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Acute Kidney Injury
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Acute Kidney Injury
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[Dr. Smith] Welcome back to Run the List, a medical education podcast in partnership with McGraw Hill Medical. Our hosts are Dr. Navin Kumar, Dr. Walker Redd, Dr. Emily Gutowski, Dr. Joyce Zhou, and myself, Blake Smith. As a quick disclaimer, this podcast is meant for informational and educational purposes only, and should not be understood as medical advice under any circumstances.
[intro music] [intro music] [intro music] [Dr. Gutowski] Welcome back to Run the List. I'm Emily Gutowski and today we're starting our nephrology series with Dr. Rahul Maheshwari. Rahul is currently a second-year nephrology fellow at the Mount Sinai Hospital in New York. He's also pursuing a masters of Health Professions Education and is passionate about MedEd.
The internal medicine residents know him for the fantastic teaching he provides when consulting on our patients. We're so lucky to have him here to talk about AKI. Rahul, welcome to the show. [Dr. Maheshwari] Hey Emily, thanks so much for having me, it's a pleasure to be here. [Dr. Gutowski] So without further ado, let's go ahead and Run the List, today we have with us a 55-year-old woman with a history of IV drug use who comes to the ED hypotensive and febrile.
She ends up getting diagnosed with endocarditis, she's started on broad spectrum antibiotics, and on the second day of her admission her creatinine rises to 2.1 from a baseline of 1.0. She is hemodynamically stable this whole time. So Rahul, how do you think about an acute rise in creatinine like this? [Dr. Maheshwari] So the first thing you want to think about is, how do you actually define an AKI?
There's been several criteria over the last 10 to 15 years that have been sort of research-dependent, but most recently we look at the KDIGO AKI criteria. The way that you define an acute kidney injury, or AKI, is a rise in the serum creatinine of 0.3 mg/dL, or a rise in about 30% from the reported baseline. This is within a timeframe of about 72 hours. So usually when I think about the general approach of an acute kidney injury, I kind of go in three steps.
First is the urgency, then the context, then finally thinking about the diagnostic approach. In terms of the urgency, you want to make sure there aren't any emergent electrolyte abnormalities. The number one thing that we usually worry about is hyperkalemia, but additionally what's the rate of rise, so is this like an RPGN, and finally, is the patient oliguric or anuric, and at which point you'd be very worried about volume-overloaded states. Secondly, what's the context?
Is this patient in the clinic or in the hospital? Are we in a specific clinical scenario, like post-op, in the intensive care unit? Is this a patient who is recently pregnant, for example? Are there any other comorbidities that might ultimately inform your last component to this, which is the diagnostic approach. So we divide this into three buckets, which I'm sure you've heard about before, which are your prerenal, postrenal, and intrinsic buckets.
From a prerenal perspective, we're just thinking about how does blood get to the kidney? So these are usually volume-down states that we think about. These are hemorrhagic shock, or bleeding episodes, dehydration, or in situations where we have poor effective arterial blood volume, so CHF or CHF exacerbations, as well as cirrhosis, as well. From the postrenal perspective, we're thinking about what is the flow of urine as it leaves the kidney and any kind of anatomic issues.
So these are issues that involve the ureter, the bladder, and the urethra. So specifically, things we worry about are stones, in men BPH, Foley dysfunctions, and even things like tumors. And finally, there's a whole host of intrinsic renal diseases, most notably ATN, or acute tubular necrosis, what we see the vast majority of the time in the hospital. These also include things like AIN, glomerular diseases, vascular diseases, et cetera.
[Dr. Gutowski] Okay, great. Thanks for that. Now that we've developed a pretty broad differential, what are our first steps in working this up? [Dr. Maheshwari] Yeah, so you know when I first get the phone call about somebody who has an AKI, this is kind of what I'm doing as I'm starting to dig through the chart as I'm hearing the story over the phone. So the very first thing I do is I go to the medication list and I think about what are some causative agents that may have been causing this, especially for patients that are in the hospital, that are sick, that have had antibiotic exposures, exposures to things like NSAIDs.
So in this specific case, we think about vancomycin which is a very well known nephrotoxin. Secondly then, we start thinking about what's the rest of the workup that's already been obtained sort of incidentally or things that we may have asked for before. So what I'm looking at are urine studies, looking at the urinalysis, the urine osms and the urine electrolytes.
The urinalysis can give us a sense of are there any intrinsic pathologies that are potentially affecting the kidney? So you're looking at things like RBCs, WBCs, or if there's any other thing that can inform you about the clinical picture. So is this a patient who has urosepsis and has leuk esterase or nitrites, for example. The urine electrolytes and urine osms we'll get to in a little bit more detail, but sometimes you look at the urine electrolytes to understand, is this a patient who is sodium avid and therefore is in a low flow state or poor effective arterial blood volume, and so do they have a low urine sodium?
Similarly, if we're thinking about dehydration, for example, is a urine osm elevated? These can also help inform other situations as well. Once we have that information, if we have a urine sample available, we'll take it to the lab and actually look at the urine sediment. And so just to kind of briefly run through some things we look at for urine sediment analyses, we can diagnose, for example, acute tubular necrosis by looking at muddy brown casts or granular casts.
If we're worried about intrinsic glomerular diseases specifically, or IAN for example, we think about WBC casts, or separately, RBC casts as well. Hyaline casts are somewhat non-specific, but still a useful diagnostic sign that we see on urine sediment. And finally, dysmorphic RBCs also make us worried about intrinsic glomerular disease.
Finally, again, this is all beyond the basic blood work, we're looking at imaging studies. So usually we're asking for a renal ultrasound. This kind of helps us more to rule out any postrenal issues. So the number one thing I'm looking for is, is there any hydro, bilateral or unilateral, on the renal imaging studies, specifically a renal ultrasound. However, looking at echogenicity is also helpful.
It gives you a sense of how long has the damage been occurring to the kidney, if there's some chronicity to it. And then finally, Doppler studies are also helpful if that's available to help you understand what's the renal vasculature, or the renal artery specifically, and how well are they getting blood to the kidneys. And so, based on those initial studies, again, depending on what's available, what's not available, this can help us broaden our workup and approach a further diagnostic workup for acute kidney injury.
[Dr. Gutowski] That's really great, thank you so much. I should also just say that before calling our nephrology colleagues we should always do a very thorough physical exam, which can of course give us a sense of a patient's volume status, whether they look to be dehydrated. I've certainly also had patients who a simple physical exam would've discovered, you know, a kinked Foley or a large bladder where they were retaining urine.
So sometimes we can avoid this consult altogether with a very thorough exam. But you did mention urine electrolytes and I know in medical school we learn about the importance of the FENa or sometimes we also learn about the FEUrea. Can you tell us a little bit about what the FENa is and whether you actually use that? [Dr. Maheshwari] So in regards to the FENa, this is the fractional excretion of sodium, this is getting us a sense as to how much is the kidney holding onto sodium and it's kind of a proxy almost for telling us if there is an effective arterial blood volume that's getting to the kidney.
Now, usually when you learn about cutoffs of FENa, we think about either is there a FENa of less than 1% or a FENa greater than 2%? If it's less than 1%, you think about prerenal causes and if it's greater than 2%, it's usually anything else. So in that context, a FENa can be helpful if you have the urine sodium, the urine creatinine, the serum sodium and the serum creatinine all drawn roughly at the same time to get a sense as to what is happening to the kidney at that point.
That being said, clinically speaking, there are lots of caveats to the FENa and it's not something I frequently use. Some of the caveats include making sure that the patient, at the time of the collection, did not have a significantly deranged GFR. The FENa was validated best in patients that had normal baseline renal function and the indication was just to see if the patient had a prerenal AKI or if they had ATN developed.
So it's not going to really be able to tell you about any other causes of AKI, sometimes for some reason, there's then this misconception that it can also help you diagnose a postrenal AKI, which is not the case, unfortunately. Additionally, this becomes challenging where you have patients that are coming in with multiple comorbidities, they often have CKD or they've had an AKI for over a week or two and then how the kidneys are actually able to hold onto sodium has changed significantly and so you can't really rely on the FENa itself anymore.
Frequently what I'm looking at in my kind of eyeball test just to see, is the urine sodium less than assay? At most places that's less than 20, and that can just kind of give you a sense as to, is that sodium avid or not, or are the kidneys sodium avid or not? The FEUrea is helpful. As you're well aware, diuretics can also significantly alter the various urine studies.
So if you have somebody who's on a loop diuretic for example, or a thiazide diuretic, they're going to have excessive sodium in the urine and so that will make it difficult for you to interpret an actual FENa. You can use an FEUrea, which is not- Urea itself is not going to be impacted by diuretics, and so there are cutoffs for that. Usually your FEUrea cutoff is less than 35% and you can use that in the same way you would interpret the FENa, where if it's less than 35% you'd think about prerenal causes and if it's greater than that it's unlikely to be that.
Again, these have the same caveats. In terms of validation studies now, the FENa, FEUrea are not great, again, as I sort of mentioned, they're roughly 75% sensitive, specific, again, depending on the clinical context and so most of the time I am kind of looking to see, is the urine sodium less than 20 and this will tell me if we're in a poor effective arterial blood volume state or a volume-down state, and from there that's kind of how I approach my diagnostics, instead of frequently calculating the FENa or FEUrea.
[Dr. Gutowski] Got it, so it's a tool, we can use it, but have to kind of take it in the larger context. [Dr. Maheshwari] Exactly. [Dr. Gutowski] So one more question for you, you mentioned CKD earlier, and I know our patient had a baseline creatinine of about 1. How would you compare a rise in creatinine from a baseline of 1 to 2 to someone with CKD who maybe has a baseline in the 3s that rises to 4?
[Dr. Maheshwari] Yeah, so that's a great question, especially because those jumps in numbers can look pretty significant and pretty scary. The way that I kind of think about it is what is the percentage deviation or increase from the baseline? So if you have somebody with normal kidney function, let's say they're coming in with a serum creatinine of 1 and something happens in the hospital so their serum creatinine is 2 the next day, similar to our current patient, that makes me very worried because the serum creatinine has increased by 100% and that drop in GFR can be fairly substantial.
Now on the flip side, if you have somebody who has a baseline serum creatinine of 3, or if you have somebody with very advanced CKD with a baseline serum creatinine of 5 and that creatinine goes up by 0.5 or 1, certainly that's a jump and that's something we need to think about and understand why did that happen, is that something we can correct and fix? But the change in the GFR is much less, so if you think about somebody who went from 5 to 6, for example, that's an increase in 20% of the serum creatinine rather than going from 1 to 2 of 100% and the corresponding drop in GFR is much less substantial as well.
And so in both cases, again, we need to work this up, but I am far more concerned about the rate of rise for that first patient that you had mentioned. [Dr. Gutowski] Got it. Makes sense, thank you. So let's get back to our case. We have a lot of potential contributors to this patient's AKI. She was hypotensive on arrival, she was septic, she was pretty dehydrated so total volume was down and she's been treated with broad spectrum antibiotics, including vancomycin.
Some of the additional studies that we got in the hospital are notable for a high urine sodium. There are muddy brown casts on her urine sediment and we got a renal ultrasound as well which shows no hydronephrosis. So putting all of this information together where does this leave us? [Dr. Maheshwari] Yeah, so you know this is a very challenging case and there's lots of potential contributions to this patient's acute kidney injury.
It's important to know that acute kidney injury, it's almost better to think of it as a syndrome rather than a diagnosis. And so this is a syndrome of lots of different nephrotoxic events or agents that are occurring. So we talked about the vancomycin, we talked about this patient who may be hypotensive, do they have a GN that's related to a post-infectious setting in the context of somebody who has endocarditis?
Are they volume-up and so therefore have a cardiorenal AKI as well? So there's lots of potential contributing factors here and so whenever you go into a scenario like this the first thing you want to do is try and remove whatever nephrotoxic events or agents that are impacting this patient. So the first thing I would think about, from a medication list standpoint is, we mentioned vancomycin, do we have any recent vancomycin levels?
Is there any reason for us to think that they've been dosed with high levels of vancomycin, especially in this patient who has a change in renal function? So the serum creatinine is a lagging marker of their true GFR, their true intrinsic renal function, and so the creatinine is 2 today, but it was 1 yesterday, and these were done at labs that were done at 600 in the morning and we're looking at them in the afternoon.
It's reasonable to think that it's already 300 by that time in the afternoon and how we're dosing our antibiotics, specifically to vancomycin. May be higher than it ought to be relative to what the true renal function is, and so checking antibiotic levels, and ideally, if we're able to find a different agent than vancomycin to treat this infective endocarditis that would be the ideal scenario.
Now if we think about volume status, if the patient is overtly volume-up or overtly volume-down, we can consider giving a trial of either diuretics or volume. If they're coming in very septic and hypotensive as soon as they get into the hospital, presumably they're volume-down in this case and we can give them a trial of fluids. If that helps improve their renal function, great.
We can always continue to judiciously give more volume and it gets to a point where they aren't improving any longer, then we can always stop and continue to reassess, as you mentioned previously, the physical exam is very important. Now in this case you mentioned that the urine sodium was high and there are muddy brown casts on the urine sediments, and so rather than a prerenal situation I would be thinking more about ATN or acute tubular necrosis.
There are two major pathways that lead to acute tubular necrosis, that's either a prolonged ischemia or a toxic ATN from nephrotoxic agents, such as vancomycin. And so again, in that same situation, making sure that they're no longer hypotensive, and so treating the underlying infection, using volume or pressors if needed to make sure that the patient's MAP stays over, classically 65.
And then again, we talked about removing agents such as vancomycin, NSAIDs, anything else that may be impacting them negatively. So that's kind of my initial approach and how I'd go about this. It's potential that the injury has already started to propagate within the kidney and even by taking all the necessary steps you may see the creatinine continue to rise over the next couple of days.
And that's kind of the unfortunate timeline or time course if you will, of this syndrome of AKI. [Dr. Gutowski] So in a lot of these patients we send them for imaging that requires contrast. What would you say about getting contrast in a patient like this? [Dr. Maheshwari] Yeah, so contrast, or specifically iodinated contrast, in terms of how it causes AKIs, is an ongoing area of discussion.
Generally speaking in patients that, first off, have normal baseline renal function, that aren't undergoing lots of other events, so usually not a sick patient in the hospital, giving iodinated contrast should not really cause any problems. In this patient, that is very sick, you are worried about some kind of contrast-induced or contrast-associated AKI that can occur as a result of giving iodinated contrasts for CTs.
Ultimately, it's a risk/benefit discussion. If you think that you really need to get the information in a timely manner that only a contrast-enhanced CT can provide, then that's something you have to do and you have to accept that risk. Ultimately, we can accept the risk of a patient whose kidneys continue to fail and may end up ultimately needing either temporary or permanent dialysis, but without the contrast CT, for example, you may not be able to diagnose a life-threatening infection, and so you do have to kind of have that risk/benefit discussion in the back of your head.
And so I don't want people to think that, "Oh, there's an AKI, we definitely can't use iodinated contrast for this CT," because then you may end up, unfortunately, causing increased morbidity or mortality in this patient. It's just another thing you have to keep in the back of your head. [Dr. Gutowski] Right, and I've definitely been on the side where I have to write a little note in the patient's chart that says, "We believe the benefits outweigh the risks." So that makes a lot of sense. You also mentioned dialysis, I remember learning a great mnemonic in med school for figuring out which patients need urgent dialysis.
You might know which one I'm talking about. [Dr. Maheshwari] Yeah absolutely, so I'm sure back in third year of med school you learn about the AEIOUs, which are a good mnemonic for thinking about dialysis indications. So briefly, A for acidosis, E for electrolyte abnormalities, I for intoxicants, O for volume overload and U for uremia. The important thing is to think about are these medically refractory indications, and so if you have a patient who's acidotic, they have a pH of 7.0 for example, are you able to give them bicarb or supplement or fix that acidosis in a way before they end up needing dialysis?
In the same way, when you think about electrolyte abnormalities, the number one thing that we most worry about is hyperkalemia, so if you have a potassium of 7-7.5, that's certainly concerning, but are there ways that we can temporize or even reverse that hyperkalemia without requiring dialysis? And so that's a very helpful mnemonic.
I just like to put that little asterisk at the end there that these are all medically refractory indications. I understand that in the future there's going to be an episode about renal replacement therapy so I won't go into the details about dialysis, but just to keep that AEIOU mnemonic in mind. [Dr. Gutowski] Thanks for taking us through that. We have talked a lot about all of the different potential causes of AKI in this patient and in any patient who we might find in the hospital.
Would you be able to leave us with a couple of clinical pearls as we finish up this episode? [Dr. Maheshwari] Yeah, absolutely. So I think when you first approach a patient with an AKI, or acute kidney injury, you want to think about your three buckets of prerenal causes, postrenal causes, and intrinsic renal causes of AKI. Secondly, thinking about what studies you have or what studies that you want to get.
What's useful, especially if you're calling nephrology, is getting some kind of renal imaging, that's usually a renal ultrasound. What's helpful is if you're going to get a renal ultrasound to get one with the bladder as well and you'll get bonus points if you get one with a post-void residual for us to understand if the patient is appropriately voiding and therefore do they have a recurrent cause of an obstruction, for example.
Other things that are helpful are getting the urine study, so urine electrolytes and urine osm as well. Getting a urine creatinine will be helpful for us to calculate things like the FENa, acknowledging all the limitations that we just discussed. And finally, urinalysis is also helpful to give us a sense of what else is happening in the kidney or in the urinary tract. Finally, if you have any questions, we're more than happy to help, so don't ever hesitate to reach out to nephrology, if possible after 700 am, but whenever is totally fine as well.
And then the most important thing is thinking about your AEIOUs when you're thinking about dialysis indications and that they're medically refractory. [Dr. Gutowski] Wonderful, well we've learned so much in this episode, so thank you so much for all of your instruction. [Dr. Maheshwari] It's a pleasure to be here, thanks Emily. [outro music] [outro music]
Segment:0 .
[Dr. Smith] Welcome back to Run the List, a medical education podcast in partnership with McGraw Hill Medical. Our hosts are Dr. Navin Kumar, Dr. Walker Redd, Dr. Emily Gutowski, Dr. Joyce Zhou, and myself, Blake Smith. As a quick disclaimer, this podcast is meant for informational and educational purposes only, and should not be understood as medical advice under any circumstances.
[intro music] [intro music] [intro music] [Dr. Gutowski] Welcome back to Run the List. I'm Emily Gutowski and today we're starting our nephrology series with Dr. Rahul Maheshwari. Rahul is currently a second-year nephrology fellow at the Mount Sinai Hospital in New York. He's also pursuing a masters of Health Professions Education and is passionate about MedEd.
The internal medicine residents know him for the fantastic teaching he provides when consulting on our patients. We're so lucky to have him here to talk about AKI. Rahul, welcome to the show. [Dr. Maheshwari] Hey Emily, thanks so much for having me, it's a pleasure to be here. [Dr. Gutowski] So without further ado, let's go ahead and Run the List, today we have with us a 55-year-old woman with a history of IV drug use who comes to the ED hypotensive and febrile.
She ends up getting diagnosed with endocarditis, she's started on broad spectrum antibiotics, and on the second day of her admission her creatinine rises to 2.1 from a baseline of 1.0. She is hemodynamically stable this whole time. So Rahul, how do you think about an acute rise in creatinine like this? [Dr. Maheshwari] So the first thing you want to think about is, how do you actually define an AKI?
There's been several criteria over the last 10 to 15 years that have been sort of research-dependent, but most recently we look at the KDIGO AKI criteria. The way that you define an acute kidney injury, or AKI, is a rise in the serum creatinine of 0.3 mg/dL, or a rise in about 30% from the reported baseline. This is within a timeframe of about 72 hours. So usually when I think about the general approach of an acute kidney injury, I kind of go in three steps.
First is the urgency, then the context, then finally thinking about the diagnostic approach. In terms of the urgency, you want to make sure there aren't any emergent electrolyte abnormalities. The number one thing that we usually worry about is hyperkalemia, but additionally what's the rate of rise, so is this like an RPGN, and finally, is the patient oliguric or anuric, and at which point you'd be very worried about volume-overloaded states. Secondly, what's the context?
Is this patient in the clinic or in the hospital? Are we in a specific clinical scenario, like post-op, in the intensive care unit? Is this a patient who is recently pregnant, for example? Are there any other comorbidities that might ultimately inform your last component to this, which is the diagnostic approach. So we divide this into three buckets, which I'm sure you've heard about before, which are your prerenal, postrenal, and intrinsic buckets.
From a prerenal perspective, we're just thinking about how does blood get to the kidney? So these are usually volume-down states that we think about. These are hemorrhagic shock, or bleeding episodes, dehydration, or in situations where we have poor effective arterial blood volume, so CHF or CHF exacerbations, as well as cirrhosis, as well. From the postrenal perspective, we're thinking about what is the flow of urine as it leaves the kidney and any kind of anatomic issues.
So these are issues that involve the ureter, the bladder, and the urethra. So specifically, things we worry about are stones, in men BPH, Foley dysfunctions, and even things like tumors. And finally, there's a whole host of intrinsic renal diseases, most notably ATN, or acute tubular necrosis, what we see the vast majority of the time in the hospital. These also include things like AIN, glomerular diseases, vascular diseases, et cetera.
[Dr. Gutowski] Okay, great. Thanks for that. Now that we've developed a pretty broad differential, what are our first steps in working this up? [Dr. Maheshwari] Yeah, so you know when I first get the phone call about somebody who has an AKI, this is kind of what I'm doing as I'm starting to dig through the chart as I'm hearing the story over the phone. So the very first thing I do is I go to the medication list and I think about what are some causative agents that may have been causing this, especially for patients that are in the hospital, that are sick, that have had antibiotic exposures, exposures to things like NSAIDs.
So in this specific case, we think about vancomycin which is a very well known nephrotoxin. Secondly then, we start thinking about what's the rest of the workup that's already been obtained sort of incidentally or things that we may have asked for before. So what I'm looking at are urine studies, looking at the urinalysis, the urine osms and the urine electrolytes.
The urinalysis can give us a sense of are there any intrinsic pathologies that are potentially affecting the kidney? So you're looking at things like RBCs, WBCs, or if there's any other thing that can inform you about the clinical picture. So is this a patient who has urosepsis and has leuk esterase or nitrites, for example. The urine electrolytes and urine osms we'll get to in a little bit more detail, but sometimes you look at the urine electrolytes to understand, is this a patient who is sodium avid and therefore is in a low flow state or poor effective arterial blood volume, and so do they have a low urine sodium?
Similarly, if we're thinking about dehydration, for example, is a urine osm elevated? These can also help inform other situations as well. Once we have that information, if we have a urine sample available, we'll take it to the lab and actually look at the urine sediment. And so just to kind of briefly run through some things we look at for urine sediment analyses, we can diagnose, for example, acute tubular necrosis by looking at muddy brown casts or granular casts.
If we're worried about intrinsic glomerular diseases specifically, or IAN for example, we think about WBC casts, or separately, RBC casts as well. Hyaline casts are somewhat non-specific, but still a useful diagnostic sign that we see on urine sediment. And finally, dysmorphic RBCs also make us worried about intrinsic glomerular disease.
Finally, again, this is all beyond the basic blood work, we're looking at imaging studies. So usually we're asking for a renal ultrasound. This kind of helps us more to rule out any postrenal issues. So the number one thing I'm looking for is, is there any hydro, bilateral or unilateral, on the renal imaging studies, specifically a renal ultrasound. However, looking at echogenicity is also helpful.
It gives you a sense of how long has the damage been occurring to the kidney, if there's some chronicity to it. And then finally, Doppler studies are also helpful if that's available to help you understand what's the renal vasculature, or the renal artery specifically, and how well are they getting blood to the kidneys. And so, based on those initial studies, again, depending on what's available, what's not available, this can help us broaden our workup and approach a further diagnostic workup for acute kidney injury.
[Dr. Gutowski] That's really great, thank you so much. I should also just say that before calling our nephrology colleagues we should always do a very thorough physical exam, which can of course give us a sense of a patient's volume status, whether they look to be dehydrated. I've certainly also had patients who a simple physical exam would've discovered, you know, a kinked Foley or a large bladder where they were retaining urine.
So sometimes we can avoid this consult altogether with a very thorough exam. But you did mention urine electrolytes and I know in medical school we learn about the importance of the FENa or sometimes we also learn about the FEUrea. Can you tell us a little bit about what the FENa is and whether you actually use that? [Dr. Maheshwari] So in regards to the FENa, this is the fractional excretion of sodium, this is getting us a sense as to how much is the kidney holding onto sodium and it's kind of a proxy almost for telling us if there is an effective arterial blood volume that's getting to the kidney.
Now, usually when you learn about cutoffs of FENa, we think about either is there a FENa of less than 1% or a FENa greater than 2%? If it's less than 1%, you think about prerenal causes and if it's greater than 2%, it's usually anything else. So in that context, a FENa can be helpful if you have the urine sodium, the urine creatinine, the serum sodium and the serum creatinine all drawn roughly at the same time to get a sense as to what is happening to the kidney at that point.
That being said, clinically speaking, there are lots of caveats to the FENa and it's not something I frequently use. Some of the caveats include making sure that the patient, at the time of the collection, did not have a significantly deranged GFR. The FENa was validated best in patients that had normal baseline renal function and the indication was just to see if the patient had a prerenal AKI or if they had ATN developed.
So it's not going to really be able to tell you about any other causes of AKI, sometimes for some reason, there's then this misconception that it can also help you diagnose a postrenal AKI, which is not the case, unfortunately. Additionally, this becomes challenging where you have patients that are coming in with multiple comorbidities, they often have CKD or they've had an AKI for over a week or two and then how the kidneys are actually able to hold onto sodium has changed significantly and so you can't really rely on the FENa itself anymore.
Frequently what I'm looking at in my kind of eyeball test just to see, is the urine sodium less than assay? At most places that's less than 20, and that can just kind of give you a sense as to, is that sodium avid or not, or are the kidneys sodium avid or not? The FEUrea is helpful. As you're well aware, diuretics can also significantly alter the various urine studies.
So if you have somebody who's on a loop diuretic for example, or a thiazide diuretic, they're going to have excessive sodium in the urine and so that will make it difficult for you to interpret an actual FENa. You can use an FEUrea, which is not- Urea itself is not going to be impacted by diuretics, and so there are cutoffs for that. Usually your FEUrea cutoff is less than 35% and you can use that in the same way you would interpret the FENa, where if it's less than 35% you'd think about prerenal causes and if it's greater than that it's unlikely to be that.
Again, these have the same caveats. In terms of validation studies now, the FENa, FEUrea are not great, again, as I sort of mentioned, they're roughly 75% sensitive, specific, again, depending on the clinical context and so most of the time I am kind of looking to see, is the urine sodium less than 20 and this will tell me if we're in a poor effective arterial blood volume state or a volume-down state, and from there that's kind of how I approach my diagnostics, instead of frequently calculating the FENa or FEUrea.
[Dr. Gutowski] Got it, so it's a tool, we can use it, but have to kind of take it in the larger context. [Dr. Maheshwari] Exactly. [Dr. Gutowski] So one more question for you, you mentioned CKD earlier, and I know our patient had a baseline creatinine of about 1. How would you compare a rise in creatinine from a baseline of 1 to 2 to someone with CKD who maybe has a baseline in the 3s that rises to 4?
[Dr. Maheshwari] Yeah, so that's a great question, especially because those jumps in numbers can look pretty significant and pretty scary. The way that I kind of think about it is what is the percentage deviation or increase from the baseline? So if you have somebody with normal kidney function, let's say they're coming in with a serum creatinine of 1 and something happens in the hospital so their serum creatinine is 2 the next day, similar to our current patient, that makes me very worried because the serum creatinine has increased by 100% and that drop in GFR can be fairly substantial.
Now on the flip side, if you have somebody who has a baseline serum creatinine of 3, or if you have somebody with very advanced CKD with a baseline serum creatinine of 5 and that creatinine goes up by 0.5 or 1, certainly that's a jump and that's something we need to think about and understand why did that happen, is that something we can correct and fix? But the change in the GFR is much less, so if you think about somebody who went from 5 to 6, for example, that's an increase in 20% of the serum creatinine rather than going from 1 to 2 of 100% and the corresponding drop in GFR is much less substantial as well.
And so in both cases, again, we need to work this up, but I am far more concerned about the rate of rise for that first patient that you had mentioned. [Dr. Gutowski] Got it. Makes sense, thank you. So let's get back to our case. We have a lot of potential contributors to this patient's AKI. She was hypotensive on arrival, she was septic, she was pretty dehydrated so total volume was down and she's been treated with broad spectrum antibiotics, including vancomycin.
Some of the additional studies that we got in the hospital are notable for a high urine sodium. There are muddy brown casts on her urine sediment and we got a renal ultrasound as well which shows no hydronephrosis. So putting all of this information together where does this leave us? [Dr. Maheshwari] Yeah, so you know this is a very challenging case and there's lots of potential contributions to this patient's acute kidney injury.
It's important to know that acute kidney injury, it's almost better to think of it as a syndrome rather than a diagnosis. And so this is a syndrome of lots of different nephrotoxic events or agents that are occurring. So we talked about the vancomycin, we talked about this patient who may be hypotensive, do they have a GN that's related to a post-infectious setting in the context of somebody who has endocarditis?
Are they volume-up and so therefore have a cardiorenal AKI as well? So there's lots of potential contributing factors here and so whenever you go into a scenario like this the first thing you want to do is try and remove whatever nephrotoxic events or agents that are impacting this patient. So the first thing I would think about, from a medication list standpoint is, we mentioned vancomycin, do we have any recent vancomycin levels?
Is there any reason for us to think that they've been dosed with high levels of vancomycin, especially in this patient who has a change in renal function? So the serum creatinine is a lagging marker of their true GFR, their true intrinsic renal function, and so the creatinine is 2 today, but it was 1 yesterday, and these were done at labs that were done at 600 in the morning and we're looking at them in the afternoon.
It's reasonable to think that it's already 300 by that time in the afternoon and how we're dosing our antibiotics, specifically to vancomycin. May be higher than it ought to be relative to what the true renal function is, and so checking antibiotic levels, and ideally, if we're able to find a different agent than vancomycin to treat this infective endocarditis that would be the ideal scenario.
Now if we think about volume status, if the patient is overtly volume-up or overtly volume-down, we can consider giving a trial of either diuretics or volume. If they're coming in very septic and hypotensive as soon as they get into the hospital, presumably they're volume-down in this case and we can give them a trial of fluids. If that helps improve their renal function, great.
We can always continue to judiciously give more volume and it gets to a point where they aren't improving any longer, then we can always stop and continue to reassess, as you mentioned previously, the physical exam is very important. Now in this case you mentioned that the urine sodium was high and there are muddy brown casts on the urine sediments, and so rather than a prerenal situation I would be thinking more about ATN or acute tubular necrosis.
There are two major pathways that lead to acute tubular necrosis, that's either a prolonged ischemia or a toxic ATN from nephrotoxic agents, such as vancomycin. And so again, in that same situation, making sure that they're no longer hypotensive, and so treating the underlying infection, using volume or pressors if needed to make sure that the patient's MAP stays over, classically 65.
And then again, we talked about removing agents such as vancomycin, NSAIDs, anything else that may be impacting them negatively. So that's kind of my initial approach and how I'd go about this. It's potential that the injury has already started to propagate within the kidney and even by taking all the necessary steps you may see the creatinine continue to rise over the next couple of days.
And that's kind of the unfortunate timeline or time course if you will, of this syndrome of AKI. [Dr. Gutowski] So in a lot of these patients we send them for imaging that requires contrast. What would you say about getting contrast in a patient like this? [Dr. Maheshwari] Yeah, so contrast, or specifically iodinated contrast, in terms of how it causes AKIs, is an ongoing area of discussion.
Generally speaking in patients that, first off, have normal baseline renal function, that aren't undergoing lots of other events, so usually not a sick patient in the hospital, giving iodinated contrast should not really cause any problems. In this patient, that is very sick, you are worried about some kind of contrast-induced or contrast-associated AKI that can occur as a result of giving iodinated contrasts for CTs.
Ultimately, it's a risk/benefit discussion. If you think that you really need to get the information in a timely manner that only a contrast-enhanced CT can provide, then that's something you have to do and you have to accept that risk. Ultimately, we can accept the risk of a patient whose kidneys continue to fail and may end up ultimately needing either temporary or permanent dialysis, but without the contrast CT, for example, you may not be able to diagnose a life-threatening infection, and so you do have to kind of have that risk/benefit discussion in the back of your head.
And so I don't want people to think that, "Oh, there's an AKI, we definitely can't use iodinated contrast for this CT," because then you may end up, unfortunately, causing increased morbidity or mortality in this patient. It's just another thing you have to keep in the back of your head. [Dr. Gutowski] Right, and I've definitely been on the side where I have to write a little note in the patient's chart that says, "We believe the benefits outweigh the risks." So that makes a lot of sense. You also mentioned dialysis, I remember learning a great mnemonic in med school for figuring out which patients need urgent dialysis.
You might know which one I'm talking about. [Dr. Maheshwari] Yeah absolutely, so I'm sure back in third year of med school you learn about the AEIOUs, which are a good mnemonic for thinking about dialysis indications. So briefly, A for acidosis, E for electrolyte abnormalities, I for intoxicants, O for volume overload and U for uremia. The important thing is to think about are these medically refractory indications, and so if you have a patient who's acidotic, they have a pH of 7.0 for example, are you able to give them bicarb or supplement or fix that acidosis in a way before they end up needing dialysis?
In the same way, when you think about electrolyte abnormalities, the number one thing that we most worry about is hyperkalemia, so if you have a potassium of 7-7.5, that's certainly concerning, but are there ways that we can temporize or even reverse that hyperkalemia without requiring dialysis? And so that's a very helpful mnemonic.
I just like to put that little asterisk at the end there that these are all medically refractory indications. I understand that in the future there's going to be an episode about renal replacement therapy so I won't go into the details about dialysis, but just to keep that AEIOU mnemonic in mind. [Dr. Gutowski] Thanks for taking us through that. We have talked a lot about all of the different potential causes of AKI in this patient and in any patient who we might find in the hospital.
Would you be able to leave us with a couple of clinical pearls as we finish up this episode? [Dr. Maheshwari] Yeah, absolutely. So I think when you first approach a patient with an AKI, or acute kidney injury, you want to think about your three buckets of prerenal causes, postrenal causes, and intrinsic renal causes of AKI. Secondly, thinking about what studies you have or what studies that you want to get.
What's useful, especially if you're calling nephrology, is getting some kind of renal imaging, that's usually a renal ultrasound. What's helpful is if you're going to get a renal ultrasound to get one with the bladder as well and you'll get bonus points if you get one with a post-void residual for us to understand if the patient is appropriately voiding and therefore do they have a recurrent cause of an obstruction, for example.
Other things that are helpful are getting the urine study, so urine electrolytes and urine osm as well. Getting a urine creatinine will be helpful for us to calculate things like the FENa, acknowledging all the limitations that we just discussed. And finally, urinalysis is also helpful to give us a sense of what else is happening in the kidney or in the urinary tract. Finally, if you have any questions, we're more than happy to help, so don't ever hesitate to reach out to nephrology, if possible after 700 am, but whenever is totally fine as well.
And then the most important thing is thinking about your AEIOUs when you're thinking about dialysis indications and that they're medically refractory. [Dr. Gutowski] Wonderful, well we've learned so much in this episode, so thank you so much for all of your instruction. [Dr. Maheshwari] It's a pleasure to be here, thanks Emily. [outro music] [outro music]
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