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S2D: The Symptom to Diagnosis Podcast - Episode 04: Acute Kidney Injury
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S2D: The Symptom to Diagnosis Podcast - Episode 04: Acute Kidney Injury
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Language: EN.
Segment:0 .
DR. CIFU: I'm Adam Cifu.
DR. STERN: And I'm Scott Stern.
DR. CIFU: And we are back with episode 4 of the Symptom to Diagnosis podcast. This podcast teaches evidence-based strategies for diagnosing common medical symptoms. Each episode is divided into four parts. We begin each episode with a case unknown to one of us. We then discuss five high yield features that help to accurately diagnose the cause of the symptoms at hand. We then return to our case before finishing up with a discussion of fingerprints, common misconceptions, pet peeves and other random pearls of knowledge pertaining to this week's symptom.
DR. CIFU: The cases that we discuss are drawn from our clinical experiences but, because protecting patient privacy is part of our oath, we never discuss actual patients and most cases are composites.
DR. STERN: Adam, I think the pet peeves are your favorite but before we get to those, our topic this week is acute kidney injury, AKI, and you are the expert of the day and I understand that you have a case to present to me, would this be true?
DR. CIFU: I do have a case to present to you.
DR. STERN: Okay.
DR. CIFU: Are you sitting down?
DR. STERN: As a matter of fact, I am.
DR. CIFU: Okay, this is not the most straightforward case. So this is a 50-year-old woman. She has SLE and a history of lupus nephritis, and she was admitted to the hospital onto my general medicine service just a month ago when I was on last with fever and fatigue for four days. She'd been treated with mycophenolate in the past, but she's been off all of her lupus medications for the last year. On admission, she's febrile, tachycardic, she has a normal blood pressure and pulse though, I'm sorry, just a normal blood pressure and has a new murmur.
DR. CIFU: She's also diagnosed with delirium. Her evaluation leads quickly to the diagnosis of endocarditis with methicillin-sensitive Staph aureus, and she's treated with Cefazolin. Her admission labs are notable for BUN to creatinine of 9 and 0.7 and that's her baseline stable from a year before last time she had labs checked. Her delirium is pretty slow to clear and on hospital day four, her creatinine has climbed from 0.7 to 1.3. Three days later, it is now 3.8. Dr. Stern, what are you thinking?
DR. STERN: [laughs] Well, I'm thinking that's a pretty complicated case. So she clearly has an acute kidney injury versus a chronic kidney injury. The rate of increase certainly makes you think that something is happening in this hospital admission that's causing this 'cause she comes in with a normal creatinine essentially and then within days, sounds like about five days or so is really dropped her GFR by 75% or so.
DR. STERN: So what would be the type of things that we might think about? Well, you know, obviously someone's going to wonder about lupus nephritis causing something like this, although the rate of onset would be very atypical. Glomerulonephritis doesn't typically occur that rapidly even in RPGN but it'd be worth thinking about. She has been quite sick. She's bacteremic, certainly ATN from the bacteremia will be possible.
DR. STERN: Prerenal azotemia if she hasn't, frankly, necrosed her tubules would be another possibility. And we've given her, you have to think about what you've done in the hospital well, you know, we've given her medications. Does she have acute interstitial nephritis from the cephalosporin? That's another absolute possibility that I would put very high on my list.
DR. STERN: I'd also review her record to make sure she hasn't had CT contrast of any type 'cause one of the common things we do in the hospitals is damage people's kidneys with contrast, so I'd want to rule that out. Obstruction seems unlikely. She's a woman and she's come into the hospital, you know, without this, so it's possible but it would seem unlikely.
DR. STERN: So that's kind of what would jump to mind.
DR. CIFU: That's a great discussion. And I love this case because of everything you went through, this woman basically has every possible reason to have acute kidney injury and so she was kind of, you know, wonderful to talk about, even though she was obviously in pretty bad shape. One of the things we talked a lot about too, just from a clinical reasoning perspective was, you know, here's a woman with lupus nephritis with AKI and so lupus nephritis sort of jumps to the top of your list, but you're totally right.
DR. CIFU: Like why should this person coincidentally have a flare for new lupus nephritis at the same time that she gets admitted to the hospital? So although there's a temptation for that to be the first thing you think about, it doesn't really make sense, right?
DR. STERN: Right.
DR. CIFU: So I'll tell you just very briefly the beginning of the evaluation and she was actually a puzzle and I'll tackle some of the things you talked about. We assessed her, we felt like she was actually well-hydrated, we checked her FENa, which was greater than 1% which made prerenal azotemia, we thought unlikely. We assessed her and actually had the rheumatologist come to see her.
DR. CIFU: They also agreed that lupus nephritis was very unlikely in her. We looked at her urine and her urine sediment was normal and it wasn't just us, we actually had the nephrologist look at it as well. We reviewed what had gone on with her in the hospital. She was actually on another team originally and her vital signs looked like they'd been actually quite stable the entire time she was in the hospital.
DR. CIFU: She did not have a CT, but she did have an MRI with gadolinium given her delirium, which was normal and her creatinine did start climbing a day or two after that study. To give you a brief sort of final finalization here, before we move on to the next part of the podcast, nephrology was confused enough that they decided to do a renal biopsy on her.
DR. STERN: Really?
DR. CIFU: Thinking about, oh, is this lupus nephritis and is this a strange presentation? And it turned out her biopsy did not show lupus nephritis. We were not surprised at that. We were a little bit irritated that they went down that path.
DR. STERN: It's a risky path to venture on without better confirming evidence, I would think.
DR. CIFU: It is, it is, they did feel like we thought that otherwise her lupus was quiescent and so we were not treating her lupus in any way, shape or form.
DR. STERN: Right.
DR. CIFU: And so they really did feel like it would change the course of our management.
DR. STERN: But the urine didn't show marked proteinuria or cast on anything that would push you in that direction, correct?
DR. CIFU: The urine did not, the initial urine.
DR. STERN: Okay.
DR. CIFU: Any thoughts of sort of where you'd go next, do you think, just before we take a break?
DR. STERN: Well, the biopsy can also help with acute interstitial nephritis, so I'd be curious about that, and you may get a sense of ATN on the biopsy as well. So now that the biopsy has been done, I suppose I would, you know, see what the results are. I'm not sure, like, as you said, that I've have gone for the biopsy, although I understand there's pressure here, you know, she's developing kind of fulminant renal failure right in front of you.
DR. CIFU: Right.
DR. STERN: And boy, if there's a window to treat this before she's frankly done irreparable damage, I think that might've been a motivating factor. It's probably hard for them to ignore the possibility.
DR. CIFU: That's exactly what we were thinking. We felt like we knew, we thought we knew what had gotten her sick was the endocarditis.
DR. STERN: Sure.
DR. CIFU: And we thought that was the cause of her delirium and in fact, everything else was improving except for her renal function. So we were at a bit of a loss.
DR. STERN: Totally makes sense. Okay, so while we ponder that, I think that we're going to take a few minutes and let's do a deep dive into AKI. Adam, do you have some pivotal points to share with us about how to approach patients in general who have acute kidney injury?
DR. CIFU: I do and actually they're pretty brief this week. So point 1, which is really sort of obvious, it's just knowing the definition of what AKI is, okay? And the definition is that AKI is an increase in creatinine of greater than three tenths of a point in less than 48 hours or an increase in creatinine by 50% of baseline. So going up by 1.5 in seven days. Lastly, it can also be a drop in urine output to less than 0.5 cc per kilogram per hour.
DR. CIFU: So in your classic 70 kilogram patient, that would be less than 45 cc per hour for six hours.
DR. STERN: And that's probably worth emphasizing on the inpatient side, right? Because creatinine takes a while to accumulate and someone can be in pretty fulminate failure and may be a day or two before their creatinine rises enough to get your attention, that they might be oliguric.
DR. CIFU: Right, and I think we miss that these days, maybe more than we used to because you know, back in the day everybody got a Foley when they walked in.
DR. STERN: [chuckles] Right.
DR. CIFU: And now we probably appropriately don't do that, but it makes you often miss oliguria.
DR. STERN: Right.
DR. CIFU: My second point is that you really can't exclude prerenal azotemia unless you really assess volume status. And often it's like, yeah, I don't think the patient's dry, but you really have to think about the history, you know, do they have a reason to be dry, examine them, look at their vital signs, maybe do orthostatics. [bell chimes] That would be our orthostatic bell.
DR. STERN: [laughs]
DR. CIFU: That usually rings for you and not me. So, so yes. So really if you're trying to figure out AKI and you're thinking about prerenal azotemia, work hard to figure out what the person's volume status is. My third key point is actually probably a corollary to that is that a pre-renal state is often not that simple, right? It's not just being dry, but it could be decreased effective circulating volume and so the person actually may be volume replete, or even maybe volume overloaded, but have heart failure, cirrhosis, pulmonary hypertension or something that makes them not get enough blood to their kidneys.
DR. STERN: That's a good point.
DR. CIFU: My fourth key point is intrarenal-- and this is sort of terrible to say, intrarenal causes of AKI are just difficult. You basically just have to memorize the differential diagnosis. But for me, I've always dreaded that, and what helps me is to at least think of an anatomic organization or framework to intrarenal causes of AKI and so think tubular causes, like ATN, interstitial causes, you already brought up interstitial nephritis, glomerular causes in this case, we're thinking about lupus nephritis or vascular causes.
DR. CIFU: Could there be a vascular event? And I guess what's great about this case is you could imagine this woman having all of those including prerenal and postrenal. And then the fifth and final point is just never, ever, ever miss obstruction. You know, obstruction as a cause of AKI is just easy, it's easy to fix and sometimes people kind of blow it off because the person says, "Oh, I'm urinating fine." You know, that's wrong, right?
DR. CIFU: People can be urinating fine or they think they're urinating fine and still have an obstructive nephropathy.
DR. STERN: And to evaluate that you do what, Adam?
DR. CIFU: So it's usually easy, right? Usually to start with an ultrasound and it may be a renal ultrasound, it may be a bladder scan and may be putting in a Foley to see if they've got a liter of urine in their bladder. And I think often, you know, we think, oh, old guy, right? BPH, but remember that could be from neurogenic bladder. It could even be from an obstructed catheter, right?
DR. STERN: Right. All right, well, that's good, let's go back to our case. Do you want to give us an update on what happened with her?
DR. CIFU: Yeah, so I'll give you an update and it actually turns out to be remarkably easy though a little bit unfortunate. So after this biopsy was done, the biopsy pretty definitively ruled out glomerulonephritis, was not consistent with interstitial nephritis, was suggestive of acute tubular necrosis.
DR. STERN: Oh, interesting.
DR. CIFU: And we went back, got another urine. The nephrologist looked at the urine and it was loaded with muddy brown casts. So at that point, that was the diagnosis. We were all a little perplexed about the first urine and you know, were we not seeing it then? What was going on and felt bad 'cause this woman basically underwent a renal biopsy because of that. But the rest of her course was sort of classic for that.
DR. CIFU: Her creatinine rose very quickly. I think she got up to a creatinine of about 5.5 and then had a, you know, striking post ATN diuresis. Never became anuric actually before that, and creatinine went back almost to normal. She left the hospital two weeks after admission with a creatinine of, I think 1.1, 1.2, a little bit up from where she'd come in, but close to normal for her.
DR. STERN: And what did you do to treat the ATN?
DR. CIFU: We did nothing, we supported her. So my, I don't know, my take on ATN and see if you agree is the hardest part about it is sometime just managing someone's volume. She was still pretty sick so she wasn't doing a great job of keeping up on her oral intake. So we had to be careful about making sure that we were hydrating her appropriately with not overwhelming her when she wasn't peeing a lot and without falling behind when she went into this post ATN diuresis.
DR. STERN: Right and just to make the point that while we occasionally need dialysis to support a patient who has ATN, it's never curative or therapeutic, it's simply to support them with the hope that their tubules will recover on their own, right?
DR. CIFU: Yes, great point, great point.
DR. STERN: All right, so that's very interesting. It's too bad she ended up needing a biopsy. Maybe we can argue with the federal government to put microscopes back on the floor so that we can actually look at urines easier. You think that would work?
DR. CIFU: I thought you could argue with the federal government 'cause maybe they won't pay for that biopsy given the--
DR. STERN: [laughs] Alright, so that's not good. That's enough to argue with. Let's go on to talk about fingerprints, common misconceptions, our favorite pet peeves and other random knowledge. Adam, you want to start us off with some fingerprints?
DR. CIFU: Sure, my fingerprint's not really a fingerprint as we define them, remember that we defined fingerprints as finding on the history or physical exam that are highly suggestive of a diagnosis and we say highly suggestive, we really mean a positive likelihood ratio of greater than 10. So I'm going to talk about a test and the test is that granular casts are very specific for ATN. So if you see greater than 10 granular casts per high-power field, that's basically diagnostic of ATN.
DR. STERN: Right, now, I'll just add to that. Another fingerprint is that a FENa that's over 1% is also very specific for ATN in the 75 to 95% range. So how about some misconceptions? Why don't you fire away?
DR. CIFU: Yes, so I may have mentioned this talking about the case, the misconception that I actually hear a lot is that patients need to be anuric to have an obstructive cause of AKI. That is definitely not the case and I would say when that is the case, it's easy, right? If someone comes in and they say, "I can't pee" and their creatinine is three, you're done. But certainly in my practice as an older doctor with a practice filled with a lot of old men, most of the times what happened is I, you know, people have their usual BPH symptoms that they've had for 10 years.
DR. CIFU: I check renal function and their creatinine has doubled, I have them come back and they're still saying, "Oh, everything's kind of fine" and then they've got a liter and a half in their bladder and their creatinine returns to normal.
DR. STERN: Yes, it can be very exciting when you put those Foley catheters in and the urine just keeps coming and coming I had that happen. The misconception I wanted to address is something about pyelonephritis. So it's often thought that pyelonephritis incorrectly can cause acute kidney injury and it really doesn't. The only time pyelonephritis is going to lead to an acute kidney injury, if it's causing hypotension and either a prerenal azotemic state or a frank ATN and in and of itself, it doesn't typically cause enough damage that you're going to see an acute kidney injury from it.
DR. CIFU: Which is complicated, right? 'Cause pyelo can cause something which can cause ATN, but pyelo itself doesn't and I mean overwhelmingly the majority of people with pyelo have completely normal creatinine
DR. STERN: Totally, all right, so turning to our favorite topic, pet peeves, do you want to start us off?
DR. CIFU: Yes, the pet peeves that we always have to limit, so we don't go on and on. So my first pet peeve is maybe a stupid easy one, but something which really does drive me crazy. It's that ATN and AKI are different things, right? AKI is acute kidney injury, which has numerous, numerous, numerous causes and ATN is one cause of AKI. If you assume that all AKI is ATN, you're going to miss the boat on the cause of the ATN, you know, probably the majority of the time.
DR. STERN: Right, okay. And the one I'm going to go with is one you've mentioned already, but I can't help but repeat myself or ourselves and that's evaluating patients' volume status is really a clinical measurement primarily, it's vital signs and I'll ring my own bell. [bell chimes] Orthostatic vital signs are key because patients can really have relatively normal vital signs when they're sitting down and it's not to stand them up and challenge them that the blood pressure drops and the pulse increases.
DR. CIFU: Perfect, I'm going to add one more just 'cause you know, we're on a roll here. Urine eosinophils, urine eosinophils are terrible for diagnosing interstitial nephritis. The likelihood ratios for urine eos, the positive likelihood ratio is 1.45 and the negative likelihood ratio is 0.83. So you can say, eh, you know, they're vaguely supportive of what your previous thinking is, but not terribly.
DR. STERN: That's really lame. I mean, why would we ever bother to do that?
DR. CIFU: Right.
DR. STERN: We should just give it up.
DR. CIFU: Exactly, I think it's a throwback too, you know, it's got some bio plausibility and sometimes it correlates.
DR. STERN: Right. All right, so our last section is clinical pearls. So why don't you start us off again?
DR. CIFU: Okay, so the first one, I know this is pretty well known, but really something that I think is important not to forget is that the relationship between creatinine and GFR glomerular filtration rate is inverse and exponential. So small changes at the beginning are large. So if you go from a creatinine of 1 to 1.5, you've had a 50% drop in your GFR. Later in the course though, a 50% drop in your GFR would be reflected by a creatinine rise of four to six, okay?
DR. CIFU: And so just keep that in mind, when someone comes in with pretty normal creatinine and they have a bump from 1 to 1.4, .7 to 1.3, that's a really big deal.
DR. STERN: And that's often missed.
DR. CIFU: Often.
DR. STERN: So my clinical pearl you've already said, but we have to do ultrasounds when we see people with AKI. You just have to do it.
DR. CIFU: All right, easy test, cheap test, non-invasive tests and may clarify at the diagnosis.
DR. STERN: And better than you urine eos, I've heard.
DR. CIFU: I've heard that said. And then maybe my last one, and this gets back a little bit to the case is that I try to remember that there are really three steps to managing AKI. First is to identify that it's occurring. That's going back to that definition that we talked about before. That's actually sometimes harder than you think, especially in the hospital when you're getting tons of labs and you're sort of used to everybody in the hospital having a creatinine of 1.5, but really focus on it, recognize when the person is having an acute kidney injury.
DR. CIFU: Secondly is get into the differential diagnosis, think about what this might be, come up with a diagnostic approach and then the thing that I probably forget most is that once you've made that diagnosis of AKI, you got to just stop, look at the patient's med list and make sure that you're stopping any nephrotoxic medications and re-dosing any renally cleared medications.
DR. STERN: Yeah, that's a real easy mistake to make, because you have to actually actively think, let me look at the meds they're already on, right? So they don't accidentally kill them, because you're overdosing them.
DR. CIFU: I actually, I think back to a woman, who's I, this is maybe a little bit strange, but I have a list of, you know, serious mistakes I've made over my career that I go back to every now and then in the hope of not making them again, but I had a woman, you know, 25 years ago who I took care of in the ICU when I was a resident. She was this woman with horrible COPD, horrible heart failure.
DR. CIFU: One of those patients where, you know, 500 cc's of fluid too much, she was in heart failure, 500 too little, she was hypotensive and you know, I spent a month sort of, you know, delicately working on her and at some point misdosed, I don't know, her gentamicin that she was on, given that I hadn't picked up on the change in her renal function and always sticks with me and whenever I make that mistake, I kind of slapped myself in the head.
DR. STERN: Yeah, Gent was a tough one to dose back in the day. Fortunately nobody does it anymore.
DR. CIFU: It's true and we seldom had pharmacists like, on the team rounding with us.
DR. STERN: All right, well, my last clinical pearl gets at the FENa and so maybe the clinical pearl has to do with interpreting the FENa when someone's on diuretics, but before I jump into that, let's talk about what the FENa is. The FENa is the fractional excretion of sodium. It's how much of the sodium that you filtered, you excrete. So in prerenal azotemia the kidneys are still working, they don't want to excrete the sodium, they think your volume depleted, you reabsorb the sodium and so the fraction that you excrete is low.
DR. STERN: In ATN, on the other hand, the cells are dead. They can't reabsorb the sodium, so the fraction of sodium that you secrete is high, hence the normal value of the FENa. One common mistake though, is to forget about patients on diuretics. Diuretics can force sodium to be excreted from the kidney and can make their FENa look high, even when the patient's prerenal and then you should use an FEUrea.
DR. CIFU: I love listening to you Scott, when occasionally I feel like you get into something that you've taught a thousand times before, and it sounds like you stuck a cassette in your head and like, cause that's a perfect, a perfect description to get people understanding FENas and FEUreas. So we hope you found this episode of the Symptom to Diagnosis podcast useful and a bit enjoyable. As a reminder, our textbook "Symptom to Diagnosis: An Evidence-Based Dive" takes a much deeper dive "An Evidence-Based GUIDE" sorry, it takes a much deeper dive into how we think about and reason through the diagnosis of medical presentations.
DR. CIFU: The book is available in print through all the usual places. It's available and fully searchable via Access Medicine website available worldwide from McGraw Hill and now available as a downloadable book on your whatever device you use, which is really, really works terrifically.
DR. STERN: It does.
DR. CIFU: Great, thank you, see you soon.
DR. STERN: Thank you. The music for the S2D Podcast is courtesy of Dr. Maylyn Martinez.