DIP Episode 140 - ABIM/Medicine ITE/USMLE Step 3 Review Series 10 (Nephro 2)

Okay, welcome. My name is Devine. I'm a resident. This is episode 140 of the Devine intervention podcasts and into this podcast I will be continuing my review series for the American Board of Internal Medicine Exam, the Internal Medicine Training Exam as well and this is also very applicable to the USML Step 3 exam and I'm going to be continuing my review of a nephrology. So I guess I'll go ahead and start. So I think one thing I want to go ahead and mention here is I want to go ahead and talk about these casts, right? Like these are, not necessarily cast but like your analysis findings that will lead you in one direction versus the other on an exam, right? So if you see a person that has like red blood cell casts, what are you thinking about? I will really hope you're thinking about some kind of nephritic syndrome, right? Like the glomerulone fridities. Sometimes you have, they may try to mess with your head by calling them dysmorphic erythrocytes instead of red blood cell casts. It means one on the same thing. And then what if you see white blood cell casts? What are you thinking about? Well, I would hope you're thinking about some kind of uti, right? Like pylon and fridis for example. Pylon fridis has like a very strong association with the presence of white blood cell casts on exams.

And then what if you notice that a person, you know, let's say it's an athlete just ran a marathon or you had an alcoholic that just passed out for hours or an old person fell down, couldn't get up, no one could help him or her up. And then they tell you that the dipstick is positive for blood. But then you do your microscopy and you you don't find any red blood cells or you find like one of the red blood cells. What are you thinking about? I would hope you're thinking about a rabbit, right? Rabbit my ass is that's a classic presentation right there. And then if you notice that a person has like, you know, like sterile pyrurea, right? So you notice that, oh, this person's, this person's urine contains white blood cells but I don't seem to be finding any bugs. If it's a person from a developing country, you really want to think about TB on exams. And you also want to think about like, you know, like an inset induced like kidney injury, right? So like an analgesic nephropathy, so that deal. That's something you'd want to keep at the back of your mind there. And then if you find like your synophils in the urine, right? Obviously, I want to think about AIN, I couldn't test it on a Fridays. There are many varying presentations on the medicine exams, but on the USMD exams, the classic thing should come to expect is the triad of like fever, rash and your synophilia, right? So like it's elevated, your synophils in the blood or elevated your synophils in the urine, right?

Those are the classic presentations there. And then if you notice that a person has like, and those other non-classic presentations, I talk about them in the series nine, right? Like the non-classic presentations of AIN, I do talk about them in the series nine of visa, visa step three, related podcasts. So what if you notice that a person has, you know, like the tell you that they have like oval casts or like fatty casts or they found like lipids in the urine? I hope on those circumstances you're kind of thinking about like an efferotic syndrome, right? And then if you see like a higher-link casts, right? That tells you the person's volume down. And if a person's volume down, what happens to the urine concentration? I would hope you're saying that it does go up, right? The urine concentration does go up. And that urine concentration going up tells you that they will have like a higher-link cast, they're like mid of like tam, tam-hosphal protein, whatever. But yes, if you see higher-link cast, think about the hydration. That is just an indicator of a person having a concentrated urine because if your volume down, right, you'll increase the activity of your urine and your tensile dose during the system so that you can maintain, so that you can maintain a, you could try to like keep some of the volume back and you don't restore your volume. Okay.

Now, I guess the big thing I think I want to maybe talk about in this podcast, I decided to sort of break them up instead of doing all of them in one because it's kind of a lot of information is to talk about these glomerular and efferidides, right? So basically the nephrodite syndrome, right? The nephrodite syndrome obviously you want to be able to compare and contrast them with the nephrodite syndrome, right? And I mean, if the nephrodite syndrome, you already know the magic number more than 300 half grams of protein in a 24-hour period. And then usually, like I said, again, you'll find those like fatty casts, those like lipid casts. And really, if you're kind of thinking about the level of the damage, right? The level of the damage is actually not at the level of the glomerular capillaries. It's more of the level of the buddhousides. The buddhousides are kind of like the epithelial cells that have food processes that sort of stamp on the glomerular capillaries. And people that have nephrodite syndrome, they tend to have like generalized a demon, right? Contrast all of this with like your nephrodite syndrome, your nephrodite syndrome, right? I kind of think of it as like anitis, right? So everything is hot, right? So it's like a big time inflammation of the glomerular capillaries, right? So these people tend to have like again, those are fancies, mancy, rib blood cells, those are dysmorphic arithrocytes in their urine.

And again, the protein area, it will be less than three and a half grams of a protein per day. It's usually like, sorry, between like one and like two or there about a grams per day on an exam. And again, like I said, unlike the phrodite syndrome, where the damage is at the level of the buddhousides, like buddhousides on the food processes. In a phrodite syndrome, the damage is primarily at the level of the, is premier at the level of the glomerular capillaries, right? And most of these people that have nephrodite syndrome, they tend to have hypertension, right? And their DMA, for whatever reason is just kind of like a pattern I've noticed or not especially on the USML step three, on the USML is in general. Their DMA tends to be like very open up for whatever bizarre reason. So that's something should keep in mind with the nephrodite syndrome. And the nephrodite syndrome, it kind of a lot, you know, it's kind of like hard for people to you know, kishnavi kind of like keep them straight. But I will try to give you, I guess like a logical framework, like a trick for remembering that. And really for the most part, to be honest, yeah, it's kind of a lot of information, it kind of sounds, you know, kind of hard. But to be perfectly honest, these are things where you just need to know some sort of high-yield history. If you know the high-yield history, they usually pretty easy to resolve, to resolve one exact right. So you don't have to like think too hard to arrive at the answer.

So the way I will kind of divide these syndromes is I think it's kind of like important to understand a concept and immunology concept. So I know this may be a little basic science, but I promise you, you'll kind of pay off as we go along. The thing is, most of these nephrodite syndrome, they arise as a result of type three hypersensitivity reactions, right. And if you remember from med school, because I'm assuming if you're listening to this, you're probably a fourth year or you're graduating from med school, or a medicine resident, but they're usually from type three hypersensitivity reactions. And as you probably know, these are type three hypersensitivity reactions, they arise in the setting of like antigen antibody complexes, right. So you have some antigen, that antigen you form an antibody against it. And then that thing begins to like, you can either like just hang out in the kidney, and you have like renal limited disease, but in some other situations, you can kind of have like those antigen antibody complexes, sort of like going to other parts of the body, by going to blood vessels, or going to the lungs, right. And then you begin to get into trouble there. And again, the hallmark is these are not all of them, but some of them are type three hypersensitivity reactions.

And the big thing you want to keep at the back of your mind with these things is that, because they form like you have like an antigen antibody complex, the big thing you should automatically expect is that remember, if you remember, we're again from just again, kind of like step one, just very basic step one stuff here. Those antibodies that are bound to the antigen, remember, they have like constant regions, those constant regions can have activated complement, right. They activate complement, and it's the complement that ultimately mediates the damage, because complement, they are very flammable, right. So they can destroy anything they have or contact with. So the complement that binds to the constant region of those antibodies, ultimately ends up causing like a lot of the problems that are that are fester in those situations. And because complement is being activated, right, to cause all this damage, people that have these problems tend to have low levels of complement, okay. So people that have these nephrodite syndrome, in general, at least for some of them, they tend to have low levels of complement, and have again, kind of explain the mechanism behind that. So I will encourage you if you're trying to learn these nephrodite syndrome, so you kind of want to like learn them by which ones cause low complement, right. And which ones cause, which ones are associated with like normal complement, right.

The ones that are associated with normal complement in general, they tend to be more type two hypersensitivity reactions than type three hypersensitivity reactions. The type three hypersensitivity reaction once we have the antigen antibody complex. You have complex comes damages everything. And then those people, those people kind of get into trouble. So sort of walk you through all those visa different diseases from kind of like this perspective. So I guess, let's see, how do I break this up? Yeah, I guess I'll just go ahead and talk about those that are associated with low complement, right. So I mean, really, there's like kind of like, it's probably like six or seven things in this category. But there is five of them that I kind of like on their own, there's one that's kind of like unique. So I'll talk about that at the end. But let me talk about like the classic ones, classic ones first. And then let me just go ahead and say something first. So the thing is whenever you see these protein rare, like protein in the urine, the first thing you always want to figure out right is, you know, just sort of go broad strokes first ask yourself, an afraid of an afraid of an afraid of syndrome, right? If the person has more than three and a half grams of protein in the urine in 24 hours, they have an afraid of syndrome. If it's less than three and a half grams in 24 hours, they have an afraid of syndrome.

Although these days, people tend to use the urine protein to create a ratio to sort of meet those calls. So the 24 hour, like whatever testing is kind of antiquated, not many people use it in this day and each. So, but still remember those hard numbers, you know, three and a half grams 24 hours. If it's greater than that, that's nephrodite, less than that, that's nephrodite. And then once you determine that a person has the nephrodite syndrome, so they'll have like the other stuff like the ribloxel casts, they'll have the, or also called the smurfy caretale sites, right? They'll have the parabular dima, they'll have the hematuria, they'll have the hypertension, right? When you see that the next thing you should ask yourself is okay. Is it like an antigen, antibody complex, kind of deal going on, right? Because if you know that, you know that those will have to be associated with low complement. So the big ones that kind of have the low complement in no particular order. So like, remember no proliferative, preliminary and fridious, that's a big one. Tensu has like the low complement. If people have like the mixed cryoglobulinemia, right? That's like the thing that kind of looks like renotes phenomenon. I'll talk about that in more detail shortly. That also has the low complement. If people have like lupus nephrodis, right? That also tends to have like, you know, pretty low, pretty low complement.

Another one that tends to have low complement is this one that shows up, it tends to show up in the pediatric population, but do not be surprised if he shows up on a medicine exam. I know internal medicine, the ideal with adults and all that stuff, but don't be surprised if he shows up like in a youngish adopt, so some like in the early 20s kind of deal, especially after like an upper respiratory infection. I would hope you are thinking about like a post-infectious glomerular nephrodis with that. And then also in ducarditis, and ducarditis can cause a vasculitis like syndrome that can look an awful lot like nephrodis syndrome. That tends to again have a pretty low complement. So I guess maybe let's just go ahead and talk about the big things with each of these diseases, right? So what if they give you a question about a patient and this patient, you know, like two weeks ago, they had like some kind of like, upper respiratory infection, or they had like some kind of like skin infection. And then they suddenly present with like hematuria and they ask you for the diagnosis, right? I would really hope on that those circumstances, you are thinking about a post-infectious glomerular nephritis. Post-infectious glomerular nephritis, occasionally we see it refer to as a post-traptococular glomerular nephritis.

The big thing you want to remember is that these people tend to have like the hematuria, the classically described like coca coca cola colodeurin, like at least more than a week after like an upper respiratory infection. If you see people having like very similar symptoms, but it's like less than a week. So like a couple of days, like two, three days, two, three, four, five days after an upper respiratory infection, you want to think more about IGNF rapidhy. IGNF rapidhy, I'll talk about that at the end. It's kind of like separate because it's it's like an immune, it's like a type three hypersensitivity related like pathology, but the complement is actually normal, which is kind of like aberrant, right? So and I have some teleological ideas as to why that maybe, and I'll kind of like describe that at the end, but it believe it or not, it's actually an immune complex mediator disorder, but the complement is usually low. I mean, sorry, it's usually normal in IGNF rapidhy. So post-infectious glomerular nephritis again, more than one week. If it's less than a week, you're thinking more about like a scinfiring gyedic glomerularopathy, which is what happens with with IGNF rapidhy. But let me focus on PIGN for now, right? So again, more than a week, usually like, you know, like 10 to 14 days, it can be up to six weeks actually, but if you do not, after an upper respiratory infection.

And again, those people, they can have it after, like an upper respiratory infection, but actually it can happen after like a strep skin infection, right? Like a strep skin infection like air sypilus, for example, or like in petagon, right? So don't don't look side of those things as potentially inside-in factors, because they know everyone has kind of memorized the whole upper respiratory, whatever business, but you can actually get post-infectious glomerular nephritis after like a strep skin infection, right? And again, it's like, it's usually like group base strep. And again, like I said, the complement will be low, right? Because you form like IGG antibodies against like some antigen, and then you have all this problem, you destroy the kidneys, and then you get into trouble. And classicly on exams, these people tend to have like, you know, again, like, like I said, a pretty low complement, and you may find like positive antibody titers for like ASO, so like anti-striptolizing, all, and also like anti-DNESB antibodies, those anti-DNESB antibodies, they tend to be associated primarily with like strep skin infections, okay? Like they are cepillars or the in-petigle.

Now, what if they give you a question about a patient, you know, that kind of presents, they tell you that whenever they, less likely, present in the winter, because this is obviously when they were symptomatic, they present in the winter, they tell you that, yeah, they've been having all like whenever they step out in the cold, they are like their hand, their fingers begin to hurt a lot, I sort of turns blue, and then they tell you that, oh on physical exam, you observe like a poppable preparer like on the legs, like in the lower extremities, and let's see this person, you know, let's say it's like an IV drug user, what are you thinking about here? I would really hope you're thinking about like a mixed cryoglubulinemia, okay? The thing is cryoglubulinemia, right? It's kind of, it's kind of explained to you why they have like visa or phenomena. The thing is, these people, they tend to have like a Reynolds-like syndrome, right? Because when they step out in the cold, the antibody, usually like IgM, it kind of precipitates from their blood, so it begins to cause like microvascular opulusions, right? But when they sort of go into the warmth, like, I don't know, like in Arizona, like Texas, just warms up real well, the thing said, the IgM antibody kind of deserves right back into blood, so their symptoms are, their symptoms are for the most part. Now, the big thing you want to know about this, right? It has an association like hep C, right?

So, again, they give it like an IV drug user or a person that got a blood transfusion like years ago, something like that. And if you see that, think about, again, with their presenting like the Reynolds phenomenon, and they also typically have like, poppable preparer on the legs, think about a mixed cryoglubulinemia with that. And again, because it's an antigen antibody complex, medicated like, spale, right? So it's like IgM antibodies, those people tend to have like pretty low complement. But here's one thing that's actually fairly unique with this. The major complement proteins you probably want to remember, is like C3 and C4, those are the big, big, big ones. I talked about post-infectious glomerular and afraid it's already. I said that the complement is low. Usually those people have very low levels of C4, very low levels of C3, right? They're kind of like equally decreased. But in this mixed cryoglubulinemia, it's kind of like a weird situation where the complement that's actually low is like C4. It's like super, super, super low. And then the C3 is usually like normal. Or if it's low, it's just like a smidge low. That's a very unique feature of mixed cryoglubulinemia, you don't want to commit to memory for exams, okay? So the C4 levels are like super, super, super low. But the C3 levels, they may be normal or they may just be like again a smidge decreased. And again, like I said, it has a big association with like aFC.

I mean, there's like many types, it's like type 1, type 2, type 3. But one that has like that type of association with aFC is the one that's called type 2. So like the type 2 cryoglubulinemia. The type 1 is the one that has like an association like Waldenstroms, a macroglubulinemia. I'll talk about Waldenstroms when I do like the hematology podcast that relates to these three exams that I'm making this podcast for. So again, that's a big thing when you keep at the back of your mind. And the thing is, pop-up prepare in the setting of nephrodite syndrome, you will be like, okay, mixed cryoglubulinemia, but I also find it in other disorders. The thing is, you're right. You also find it in other things like IGN ethyropathy, for example, especially like the systemic form of IGN ethyropathy, like hernexion line paper. So those people will have, you know, they'll have like the pop-up prepare, they'll be below the products. But the key thing with IGN ethyropathy is that the complement is normal. And again, I will explain why that's the key. At least my thinking as to why. I've not really found any proof of this, but I'll explain why thinking as to why that may be the case. And then people that have the hernexion line paper, they'll have 10 to 12 other things, they'll have like the arthritis, they'll have like the abdominal pain, they'll have like the joint pain, right. So those things all can go together. You will not necessarily find those things in a mixed cryoglubulinemia.

And then, the next one I will go to, what if they give you a question about, you know, like a 35-year-old female, she's had like a middle rash and maybe she's had like, immune throat, like ITP back in the day, or she's had like autoimmune hemolytic anemias. And then, and again, this is usually like woman, usually African American woman on exams. And they tell you that, you know, she has hematuria. If you see that, right, I hope, again, you're thinking about like a like a lupus, kind of like a lupus arthritis. And again, they'll give you all these lupus symptoms, they'll give like the hematuria. And they may ask for the next step in management and actually, I mean, in diagnosis, and believe it or not, they can actually involve like just checking their a and a, right. Because remember, a and a is super sensitive for lupus, but it's not very specific. Because if your a and a is negative, you essentially do not have lupus, right. So for these people, you check their a and a, and then if the a and a is positive, then you start going a little more specific with like complimentary tests, like checking like the anti double stranded DNA antibodies, that are characteristic of a lupus. Remember, lupus also has like the anti smith antibodies, right. And again, because this is an immune complex meditated disease, complement is super low. Right. So like the C3 levels are super super low, C4 levels, super super low, right.

And in fact, all the complement proteins are like low, like C1, C2, everything is low. In fact, I remember in med school, I learned that in lupus nephritis, there's something they call the full house pattern. Full house pattern just means that every complement protein you can think of essentially that is used in those tests pretty low. For most others, it's like C3, C4 that are low for the most part. And knowing the treatment for lupus nephritis is actually kind of high up to no on exams, right. So the thing is, when the person is having the flare, right. There are certain drugs that are used to, you know, acutely suppress their symptoms. And then after you acutely suppress their symptoms, you can then kind of put them on like maintenance therapy. So the drug you use to like suppress their symptoms, you use like these are supersidotoxic agents like a cyclophosphamide. Another alternative you can use is like my cofenolita mofetil. Remember, cyclophosphamide is the thing that can cause hemorrhagic studies from like the acrylene byproducts that you can prevent with mesna. I remember that actually increases your risk of a bladder cancer in the future. So you can use cyclophosphamide. So again, like to acutely suppress their symptoms, like to induce them, like induce remission. You can use cyclophosphamide, you can use my cofenolita mofetil. I remember for people especially taking step three, my cofenolita mofetil is an I know sin monophosphate dehydrogen is inhibitor.

And then in addition to either of those things, so you can use cyclophosphate like a microphenolita mofetil. In addition to those, you then add steroids. So again, like induce remission and then chronic maintenance therapy, you can use my cofenolita mofetil still. That's fine. Or you can use like six-megapthopurin. Remember, I'm not the name for that, it's like is a thioprin. Although, one thing I'll go ahead and say, remember that association between is a thioprin, six-megapthopurin and alopurin. Remember that is a thioprin is broken down to inactive metabolites by xanthin oxidies. So if a person has gout, let's say they're taking xanthin oxidies inhibitor, alopurinol of a buxostat, you'd want to dial down on the dose of alopurinol. I mean, of is a thioprin because inhibiting xanthin oxidies with alopurinol of a buxostat, their isotherapeutic levels can shoot really high, they can have profound bone marrow suppression, just bad bad bad symptoms so you want to try to avoid that if you get. And this lupus nephritis, there are many types, I think there's like five or six types, like some like really large number. The big one you want to remember for your exam is the type four, right? So that's the one that I remember Goli and back in the day, not just Goli and but even now, like in this day, in the hospital, like literally like nephrologists and also on exams, they call it like a diffuse proliferative glomerulonephritis, okay?

This one is like the most common of like the five or six that exist and it has a, you know, like a pretty bad prognosis. So it's something you want to, you know, be able to recognize not just on exams, which I guess is the primary reason for this, but you also want to be able to recognize it clinically, right? Because it's not something you want to miss because those patients can, you know, die pretty quickly, right? So you want to, you want to sort of keep an eye out for this because lupus is a fairly common condition in the US. And then the next one I'll talk about is really this one, I'll just tell you what it is, the really tested, what if you tested, you want to kind of like be prepared. It's like membrane proliferative glomerulonephritis, like NPGN, there's like many types, the big one you want to remember is like type two. You want to remember that it has an association when like, you know, HB, HFC, and again, because it's immune complex, when you get it, they'll have like low complement levels. And again, so because it's a zero to like, HB, HFC, right, they can again describe like IV drug user person with like risky sexual behaviors, blood transfusion from like way back when stuff like that, right? So you may say, oh, divine. IV drug user blah, blah, blah. How do I differentiate this from from a curable inemia?

The thing is people that have curable inemia, they have a lot of like who like really like, you know, like legit physical exam findings, popular paper, and the lower extremities, they'll have like the Reynolds phenomenon. So if you see those things, you should be thinking about mixed curable inemia. If you don't see those things, you should be thinking about a NPGN. And then I said that I will talk about like the, the nephritic syndrome that, you know, kind of has an association with, it's actually like an immune, like a type three hypersensitivity kind of business. But in general, it doesn't have, it doesn't have low compliment. It's kind of special, right? It's one of those things where you're fairly positive, you'll see it on your exam. That's a IGN et Frappathy, right? IGN et Frappathy tends to have normal compliment. So why do I think, again, I've not researched this, not 100% sure, but this is my teleological explanation. The thing is in IGN et Frappathy, it tells you that the antibody involved is like IGN. The thing is IGN has no ability to activate the complement cascade, at least as far as I remember from Med School. The antibodies that activate the complement cascade are like IGG and IGM. So if you're dealing with IGA, you have no ability to activate the complement cascade. So if you cannot activate the complement cascade, your complement levels will be normal.

Although if you kind of read the literature, you'd usually hear that, oh, in IGN et Frappathy, the actually activate complement just happens like just in the kidney. So that's like not enough to lower complement all over the body, but I don't know about that. But again, the big thing I just want to remember is that the complement is normal with IGN et Frappathy. And again, the classic presentation, all respiratory infection, right? All respiratory infection like two to three days ago, right? And then the person comes to the clinic says, oh, dupch, got a lot of blood in my urine, like my urine is red, right? They come in like super worried and then they will show you the analysis, you will find like the red blood cell cast, the EKA, the smurfing area through sides, right? But some other things you may see, right? Because for the most part, if that's all you see, if you just see like the hematuria and you see nothing else, that's IGN et Frappathy, right? But the thing with IGN et Frappathy is it can become systemic. When it becomes systemic, then the disease kind of changes to HSP, right? So like Hennonkshon Lina, pepper. And one thing I will see there is IGN et Frappathy, another thing we see on the exam is like burgers disease, it's like B-E-R-G-E-R, so burgers disease, right? That's another thing for IGN et Frappathy.

But yes, if you see a person have like, you know, the hematuria, but they also have things like, paparbo pepper below their buttocks, they have like abdominal pain, they have like joint pain, think about Hennonkshon Lina, pepper. And the reason they have that abdominal pain is right, they have like that, they have that anti-genantibody crap happening like the mesenteric vessels, right? So that will obviously cause like a skimmy of the bowel, so they begin to have like a skimmy bowel like symptoms, right? So like abdominal pain, they also have like joint pain, right? So they have like arthritis, a throches, stuff like that. So those are the big things you should keep in mind with with IGN et Frappathy. Now, these are all the things that are so you don't like increase complement, the ones that have like normal complement again like IGN et Frappathy is again kind of special because it's anti-genantibody we get it, but the complement is normal, right? And then I talked about the group where the complement is elevated. Now, I want to talk about the group where complement is completely low. And for the most part, these are not mediated by like anti-genantibody complexes, these are more like type two versus the other ones I just mentioned that are more like type three hypersensitivity reactions, right? And really in this group, there's just only like two big things you want to worry about.

You want to worry about like the anchor mediated of vasculities and the anti-GBM syndrome, right? So like the anti-GBM syndrome. And one thing I'll go ahead and see with anchor, right? So let me give you a question on the exam and see that over persons anchor, they have like anti-neutralphilic acetylplastic antibodies are positive and then they ask for your next step in management. Your next step in management is you want to do like an ELISA, like an immunofluorescence kind of business to determine exactly what the antibody is targeted against, okay? You want to determine exactly what the antibody is targeted against, right? If it's anti-proteinist three, right? You know that you're dealing with like C-enka. If it's like anti-mylo peroxidis, you know you're dealing with P-enka. But the thing is believe it or not, they actually people that are anchor positive that's not necessarily directly against like protein is three or mylo peroxidis, right? So whenever you see that, you maybe want to begin to think about like atypical anchor, right? The reason I keep harping on this is that atypical anchor has a very strong association with like all three of colitis, right? So I'm trying to match school everyone has memorized over atypical loyalties associated with P-enka. That's actually not really true. All three of colitis don't get mirror as real the anchor. It's like anchor positive. But the anchor is something that is called atypical anchor, okay?

I think I'll be probably talk somewhere about that when I get to some of the GI reviews for these three exams. So what are the big things you want to know about these anchor problems? You know, you want to know that like let's say for example they give you a question about a person that you know has like a saddle knows the formity or the half arm like ear infect like recurring ear infections that doesn't seem to be responding to antibiotics. And then they tell you that they have like hemoptysis and hematuria. Obviously if you see this you know that they're dealing with like wagners where lomatosis although it's no longer wagners anymore, right? There's like this Nazi connection post someone does that stuff anymore. The thing that people go after these days is at least the the the current name is GPA, right? So like granulomatosis with with polyhengeitis. So the classic presentation is again they'll have like hematuria, right? So they will have like kidney problems. They will have hemoptysis. So they have like lower respiratory tract problems, right? So they can have like pneumonia and they have like something that you kind of find in people that have like anthrax. So like a diffuser of yellow hemorrhage. But the key thing to watch out for an example are the upper respiratory symptoms, right? And the upper respiratory symptoms they can be super diverse, right? They can have like nose bleeds, right?

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Red blood cell casts in the urine sediment.

Pyelonephritis (e.g., pyelonephritis).

Rabbit my ass (a common exam trick/mnemonic).

IgA Nephropathy.

Mixed cryoglobulinemia shows marked low C4 with relatively preserved C3; Lupus often shows generalized low levels of all major complements (C1, C2, C3, C4).

Mixed cryoglobulinemia.

Low levels of all major complement proteins (C1, C2, C3, C4), sometimes described as a "full house" pattern.

Normal complement levels, because the associated antibody (IgA) cannot activate the complement cascade.

PIGN typically presents $>1$ week after infection; IgAN is usually within days of mucosal illness.

Antibodies targeting GBM proteins (e.g., anti-Parietal/anti-Myloperoxidase); Diagnosis requires ELISA or immunofluorescence to identify the specific targeted protein.

Mixed cryoglobulinemia involves systemic symptoms like Raynaud phenomenon, palpable purpura, and often has a history of HCV/IVDU; IgAN is primarily associated with gross hematuria following mucosal infection.

Low levels of all major complement proteins (C1, C2, C3, C4), sometimes described as a "full house" pattern.

Normal complement levels, because the associated antibody (IgA) cannot activate the complement cascade.

PIGN typically presents $>1$ week after infection; IgAN is usually within days of mucosal illness.

Antibodies targeting GBM proteins (e.g., anti-Parietal/anti-Myloperoxidase); Diagnosis requires ELISA or immunofluorescence to identify the specific targeted protein.

Mixed cryoglobulinemia involves systemic symptoms like Raynaud phenomenon, palpable purpura, and often has a history of HCV/IVDU; IgAN is primarily associated with gross hematuria following mucosal infection.