Chapters Transcript Hematuria Kaye Brathwaite, MD, identifies the presence of hematuria. So I'm talking about hematuria today. Thank you, Madison. My name is Doctor Brathwaite. I'm one of the kidney doctors here at children's. Um So I have nothing to disclose today and just going into some of the goals for our talk. So identify the presence of hematuria and looking at initiating the proper diagnostic work up and thinking about when to refer to nephrology would be important. So let's start off with identifying the presence of hematuria. Um So we know that hematuria can be quite alarming for families, for patients, for providers as well. There are some benign causes of hematuria, but there are also some markers can be a marker for significant kidney disease. So it's something that we do like to pay attention to. Um but before we even think about hematuria, there are several causes of red urine. You know, there are medications that can cause the urine to have pigments as well as some foods, um and several metabolites as well. So it is good for us to assess to see if this is true hematuria that we're seeing um when whenever we see a patient with colored urine. So, hematuria, as we know can be macroscopic so visible with the naked eye. And more often this is either bright red or can often be tea colored if it's related to a globular cause and or it can be microscopic Hema material. So that's detected by our urine dipstick or a urine sediment when we send your future sample and do a formal urinalysis. So, looking at the definition of hematuria, so we use the urine microscopy to look at the number of RB CS or red blood cells that we see in a freshly voided urine sample. So what happens is we take about 10 MLS, we can centrifuge that at about 500 G for five minutes and you discard the sup and resuspend the pellet in the about a half of an ML that's remaining in the tube. And that's what you're gonna look at under the microscope. So, in a centrifuge sample, if there are greater than three red blood cells for high power field, and that is considered true hematuria. If the sample is in centrifuge, then you know, then you can look at greater than five red blood cells. But for us to have a diagnosis of imagery on urine microscopy, technically, we should have greater than 3 to 5 red blood cells for high power field. The urine dipstick is what we typically would look at initially. And the urine dipstick, it utilizes this peroxidase like activity of hemoglobin. That's any he hemoglobin that's present in the urine and it converts the chromo tetra methyl benzene that's incorporated in the urine dipstick. And when it gets oxidized, it turns the color to this green blue that we see on a positive dipstick. So really, we dip the, the um the marker into the urine and then we take it out immediately, you shake it off and then you leave it for the um amount of time that it says on the package that you have. So the Dipstick detects the free hemoglobin in the in the urine. So it's, it's under the assumption that there is hemolysis of the red blood cells. And if there's a significant amount of hematuria, then it will be enough to detect um hematuria because enough, we're assuming that enough blood cells would lice. So it's a sensitive to as little as 100 and 50 mcg per liter. But there are some things that can cause a urine dipstick to be false positive. Most often myoglobin, urea and hemoglobin urea, but also some oxidizing agents in the urine can do this as well. And for false negatives, if there are a large amount of reducing agents in the urine, um or it has a very high specific gravity, those can be instances where we see a false negative. So our urine microscopy is really key. And when we again, we sent your future the sample and with the after we remove the sate and we resuspend the pellet in the remaining urine and that's what we're looking at under the microscope. But even in the microscopy, if our urine has a very low specific gravity or the PH is alkaline, sometimes we can see false negatives here as well. But the urine microscopy is important to diagnose um true hematuria. Ok. So just thinking about a case. So a 16 year old male teenager who's an avid runner, he just participated in a local marathon. He's in the led due to brown urine um and his blood pressure is normal. He his vitals overall are normal, what would not be seen on a formal urinalysis. So, in this case, you know, we we can see that it's positive for urine um in the urine, for red blood cells, it would be very concentrated. He he just ran a marathon and you might even see some trace protein urea in the setting of exercise. But you wouldn't necessarily see greater than five red blood cells for high power fields because this is most likely it's gonna be myoglobin urea after running a marathon. Um ok, so let's look a little bit more now into work up. So, hematuria is, is quite rare actually in normal physiology because our glomerular basement membrane kind of prevents any blood from getting into the urine. So it stays within the bloodstream. But the red blood cells also have a very flexible cell membrane. So it does allow it to squeeze through if there's any disruption to the barrier in any way. So we often can see hematuria in, in place in moments of inflammation, whether it be we are exercising significantly in a setting of fever. If there's any trauma, of course, um UTIs and any inflammation of the urethra or the bladder, there are also more significant causes including malignancy. All of these things can cause transient hematuria in patients. And we also can see actually microscopic hematuria just because of the nature of the red blood cells in about 3 to 5% of healthy Children when we screen. So that's also something that um is can be present as well. So, in hematuria, it's important to distinguish non glomerular from glomerular hematuria. And the difference is that on extra glomerular hematuria, they typically are these isomorphic red blood cells. So, normally shaped, there's not any significant um distortions of the red blood cells. Um They're very isomorphic and you don't really see any additional like things like urinary casts, red blood cell casts in the urine, the urine is typically either red or pink. Um and you might even see some clots present depending on the etiology in these cases, protein Urrea, however, is typically absent and there are several causes of extra glome hematuria. Um You know, if most common, of course, we want to assess if there's a urinary tract infection, cystitis can lead to other causes as well. And viral causes as well as parasites um can be seen some medications, as we know, cyclophosphamide can cause a, an acute chemical cystitis and stones. We see very often in, in our pediatric population. So, hypercalciuria, whether it be related to a diet or genetic causes and kidney stones as well. Um, and then if there anything significant going on as far as other bleeding or, or any other cardiac things, you want to think about coagulopathy or v or vascular malformations or not Cracker syndrome as well. And malignancy in the kidneys or of the bladder can of will often present with hematuria. Although non glomerular, um we don't talk about this often but in sickle cell disease as well. Um we see hematuria can be gross hematuria or microscopic hematuria and most often related to papillary necrosis. So, glomerular hematuria, we know we can see we can see red urine, but we can also see this smoky brown or Coca cola colored urine. We do not typically see see clots in glomerular hematuria, but protein urea may be present. So this is a case where you know, we would potentially see protein urea as well. And again, the blood cells here are quite dysmorphic. So you have these acanth aytes where you have these bloods over off of the red blood cells. Um sometimes you can have a pale central groove as well. So, and here we also see that urinary cast may be present. So our red blood cell casts where the blood cells could get trapped into the tubular lumen to form this kind of characteristic shape. Um gives us an indication that there's glome hematuria. Now, you may not always see cast. So it is something you know, there are other things in our history that we want to pay attention to. Um but if we do see cast, then we can be almost we can be very certain that this is glome hematuria and thinking about some causes of glomerular hematuria. So our post infectious glomerular nephritis, which is extremely common that we see. Um but other causes that are more significant, including the rapidly progressive glomeruli, nephritis and and other forms of GNS um ig vasculitis, which we also see quite commonly in our general population. So, and then we also want to think about our genetic causes and some cystic diseases as well as um if there's any thrombosis, any coagulopathy, we want to think about these as well. So there are several causes that can cause glomerular hematuria. And really when we see that there is protein urea or there are urinary cast, um hypertension, you know, if there's any family history of significant renal disease or other things that could potentially suggest a renal ideology, you know, we want to think about that. These are the things that that could be more pathologic. And this is when um we want to think more a little bit more and be more involved with our investigation. So as far as our investigation of hematuria. Um we often like to look at the urine protein creatinine ratio. Um The urinalysis does tell us that there's protein, but the urine protein creatinine ratio is a little bit more accurate and quantifying because we know that if there's over 0.0 0.2 of protein urea as far as our, our c protein creatinine ratio, then that is not necessarily physiologic. So, physiologic, anything up to 0.2 but anything over that, it could be something, something else going on. Um We like to look at our kidney function because kidney function, of course, in the setting of, if we're seeing signs that there's an acute glome nephritis, that's a quick way to tell us if, if it's more significant, the more significant involvement that there's more than we need to do. Um Of course, if there are any other cases of bleeding you or, or clotting, you know, we want to think about um making sure we, we look at the CBC coagulation screen and then when we see hematuria, particularly gross hematuria um or, or microscopic, you know, we, we do like to get our C three C four initially and A N A is also helpful um as well because in our setting of gross hematuria, if it is a post infectious GN, we can see right right away if that C three is low and if it is low, then we are able to um when we see these kids as nephrologists later on, then it's, if, if it's normalized by then we do, we can look at your labs to say that this is that this was truly a post infectious gene. If there's no labs, then it's a little bit harder to assess that. In some cases. You know, if there's pulmonary hemorrhage, we would look at an anti GM antibody. Um, you know, of course, in any of these situations, if it's, if it's more comfortable to send the patient to nephrology to get some of the more involved labs. And that's ok as well. Um But that's something that's a quick check as well, that can be easy to do. And urine culture is, in some cases, we can also look at viola paraic causes and you know, looking at our patients with calcium creatinine ratio, this is helpful as well because it's especially if a patient is at risk for hypercalciuria, this is a quick check. Um and in older kids, if it's greater than 0.2 so similar cut off to the protein, then that's something that we can um say that is, is contributing as well to potentially the Hemery. If there's any evidence of stones, again, the 24 hour urine is something that is is more accurate than our our spot calcium, the creatinine ratio. However, of course, if this is something that you feel more comfortable sending to the nephrologist to do, this is ok as well. And then imaging studies are also really helpful because our Doppler sometimes can let us know if there's any, if there's any clotting of the renal vein there. Um in cases of trauma, of course, AC T and if we're concerned for Nutcracker syndrome, then an MRI would be helpful. I really do like this diagram because it kind of lets us put things into perspective and, and our history and physical are really key um in thinking about hematuria and whether it's a glomerular versus non glomerular causes as well. And you know, when we look at the urine as well, if there, if there are any clots, if you know there is an exam, if there's any flank pain, you know, those are things that we want to think about. Maybe there's stones and in those cases, we would, you know, think more, we would want to think more about doing our calcium to creatin rate for our 24 hour urine or of course, if there is dis or frequency, we think about our common UTIs. So our history and physical are really, I think are key in, in helping us to look at this evaluation more in depth. And then of course, with our glomerular causes, if we see those casts or dysmorphic red blood cells, then we're really thinking about a glomerular nephritis, whether it be a post infectious or other cause. And, and then from there, we know that we can get some labs including our complement levels. Um ok. So looking at a case, so a nine year old girl has isolated microscopic hematuria that's incidentally noted on urinalysis, obtained for abdominal pain and she has some intermittent diarrhea, urinary frequency. And however, her urine studies that during these periods haven't really revealed a ut I. So they've not been positive or signific significantly positive for a UT I. She is toilet trained and you know, urinating well without difficulty and has no diurnal or nocturnal auris. Her father has had kidney stones and there's no family history of significant renal disease or deafness, um or hemat her blood pressure at this time is normal. So in this case, there are a couple of things that are already to the top of my mind when I read this case and a patient who has these periods where it seems like she has a UT I, but they're not true. Truly, a UT I right away makes me think that a patient could have avoiding dysfunction or bowel bladder dysfunction. Um she is toilet trained so that in some ways helps. But at the same time, she does have these symptoms of urinary frequency and diarrhea and there's no true ut I. So it could be that, you know, there's some holding patterns there, some constipation as well. Those things can contribute to avoiding dysfunction or bowel bladder dysfunction in kids this age. And it would be really important to get a good history just to discuss you know, her bladder habits as well as um, you know, looking at the just kind of looking at at her her bladder habits as well as well as um looking at the U A formally getting a urine culture, things like that. But also there's a family history of family history of kidney stones. So looking at in her case, uh calcium to creatinine ratio would actually be also very helpful. So this patients, you looked at the urinalysis and they're there's true red blood cells, you know, they're quite EOR fic. So that's a good sign that this is likely non glomerular hematuria. Um and then you do the calcium to creatinine ratio um which comes out to be about 0.15 less than 0.2 which is good. It's reassuring that there's not significant hypercalciuria um which we can see in, in much younger kids if there's some sort of genetic ideology. But in her case, even though you know, there is a normal calcium to crowning ratio, there, there are stones that could be related to other causes and it there. So that doesn't necessarily mean that there aren't stones. So it is important to still think about, you know, can we get a 24 hour urine collection as well? Um So normal calcium to creatinine ratios in kids really depends on age and older kids less than 0.2 is normal. And again, so we wanna look at the urine with under microscopy in her case, given that she, there are some signs that she could potentially have avoiding dysfunction. I would look at a kidney function and even think about getting a kidney ultrasound just to make sure that there's no other structural abnormalities that are contributing. Because sometimes if there is evidence of either hydronephrosis or, or another structural abnormality, then those as well in the setting of bowel bladder dysfunction can, can really be um exacerbated. The kidney function can be affected in those cases. So we really do want to get the bowel bladder function, gall bladder dysfunction under control. But again, if there's any other abnormalities, then those would be times to really um sense of nephrology. But also think about how we can manage this bowel bladder dysfunction to not affect the whether it be hydronephrosis or another cause more significantly. And in this patient, of course, we would look at the urine culture depending on the history, we would consider other causes of in the urine of infections. Um And again, are looking into our evidence of stones. Our stones sometimes can be seen on kidney ultrasound, we see a twinkle artifact that can be observed. Um And then if there are any signs of coagulopathy, of course, we would look at that as well. Ok. So looking at another case here, this is an 11 year old girl who presents with tea colored urine, she's a febrile, her blood pressure is quite high. Um and in physical exam, she has a little bit of non pitting edema. So here she, you'd get some labs done. Her creatinine is probably a little bit on the higher side for her age. Her compliments her C three is low, her C four isn't normal. Um and she does have both blood and protein in the urine and a lot of our significant r red blood cells on, on um her urine microscopy. she has some white cells as well and her u urine protein creatinine or U PC is elevated. So, in this case, um right off the bat, you know, we're thinking about a glomerular nephritis. But also because her C three is low and her C four is normal, we probably are more likely thinking about a post infectious glomerulonephritis. Um postinfectious glomerular nephritis can present with, with hypertension, it can present with edema. So, although we see some of those signs that, that appear to be um a more involved process, post infectious glome lymphs can present this way as well. So, uh any glomeruli nephritis, really what we see again is this dysmorphic red blood cells. There's can be protein urea hypertension, edema, alla and renal insufficiency or this is our classic lime lines. Um and some patients can present with a rapidly progressive glyphs where they lose kidney function quite quickly, um less commonly, but but also can be present as a nephrotic syndrome and as well as Nephritic syndrome. So, in nephritic syndrome, the patients, the they really have mostly hematuria but they do present still with hypertension and edema and then are sort of more chronic ones where we see our persistent hematuria with or without protein, ur rhea and a recurrent gross hematuria as well. So, in post infectious glomerulonephritis, we typically see these kids um boys more than girls, but really ages 4 to 12 and there's a latency period of about two weeks for a post pharyngitis. So two weeks after, for example, a post in a post strep pharyngitis, you may start to see symptoms of hematuria, edema, hypertension if there is a a skin infection and inveigle, for instance, it it may take longer. So it can be up to after six weeks after the acute infection and and then in these patients, the gross hematuria is in about 33% but all of them will have some hematuria. Um So mo so more often microscopic and they can also present with renal insufficiency, you know, decrease your output all of these things. So it's important for us to still think about post infectious. Even though we're seeing some of these more acute signs, I would send these patients to nephrology because, you know, we know that post infectious is a glomerular nephritis and it is self-limited and you know, we're really doing supportive care. However, if that compliment level doesn't quite normalize after 6 to 8 weeks, you know, we want to be thinking about other things. So it is we do like to follow up these patients for that reason. Um So again, just there's a latency period if there's a pharyngitis pharyngitis typically about two weeks. And then we start to see our hematuria, our gross hematuria typically goes away within the first two weeks or so. But we can see microscopic hematuria for up to two years. Some patients, it has been up to four years. Um and then that complement level right here tends to normalize within about 6 to 8 weeks of diagnosis. So, you know, for sometimes it can take a couple of 12 weeks, 12 weeks as well. But this is something that we do like to follow because if it's not, then we want to be thinking about other um causes mortality rate for post infection is very low, but sometimes they do present with more significant disease again, with a, for instance, a rapidly pro progressive glome nephritis. Um ok. So in this patient, we would have looked closely at the urine, we would have gotten the urine protein creatinine ratio, look at some labs to look at kidney function and get our compliments. You could also do an an A N A in these patients. You know, if because sometimes if our compliments are both low, we want, you know, lupus may be more likely. Um and then plus or minus the A slo this can be positive for quite some time as Well, OK. So looking at another case here. So this is a 10 year old girl presenting with a demon and gross immature of four weeks after a, her brother has a strep pharyngitis. She has no significant skin joint or G I complaints her medical history. She's positive for two episodes of post infectious cleer nephritis. She's hypertensive. Her creatinine is elevated at 1.9 and she has some, some blood and some dysmorphic blood cells as well as urinary casts, red blood cell casts her C three is low. Her C four is normal and her A N A is normal. So, you know, with the C four being normal as well as her A N A, we know that this is unlikely to be a lupus nephritis. But her C three being low, we can think about a post infectious glime nephritis. But the thing that leads me away from this is that it says that she has multiple episodes in post infectious Clymer nephritis and typically a post infectious is self-limited and, and it, and it really doesn't recur. So if we're seeing a patient with these, you know, these recurrent quote unquote infection, post infectious GN events, it's typically more likely it's gonna be ac three glom nephritis. Ok. So thinking about when to refer and coordinate with nephrology a little bit more. Um really when we see that there's significant disease, if there's protein urea, if there are urinary casts, if there is hypertension or family history, um or any other clinical lab findings that are suggestive of um you know, renal or urinary tract disease. I would, that would be my indication to refer, you know, whether it's a post infectious or some other cause. Um This would be kind of the hallmark for glomerular disease is we to refer for some of the other non glimer diseases, you know, we, we can talk about those as well about when to refer. But I think most of the times that there's any structural abnormality um over there or really also, if there is a significant hematuria that, that you feel more comfortable with a nephrologist managing, then or if it's persistent for a year, then those would be times that I would refer as well. Ok, I do like this schematic here as well. Um because it kind of gives, you know, we when we have our significant hematuria, um you know, what are some of the things that we're looking at? But also looking at some of our differential and, and it helps kind of look into when to refer as well because, you know, sometimes in our, in our kids with sickle cell, if there is anything abnormal, you know, we, we think about papillary necrosis, that could be, you know, we do like to see those kids um as far as our post infectious, if there's anything, you know, our GFR is decreased or, or the patient is hypertensive then that would be in the setting of the glim nephritis, that would be a time to refer as well. If there's any significant family history of kidney disease or family history of hematuria, that would be an important time to refer because we're thinking about our genetic causes as well. Our output syndrome and thin basement membrane disease for, for anything abnormal and kidney ultrasound. So if there are kidney stones or, or cysts, sometimes the kidney stones can be more significant or related to a genetic ideology. And there and in those patients, we tend to like to treat um as well as their kidney stones. And then if you know, the kidney stones are, are significant, it is hypercalciuria as well. You know, looking at more sign, more involved causes of why that those would be reasons to refer. So I like the schematic because it, it really helps to kind of put things into perspective. Um and let's go through a couple of cases just to kind of solidify that. So a six year old boy is evaluated for a family history of asymptomatic microscopic hematuria. His mom and father both had microscopic hematuria and routine health visits. Um And there's a history of microscopic hematuria and a maternal grandfather and a paternal grandmother. There's no history of hypertension or proteinuria or renal failure or deafness on either side of the family. Um But on physical in a physical exam, this patient, he's grown normally. His vital signs are normal. His blood pressure is normal. He has one plus blood and negative protein, but there are 5 to 10 dysmorphic red blood cells for high powered fields. So overall, you know, his exam and and his exam findings are quite benign. He does have these dysmorphic red blood cells. So that lets me know that there's some glime or hematuria that we're seeing. Well, this family history is interesting because he does have hematuria on both sides of the family. Um none of them progressed, had, you know, had significant kidney disease. So that's reassuring. But this patient is a patient that is still at risk for Albert syndrome and it really is related to the mutations that are involved in in an Alpert syndrome. So, most likely Alpert Syndrome patients do present with the X link, which is the collagen 45. Um but there are autosomal recessive forms of disease. They can be auto recessive or autosomal dominant. But in our case, this patient probably has a family history of an autosomal recessive, whether it be a 43 or 44 mutation going on and on either side of the family. And those collectively can then if this patient um has both of the alleles can present with um Alport syndrome. So this is a patient even though, you know, it seemingly is benign this his history and and physical. So far as a patient that I would refer because he could potentially develop outward syndrome and be at risk for um end stage kidney disease and adolescence or adulthood. Ok. Ok. So this patient here is a 14 year old adolescent girl seen for recurrent episodes of gross hematuria for the past few months and she's seen been seen multiple times. No cause has been found. And there's no history of diarrhea, back pain or swelling and she has had a few febrile illnesses in the past month. She can't really remember the timing of the correlation with the episodes of hematuria. However, there's no history of joint pain or rashes. She is adopted. So the family history is unknown and the ultrasound of the her kidneys is normal. Her vital signs are normal and her urinalysis shows that there's some blood and some protein in this patient with the recurrent episodes of gross hematuria. This is more than likely gonna be an ig nephropathy. You know, they in the setting of, you know, they're telling us there's no disarm, no back pain or swelling, maybe, you know, it's, it's very asymptomatic, right. So ig nephropathy very classically are asymptomatic hematuria. It can be gross, it can also be microscopic. Um but it's these recurrent episodes and they're typically associated, you know, during the time of an infection. So this patient is they're not really clear on their timeline. But in an it nephropathy, it's typically the the hematuria coincides with an, with the infection, whether it be a upper respiratory tract infection or a G I infection. So these patients, when we're seeing, you know, this recurrent hematuria are patients that I would also refer, um patients, you know, tend to have worse prognosis if they have proteinuria as well. So I would also, you know, look at these patients more closely and have them seen sooner uh to a nephrologist. Ok. So a 16 year old boy with a three day history of lethargy is seen in the pediatrician's office and he has decreased in output and gross hematuria without any diarrhea or fevers. So this patient, he's mildly puffy. His blood pressure is 1 56/92. So quite high, his compliments are normal. His creatinine also is quite high. So this patient, um you know, it's good that he's already in the ed because with it's it seems that he has an acute glom nephritis, right? He is puffy, he's hypertensive, you know, um he has gross hematuria, his compliments however, are normal but there are and also he um his craning is quite elevated. So this is a patient who, because his craning has changed so significantly, you know, he's losing kidney function quickly. This is a rapidly progressive glymph fights, this is considered a medical emergency. So any patient that we see, you know, these symptoms, we want this patient to get immediate attention. So, so he needs to be seen in the emergency room. Um so rapidly progressive glomerular nephritis, you know, it's really this abrupt onset of severe nephritic syndrome, nephritic symptoms. Sorry. So they will have, they can have gross hematuria. They can have all of urea and hypertension as well as fluid overload or are commonly seen. Um, and real insufficiency is really the hall max. They lose kidney function rapidly. They may have protein urea, they may not, but also they, they don't typically present with nephrotic syndrome. And that's really just because the kidney function is much lower. So you're not getting that, that much protein filtration there, but really a prompt prompt diagnosis and early therapy is, is, is key for these kids. And most of the, you know, we often see either an anco vasculitis being one of the common causes. But there are other, you know, even with uh um interstitial nephritis or even our post infectious glomeruli nephritis can sometimes present with a rapidly progressive glome nephritis. But I think just the key would be to when we see our signs of, of all of urea or hypertension or fluid overload. Those would be signs that the patient needs to be seen um much sooner. Ok. So a 20 year old college student with no past medical history develops hemoptysis and shortness of breath denies any joints or skin um complaints and urinalysis shows that there's blood as well as protein. The creatine is quite elevated at 3.8. Albumin is ok. It's a little low at 2.2 and a A an an are normal C three and C four are also normal. So this is a patient who you know, in our rapidly progressive glyphs patients, we think we think about Anka a lot, you know anco vasculitis, but also patients with um anti GB M disease can present this way as well. Also given that hemoptysis, this is another key indicator. And when we think about our our normal complement genes, this is, you know, typically one of the common causes. So this is a patient that would also need to be seen acutely. So in, in, you know, you would send this patient to the ed because really getting plasmas to change and you know, as quickly as possible, potentially phos cyclophosphamide as well. It can really be life saving for these patients. Ok. And then we'll do one more case here. So a 15 year old adolescent girl is evaluated for gross hematuria and she has a history of a photosensitive rash. In prior summer, it doesn't improve at topical steroids. You know, she's otherwise has no symptoms or concerns, but her blood pressure is on the elevated side and she's not a demas today. Her skin is clear. The her exam is is overall otherwise it's normal, but she presents with this tea colored urine. She has some protein there. She has a large amount of blood, 100 red blood cells per high power field and many urinary, many red blood cell casts as well, a first morning protein creatine ratio is 1.2. So also quite elevated, not nephrotic, not over two, but she still, it's still quite significant. Um So this patient, you know, given that she does have this photosensitive rash, you know, we are thinking that this could potentially be a lupus, a lupus presentation involved. Um The fact that she has protein urea and she has hematuria, you know, we were thinking lupus nephritis as well. So when we think about these systemic symptoms, you know, if a patient presents with fevers, if they are arthralgia, if there's, you know, our, our rashes, um you know, we wanna think about more systemic things and potentially lupus nephritis and these patients. Absolutely, we wanna refer and there's protein urea, you know, you can send, if there's proteinuria, we definitely would want to get a kidney biopsy. So those patients, we, we do like them to be referred quickly. But again, if, if we're seeing signs of, you know, significant, either hypertension or edema or, you know, decreased urine output, those would be signs that maybe they should, they should go to the emergency room rather than having an outpatient referral. Um the patients with lupus, if they are, they do have protein urea, we wanna, we do wanna see them um very soon because we would want them to get a kidney biopsy to class, to classify their lupus and to start therapy as quick as soon as possible. Ok. So again, looking at, um, this just kind of putting things into perspective, you know, we talked a little bit about the genetic problems that we can see in nephrology and some of the glomerular nephritis. Um, you know, often we didn't talk much about cysts. But, you know, if, if there are cysts on the kidneys, sometimes we can, that can be related to something, um, a syndrome or something genetic. But, you know, those kids we would like to see as well. Um, so I think at that with that, I think I'll take questions. Created by Presenters Kaye Brathwaite, MD Pediatric Nephrology View full profile
