernourished or over nourished, right, we can have issues with low birth weight infants or premature birth age, either very young or very old. Um any chronic disease and interval the interval between pregnancies. We know that having both a very short and very long interval between pregnancies can be associated with preterm birth if there was any prenatal metra toxic exposures. Um That's particularly I think about things like Nsaids and ace inhibitors. Um but also um any sort of substance misuse during pregnancy and then other pregnancy complications that may result in placental insufficiency like Prick Lancia or help syndrome. Perry natal e um I'm really thinking about what are sort of the delivery complications. It was something going on with mom that she needed to toxic medications, Very Natalie, did she have some terrible infections um and needed sides. Were there bad delivery complications where there was their prolonged rupture of membranes. Is this a baby that's gonna have congenital sepsis or um was there some terrible hypoxic event. And now the baby has hypoxic ischemic encephalopathy and is on cooling protocols, all of those are things that may result in acute kidney injury, post natal e um it's sort of the same kind of things that I've talked about, right. I'm thinking about anything that would result in Lone Effron endowment because we no lo lo having Lauren Effron masks predisposes you to acute kidney injury. So that's like prematurity, low birth weight, um inborn errors of metabolism, potentially. Um and then anything that is going to be sort of cut renal toxic, so congenital heart disease um and patent or curio sis's, they're not good blood flow to the kidneys. Is the patients, has the baby been septic and hypotensive? Um or are they so sick that they're requiring extracorporeal therapies? Like do they have bad congenital heart disease and they've had surgery and now they're on ECMO. Um so basically, anything that is is gonna be harmful to the baby can also be harmful to the kidneys. Um and when we do see acute kidney injury in these infants, it has some pretty significant consequences sort of in that period. So, one of the biggest studies that looked at a. K. I in the is the awakened trial. This awakened trial is this huge multi center in multinational cohort study um in four countries. Um they looked and looking in 24 neck use. So these were patients in Australia Canada Canada India and the United States. Um and they looked at them over actually a pretty short, just three month period. They used a modified modified kg go criteria. So they used they defined A. K. I. As an increase in serum creatinine 0.3. Um or more or 50% or more from the previous lowest value. Or a you're an ordinary output of less than one. Um They included patients who were admitted to a level three or four NiCU and who were on 48 hours or at least 48 hours of I. V. Fluids. There were some patients that they uh excluded. So they excluded anybody who didn't have who was admitted at over two weeks of life to the niCU. Anybody who had congenital heart disease that required a surgery within the first week of life. Um any patients with lethal chromosomal anomalies or anyone who died within the 1st 48 hours. They also excluded patients with significant congenital renal disease. They wanted to see at least two serum creating measurements um and urinary output data. Um and so of the roughly 4000 patients who were screened, they had a sample size of 2000 which is pretty darn good for a pediatric study. Um so up there 2000 patients Um 14% were those you know really early preemies between 22-29 weeks. Um and then the rest of them were sort of split evenly evenly between 29 weeks to 36 weeks and over 36 weeks. Their highest incident of AK. I was not super surprisingly in those littlest babies between 22 weeks to 29 weeks gestation Mitford. But this to me was a little bit of a surprise is that actually of these infants um had been into the Nicu the 29 week to 36 week group had the lowest incidence of acute kidney injury. And then it was the over 36 weeks who were sort of second in terms of incidents. And that's um probably related to those 36 week uh infants. They don't necessarily need to be in the nicu if they're healthy. So they've probably got some some other sort of um issue going on their septic, there were birth complications. They have congenital anomalies, things like that. Um So when they looked at survival and length of state in patients who had A. K. I. Versus new A. K. I. They found that patients with A. K. I. Were about 10 times more likely to die than those who didn't have A. K. I. And had a significantly longer length of state. Um Up to um uh And that sorry and that length of state was sort of increased in based on the severity of the of the A. K. I. So if they had worse ak I. They tended to have longer length of state. Um So they broke down that overall survival into New Ak I. Um And A. K. I. Using these are survivors Kaplan meier survival curves. Um And uh as you can see the A. K. I. Group again much lower overall survival. That was very significant. Um And when they broke that down into um by A. K. I. Stage again unsurprisingly the worse the A. K. I. The low the higher the chances of mortality. Um So I apologize. Power point has broken my bullet points. Um So what we really want is to prevent acute kidney injury. And so that's the first thing that we think about. So in addition you know social programs that support um maternal health and well being are A. K. I. Prevention. But what can we do with actual pediatricians? So we know that prenatal administration of glucocorticoids and patients who are expected to deliver early will improve systolic blood pressure and renal blood flow. So we've there are studies that should improve G. F. R. And it also helps to accelerate the maturation of tubular function. Um Because uh infants have immature tubular function. I sort of think of all of them as units as having sort of a transient um Fanconi syndrome. Um So they may have significant policy area or electrolyte wasting. They can also put them at higher risk of kidney injury. Other medications that can have a preventative effect. So there's the offline or online offline that's a lizard, a dentist in receptor antagonists and they basically help inhibit a dentist induced phase of construction. So they help to maintain renal blood flow. Um And currently theater allen is recommended for any infant with severe um perinatal asphyxia. Um Though there are potentially some significant neurologic side effects from the and um an awful in caffeine is another actually at a dentist in receptor antagonist. And um data from the awakened study has shown that infants treated with caffeine actually had a lower incidence of acute kidney injury. Um Other things that we use sort of to treat A. K. I. So once we have a. K. I write it's mostly supportive care. And then we're trying to prevent the need for more significant interventions. So generally in any patient with A. K. I. We want to make sure that they are adequately hydrated. We want to avoid natural toxic exposure as much as possible. Um But if we have infant tours starting to have significant A. K. I. Or may have um uh decreasing urine output. Then that's sort of when we nephrologist think about diuretics. So they're used to. Diuretics are really common in A. K. I. To maintain your output but they actually don't improve outcomes. Um And may in fact be may worsen in kidney function or exacerbate A. K. I. In these patients um in Neo needs its overall not well very well studied but we do sometimes use diuretics because of how risky and complicated renal replacement therapy can be in these little babies. So if we can kind of limp along with with aggressive diaries, is to prevent the need for renal replacement therapy. We usually will Um talking about prevention. Um there was a study called baby Ninja that came out, this was from 2019. Um and this study only looked at this is actually a quality improvement project, looking at um screening for acute kidney injury. It's based on the there's a net toxic injury negated by just in time action. That's where that ninja acronym comes from. This was originally done in patients in the Nicu. Um And um this was I think University of Alabama applied sort of that same framework to their Nicu. Um And so what baby ninja recommends is daily or the ninja sort of protocol recommends is daily creating measurements during high network toxic medication exposure exposure. So they considered that greater than three known Neffa toxic agents um or greater than 10 days of nef ra toxic exposure. Um and then they continued to do daily creating for two days after that exposure ended, or until A K. I had improved. Uh And what they found was just by measuring and paying attention that they actually saw a significant decrease in net for toxic exposure and A. K. I. So as I said, this was a Q. I. Project. So they looked at, they sort of divided it into these three eras, the pre ninja era, the ninja initiation era, and then the sustainability era. So they so when they were putting this into place, they actually saw a slight bump in new A. K. I. A new nephew, a toxic medication exposure, but after um in that maintenance or sustainability phase of this quality improvement project, they saw that um A. K. I. Events were significantly reduced and so is never a toxic medication exposure in these patients. And part of I think a big part of what this study really was doing was forcing people to to think about the implications. Right? So if if you know the the neonatologists were thinking about their babies and their babies on in the medicine and is on um and I mean like aside and they need another medication for something they make think more about, Okay, can we avoid using an effort toxic medication. Um are there other options that we can use? So this is this is I I was very impressed by this, but just by basically just by thinking about and screening for acute kidney injury, they found that they had a significant reduction, but there was no sort of intervention piece of this study. Okay, so we always want to prevent acute kidney injury because what we've part of it is we want to prevent any future kidney issues. Um and we also really don't want to use renal replacement therapy in these little babies if we can help it. Um so indications for renal replacement therapy in infants are sort of the same as in um other, you know, patients, we use a an acronym, A. E. I. O. U. Acidosis, electrolyte abnormalities. Um usually that the eye and A. E. I. O. U. Is intoxication. Um Generally we don't have uh you know near inmates who have gotten into something they shouldn't be. Um So we talked about that in that case an adequate nutrition. So um preterm infants are often um and even term infants and even term infants are really, their nutrition requires high volumes of fluid. And so if we're not able to adequately feed these babies whether n truly apparent parents really um and maintain their fluid status um That is an indication for us to do dialysis. We also think about fluid overload. Um and yuri mia as possible indications for renal replacement therapy. So there's sort of two main options that we have for renal replacement therapy. And those are perennial dialysis vs. Continuous renal replacement therapy or C. R. R. T. Unlike in larger people we almost never we basically never do what we call intermittent hemodialysis. That's sort of the dialysis that most people think about where you get hooked up to a machine for 3 to 4 hours, you know um once a day or 3 to 4 times a week. Um And that's because like I said in part because infants are so volume dependent on volume for nutrition and because of the risks of sort of the hemo dynamic shifts that happened during hemodialysis. Um Generally infants will tolerate that. So if the babies are needing you know these huge volumes of fluid for nutrition much higher than adults. And older Children generally get, there's no way for us to remove that amount of fluid in just a few hours. That is all safe for these neo Neitz. Um So then we're sort of thinking about peritoneal dialysis versus your RT. You don't go back to this. So this is a peritoneal dialysis set. Um I don't know, and this is specifically a set that's for infants. So in peritoneal dialysis, we insert a catheter into the peritoneal cavity um that uh this is hooked, you can see this part is actually attached to that catheter. Um there's a three way stop cock here that is attached then um to a drain bag. Um and also to the uh there are tracks that we fill, so fluid goes into the baby and then comes out through the drain bag. Oh sorry, this is the drain back here. Um So we put fluid into the baby through here. The fluid sits for um generally about an hour. And then is we open up this three way stop cock and allow it to drain into the drain bag. Um This is very, very labor intensive and I'll talk about that. So peritoneal dialysis is generally for one thing less expensive, It's um the um equipment for PD is is pretty inexpensive and it's technically a lot easier than continuous renal replacement therapy. And neonatal. Um it's also much more physiologic than continuous renal replacement therapy and it's generally very well tolerated even in unstable patients. Um But it's super labor intensive. So you may have seen patients on peritoneal dialysis who are hooked up to a machine that does the fills and drains for them. That's called the cycler. Um That cycler is only able to accurately do that for volumes of generally the minimum is 100 mL, realistically it's probably 100 and 20 mL. Um and we sort of max out our perennial filled volumes and about 45 ml per kilo. So if you think about these teeny tiny babies it takes a long time for them to get to that filled volume and we always start smaller because we kind of need that perennial spaces stretched as this goes along. Um It is less efficient and sort of less precise um at correcting um electrolyte imbalances and um And in fluid removal we use different dextrose concentrations to pull fluid into the peritoneal cavity through osmosis. Um And uh but unlike in C. R. T. Where we're basically precisely telling the machine you know I want you to take off this exact amount. The machine will take off that amount and pd were sort of guessing you know if we use this concentration. You know we use this concentration yesterday and this is what we got. So if we adjusted a little bit it'll be a little bit more a little bit less. It's much much less precise. We're also increasing increasing intra abdominal pressure. So basically all of these babies who start P. D. Um as infants end up with hernias um And we can't do P. D. If there's any abdominal wall defects. Um So if that's a baby who's had a recent abdominal surgery or who has an osce to me generally there's a big risk risk that there will be leakage and infection um from the peritoneal cavity. Um And then we're again increasing intra peritoneal volume in babies with pulmonary hyperplasia or who have a lot of respiratory distress. They may not be able to tolerate that from a respiratory standpoint. Okay? Um So in our infants where P. D. Isn't an option or isn't a good option. Then we think about continuous renal replacement therapy. Um And it's important to note that in most cases we're doing this totally off label. So um but I'll talk a little bit more about some new things that are coming along for CRT. So um if you think about this is a standard C. R. R. T. Machine um this uh so this is hooked up to a patient. Um and then there's a through an arterial line and well not an arterial line but we call it the red line. And then there's a return line where the blood is returned to the patient. Um This is a standard filter called which is uh called an HF 1000 to the high flux style laser. Um And then we've got all of this tubing. So when we take the blood from the patient, we have to take that blood and fill all of this space. Um And usually most commonly we prime the circuit with normal sailing. So in this sort of standard setup that volume is 100 and 60 mL. So if we think about a patient um and babies we say they have about 80 mL of um per kilo of blood. So if we hook a two kg baby up to this, we essentially take all of their blood out and replace it with failing, which is obviously not a good idea. Um So we have a few options for mitigating that we can do a blood prime where we prime prime the filter with blood instead of sealing. That's quite technical and time consuming. Um Or we can use there's actually a smaller filter um that has emergency authorization. Um Under it's actually under the shadow of the covid umbrella of eu A Um and that but that still has a volume, a circuit volume of 60, which is still a lot of volume for a little tiny baby. So oftentimes we are even in I mean almost all the time, right? You really need to be closer to like eight kg before. Um You need you wouldn't need a blood prime even for that much smaller filter. Um And you know, we don't have a ton of eight kg babies in the nicu that's a pretty big kid to be in the Nicu. Um There's also um a risk of clotting. So we have to do slower blood flow rates, Blood flow rate on the machine, we based on body size. So we're oftentimes doing these very slow blood flow rates into the circuit and having that blood that is just not moving that quickly. Um There's a high risk that it will clot. And again, we're taking blood out of the patient, even if we're giving blood back, there's still a lot of sort of fluid shifts in that infant and there may be significant thermodynamic and stability on continuous renal replacement therapy. There are some emerging therapies that are coming down the line though. So the carpe diem. Uh they call it the cardio renal pediatric dialysis emergency machine. The Carpe diem was initially um developed as a sort of home fluid removal system for adults with congestive heart disease. Um So but they have the company that makes carp ADM has adapted that um for as a neonatal cr. R. T. System. Um And that was just approved in 2020 and um for 2.5 to 8 kg. Again, eight kg is a big kid. Um And then there's also the aqueducts, which is the same sort of idea as the initial carpeted. Um It's generally mostly fluid removal, but you can still put a filter in line with that for to do dialysis. Um uh that currently has not um there is no FDA approval for the use of the aqueducts machine um in neon aids. But there have been uh we've seen success in that reported in infants as small as 1.4 kg. Um So these are both machines that are much smaller and use a much smaller blood volume and a much smaller circuit volume. Okay so we have our baby in the nicu terrible things have happened, they've been sick, they've had kidney injury, but now they're getting better and they're ready to go home. And the question that we get all the time about these babies from their parents is will my baby have permanent kidney problems. Um And the answer to that is honestly pretty complicated. It can be very hard to predict which of these patients will develop CKD um If they've had a K. I. Um there even if they haven't had a K. I just having preterm birth is a risk factor for CKD and hypertension later. And a lot of it will sort of depend on, you know, how bad was the A. K. I have. They do we think they've fully recovered. They probably have lost some net franz how many did they have to start with? It's a very very complicated. Um It's a complicated answer and we often can't say yes or no unless it's pretty clear, you know, well your baby the creating has not come down, right. But in these infants who have a k. And appear to have recovered, they're still at risk later. So there's been a lot of studies on this. Um, So we know um, that low birth weight um really increases your risk of chronic kidney disease as an adult. Um that's again sort of related to loan Effron endowment, but others also to these other things that sort of feed into low birth weight, right? They get catch up growth. We know low birth weight is actually at risk for overweight and obesity later in life. If you have loan ephron number, you may have hypertension or hyper hyper filtration, which also can lead to chronic kidney disease. So it's all of these sort of things that feed into each other. Um We also see that um the smaller you are, the higher your risk of cKD um and in patients who have both very low birth weight and a history of acute kidney injury, their risk is much higher for things like hypertension, protein area and renal dysfunction later in life. So risk factors for chronic kidney disease. And nicu graduates. Um, we know anything basically anything that gives you that loan Effron endowment. So, preterm birth, low birth weight, also, some of that may be genetic, um, and then kidney injury, Neffa toxic exposure, hypoxia and congenital heart disease are all also risk factors. So anything where you're knocking off a few nah franz sort of your risk is going to go up and up and we know that in most patients who have significant a. K. I even if they're creating goes down to a place where it's normal. We assume that they've probably lost some of their net franz. So how do we follow these babies in the long term? Um, So, uh here are the K. D. Go and the American Academy of Pediatrics guidelines for following ckD screening in a preterm infants or in infants with the history of acute kidney injury. There are none. Um, we're a little bit on our own and using our best judgment. Um, but there are some things that we definitely do know. Okay, so the rule of neonatal A. K. I. C. K. D. Development, we assume there's something that it hasn't been well studied, but we know that prematurity and low birth weight are risk factors for chronic kidney disease and for acute kidney injury. So it's a little bit of a chicken or the egg kind of thing. Right. Um, so Que Debo does recommend anybody who's had acute kidney injury. Um, should have a three months later, shouldn't be reevaluated, have serum testing um, to look at kidney function. They should we should check their blood pressure. And then the American Academy of Pediatrics also recommends that all nicu graduates should have yearly um urine testing once there. I usually wait until their continent um and can give us a urine sample. Um and blood pressure checks. So we're sort of screening for humanitarian protein area and those urine tests and we're making sure that their blood pressures are normal. And generally what I recommend for babies that I've seen in the Nicu, especially if they're under 32 weeks is every time they go to the doctor try to get a blood pressure, we won't always be successful. They don't um they don't cooperate and that's okay. But we should be trying each time they're seen in their pediatrician's office. Um So there are there is a suggested algorithm for the assessment of Nikki you graduates at risk for CKD. This was published by um Uh Dr. Charlton and her group um in 2018. Um and I think this is actually quite a reasonable one. Um So they say, you know, what's your CKD risk assessment? Were you premature? Did you have a K. I was there, you know, what was the birth weight? What was were there any structural abnormalities on the ultrasound? And they recommend with each healthcare visit blood pressure, check their growth, and do counseling and education about the risk of CKD. So, I generally tell patients of anybody who's Nikki graduate or anybody who's had a K. I like, you know, I don't know for sure if your baby is going to have kidney injury later. But let's do the thing. You're gonna have chronic kidney disease later. But let's do the things now that can minimize that risk. Right? So I talk about you know once they're eating solid food we want to do healthy things um maintaining a normal weight, avoiding overweight and obesity, drinking plenty of fluids and then avoiding insects when possible. They recommend um at ages 4-5. Um and at the first adolescent visit a serum creating a serum system in c. and a urine albumin to creatinine ratio. Um And in patients who have are higher risks of patients who've had recurrent aK I or known um any chronic disease obesity or if their blood pressure is abnormal doing some more frequent screening. And I think this is this is quite a reasonable sort of place to start. And of course if there are any concerns you can always send them to nephrology. And to be totally honest with patients that I have seen in the NiCU um who have who have seen in the NiCU for things like acute kidney injury. I always follow them up at least once or twice in clinic and then give the option to the parents of you can you know if everything is looking okay, you can go back to your PCP or you can just come and see me once a year and we can kind of do all of these things. All right. So in conclusion we know that neonatal are at increased risk of a. K. I. And that's even higher in preterm neonatal A. K. I. And the Nicu is associated with increased mortality and a longer length of state. Um But we really need more research on the long term implications of neo natal A. K. I. Um But anybody with a history of neonatal A. K. I. And really all of our NiCU graduates should have some long term screening for CKD. Um and then I'll just move on to this left side, fly to bed. If you have patients, you're concerned about how you can refer them over to us.
