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Acute Kidney Injury (AKI): Staging and Etiology

by Amy Sussman, MD

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    00:01 Hello and welcome to the next lecture in your nephrology curriculum.

    00:05 Today, we're gonna be talking about acute kidney injury which is very near and dear to my heart as a nephrologist because it's something that I see everyday And it's something that you're going to encounter in your professional life as you take care of patients.

    00:20 So acute kidney injury is defined by the abrupt loss of kidney function, retention of urea and other nitrogenous waste products as well as the dysregulation of extracellular volume and electrolytes.

    00:32 Before we move on though, there's some important terms that I really want you to understand so you can better understand the cases that we're going to be talking about.

    00:40 The first is creatinine.

    00:43 Creatinine is a breakdown product of creatine phosphate in muscle.

    00:47 It's filtered completely by the kidney and it's not metabolized and therefore is used to estimate kidney function and filtration.

    00:55 It does have an inverse relationship to function meaning that the higher the creatinine is, the lower the GFR or filtration rate is.

    01:04 You will also hear the word BUN or blood urea nitrogen.

    01:08 So urea nitrogen is formed from the protein catabolism by the liver.

    01:13 It's filtered by the kidneys and it's used as an additional measure of kidney function.

    01:18 Although a high BUN generally reflects lower filtration, there's some caveats when it comes to BUN and it can increase independently of kidney function.

    01:27 This includes things like glucocorticoids or steroids when our patients are on steroids, tetracycline antibiotics or reabsorption of blood from the GI tract.

    01:38 In each of those instances, the BUN may rise and the creatinine might be normal as well as kidney function.

    01:44 So do keep that in mind as we're talking about BUN.

    01:48 Oliguria is another important term to know.

    01:52 Our patients are commonly oliguric when they develop acute kidney injury and this really means that our patients are producing less urine.

    02:00 Typically, it's defined as less than 500 ml of urine output within the 24 hours but do keep in mind there are a few definitions that will define oliguria as less than 400 ml in the 24-hour period of time.

    02:12 Finally, there's anuria.

    02:14 Anuria is defined by less than 100 ml of urine output in the 24-hour period of time and this is essentially one of the worst signs of of acute kidney injury because our patients are essentially not producing any urine.

    02:29 If you remember nothing else from this lecture, do remember that acute kidney injury is significant.

    02:35 In our critically ill patients who develop AKI, their mortality is increased between 40 to 60% at 60 days and their hospital stay is prolonged.

    02:46 Part of the reason why it's been so difficult in order to care for and treat these patients is because it took forever to develop criteria in order to define what AKI is and to stage AKI in order to develop therapeutic targets in this population.

    03:01 So finally, in the early part of the 2000's, the acute kidney injury network came up with staging criteria and this is based on absolute creatinine, a change in serum creatinine, and reduction in urine output.

    03:15 So beginning on stage 1, this includes a creatinine increase of greater than 0.3 mg/dL.

    03:24 That's really significant because of the fact that if you think about a patient whose creatinine goes to 0.7 (mg/dL) to just 1.0 (mg/dL) that means that that patient has developed AKI and when you look at that particular patient, their mortality is increased.

    03:39 We also look at the urine criteria as well, so less than 0.5 ml/kg/hr over a 6-hour period of time.

    03:47 Stage 2 is an increase in creatinine of 2 to 3 times normal and then again, a reduction in urine output over the 12-hour period of time.

    03:56 And finally stage 3, where patient's serum creatinine is increased 3 to 4 times that of normal or a serum creatinine greater than 4 mg/dL with at least an acute increase of at least 0.5 mg/dL and these patients oftentimes are anuric.

    04:14 The higher the stage, the worse the outcome.

    04:18 So, it's great that we have a staging system however there are some caveats that we need to think of.

    04:24 So despite having the consensus for defining and grading AKI, it still is based on serum creatinine and urine output, and these two are really imperfect biomarkers And again, if I'm talking about a biomarker, I'm talking about a biological marker for organ injury.

    04:41 Why is this? Because when the serum creatinine rises or urine output decreases, already substantial injury has taken place to that patient.

    04:50 It diminishes, if you think about that, the ability to begin treatments aimed at preventing the loss of renal function.

    04:57 In the low, we have had development of novel biomarkers.

    05:01 There's things like NGAL, kidney injury molecule 1, or NAG, they're not ready for prime time yet and we're not using them commercially in the US at this time.

    05:12 So, let's kind of think about this in a more conceptual fashion.

    05:17 If we have a patient that's coming in, but there's something about that patient during his hospitalization that increases their risk for acute kidney injury, that makes them susceptible.

    05:27 It might be because they have advanced stage.

    05:30 They might be hypovolemic, they might have diabetes mellitus, or they might be on medications like non-steroidal anti-inflammatory drugs which impair autoregulation.

    05:41 An insult occurs to that patient that creates acute kidney injury and this is where we should be looking at our biomarkers to detect that something's happened.

    05:52 But instead, what happens? it actually takes a substantial amount of time for GFR to decrease and our patients really aren't manifesting to us as being injured until they already have kidney failure.

    06:05 So it's really when they have complications of their chronic kidney disease are they coming to our attention.

    06:11 And you can see now how having creatinine and urine output as biomarkers are just inadequate when it comes to defining when kidney injury happens so that we can actually develop therapeutic targets to help our patients at the time that they need it rather than just taking care of complications from their AKI.

    06:30 So, let's move on to thinking about the etiologies of different types of acute kidney injuries and I think from our first year of medical school, everybody could really think about the 3 main categories that you've been taught since day 1.

    06:43 Which are really pre-renal, this includes things like volume depletion and a decrease in effective arterial blood volume.

    06:50 Intrinsic renal disease, and then this is separated or I'd like to separate them by different compartments of the kidneys.

    06:57 This includes the tubules and interstitium.

    07:00 That includes acute tubular necrosis, acute interstitial nephritis, acute tubular obstruction, the vascular compartments so any kind of vascular disease and of course my very favorite which is glomerular disease.

    07:11 And then finally, the post-renal category which means that there's urinary obstruction anywhere from the renal pelvis to the urethra.


    About the Lecture

    The lecture Acute Kidney Injury (AKI): Staging and Etiology by Amy Sussman, MD is from the course Acute Kidney Injury (AKI) (Quiz Coming Soon).


    Author of lecture Acute Kidney Injury (AKI): Staging and Etiology

     Amy Sussman, MD

    Amy Sussman, MD


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