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Disturbance of Acute Renal Failure

by Carlo Raj, MD
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    00:01 Alright, now, there is a particular topic here and you’ve heard of this before but you’re not maybe quite sure as to when to use it, how to use it, and do you use it every single time? Well, I want to now clarify and elaborate on your usage of azotemia.

    00:21 Okay? Azotemia.

    00:23 Students tend to get confused with uremia and azotemia.

    00:27 Uremia is the clinical manifestations of renal failure and I just gave you metabolic acidosis, hypocalcemia, so on, and so forth.

    00:34 Whereas, azotemia is something that you could actually measure.

    00:38 Azotemia, you need to think of this as being a disturbance in your BUN/Creatinine.

    00:44 Disturbance, the ratio.

    00:47 So, when would you think about using this? You in your journey in where you are with your medical education, you wanna only use this for acute, is that clear? You don’t wanna use azotemia for chronic and the reason for that is because in chronic, you’re going to have many, many, many other signs and symptoms in which you can easily identify your patient as having chronic renal failure.

    01:11 If it’s acute however, you do wanna start thinking about using this.

    01:15 You will.

    01:17 Now, what does it mean in terms of disturbance? Let me walk you through the picture so you’re clear about what you’re seeing and the characteristics of two major components.

    01:26 The big fat arrow that you see there in red is your blood urea nitrogen.

    01:31 That little blue narrow arrow that you see there is referring to creatinine.

    01:35 Okay, now, you tell me about the normal properties of your BUN/Creatinine.

    01:39 Close your eyes. Both are arriving through the afferent arteriole to the glomerulus.

    01:46 Will both of these be filtered? Yes, they both will be filtered.

    01:50 Of the two, creatinine and BUN, which is only reabsorbed? Good, blood urea nitrogen, we had a huge discussion, we talked about creatinine why it is never reabsorbed.

    02:03 If anything, it is slightly secreted, is that clear? Next, so if you are now reabsorbing BUN, blood urea nitrogen, the ratio is BUN over creatinine.

    02:16 Take a look at the right side here.

    02:18 You see BUN over creatinine, and this is the ratio that you’re paying attention to.

    02:23 Now, what I’m showing here is a pathology, but know that 15 is approximately normal, 15.

    02:30 So what is occurring in this picture of acute kidney injury in which it’s causing damage to the kidney but - or may lead into.

    02:42 Once again, it may lead into causing damage to the kidney, quite common, but not quite yet.

    02:49 And what is the pathology that we’re looking at here? This is called prerenal azotemia.

    02:55 Prerenal azotemia is my topic.

    02:59 For example, say that you have congestive heart failure, decreased cardiac output, maybe there’s hypovolemia. Okay? So if it’s hypovolemia or decreased cardiac output, you can expect there to be decreased perfusion to the kidney, right? Exactly. And is this before the kidney? Yes, prerenal.

    03:17 Now, you walk me through this.

    03:19 BUN/Creatinine, is it being filtered? Yes, it is.

    03:24 But at what rate compared to normal? If the perfusion is slower and you don’t have as much perfusion to the kidney then you don’t have as much being filtered.

    03:35 So there’s more remaining within your capillaries in your arterioles.

    03:41 You go to the efferent side, there’s a little bit more of your BUN.

    03:45 Now, of these substances that are being filtered, a little bit of BUN, a little bit of creatinine, of the two, which is the only one that is being reabsorbed? Once again, BUN.

    03:58 If your BUN is the only component of that ratio that’s being reabsorbed, where is my BUN in the ratio? Oh, it’s on the numerator.

    04:07 Good, so if you continue increase in numerator, numerator, numerator, numerator, concept.

    04:13 What happens to the ratio? I can help you here.

    04:17 It’s an increased ratio, isn’t it? So that increase in ratio, you must then memorize, is greater than 20, maybe perhaps up to 30.

    04:25 And what does this indicate to you? This is prerenal azotemia.

    04:30 I told you this may lead into kidney damage.

    04:34 Would you tell me what one of the most common causes are of acute kidney injury, AKI, or acute renal failure? Ischemia.

    04:43 So if there’s decreased cardiac output, doesn’t that mean decreased perfusion? Doesn’t that mean ischemia? Of course, let’s move on.

    04:54 So, continuation, let’s say that your patient has decreased cardiac output, maybe hypovolemia, decreased perfusion to the kidney.

    05:02 At some point, what’s gonna happen? Oh, there’s going to be a kidney damage.

    05:07 So one of the - you’ll see this and you read this, and you might be told this.

    05:12 One of the most common causes of renal azotemia which is my topic here is prerenal azotemia.

    05:18 Okay, so if it’s renal azotemia, what is this referring to and how do you wanna use this clinically for the sake of time? Acute only, do not use this for chronic, why? I’ll show you.

    05:32 In chronic renal failure, you’ll have a host of other signs and symptoms where your patient, it will be obvious that he or she is suffering from CRF.

    05:41 With AKI, well, not so much.

    05:43 So now, say the perfusion as decreased, you have ischemia who’s going to be affected? The tubular epithelial cells.

    05:52 You focus on the filtrate please.

    05:55 You see that? The filtrate, so acutely, are substances being filtered.

    06:01 Sure, they are, but if they are being filtered and the tubular epithelial cells are dead, are you able to properly reabsorb your BUN? No, you’re not.

    06:13 And so therefore, if your numerator continues to drop, drop, drop, drop, drop with my concept, the ratio decreases, less than 15.

    06:24 To make your life easier, anytime that you get a question where your azotemia referring to BUN/Creatinine ratio is decreased, guaranteed, it's intrinsic or renal azotemia.

    06:37 If you find your BUN/Creatinine ratio to be elevated it will either be prerenal and I'm not covering postrenal, and the reason for that is because as we move on to other lectures, we talk about what’s known as nephrolithiasis or renal stone, that’s obstruction.

    06:56 It will be so obvious to you that your patient has obstruction.

    06:59 Maybe it’s a 72-year-old male and he goes to the bathroom, he goes to the bathroom, he goes to the bathroom, and he keeps going frequently, and every time he goes, he’s not able to properly void.

    07:08 Diagnosis, good, BPH.

    07:11 Is that obstruction? Oh, yeah.

    07:13 What about calcium oxide stones? Obstruction.

    07:17 The point is there, you also find an increase in BUN/Creatinine but all I’m gonna do is have you work through azotemia only for prerenal and renal.

    07:27 Understand those, you’ll be in good shape.

    07:30 The only thing that you’ll need to add in here is something called fractional excretion of sodium which is a heck of a lot more reliable than your azotemia or BUN/Creatinine ratio.

    07:41 But this is how you use it.


    About the Lecture

    The lecture Disturbance of Acute Renal Failure by Carlo Raj, MD is from the course Tubulointerstitial Diseases.


    Included Quiz Questions

    1. The BUN-creatinine ratio is always elevated in acute kidney injury.
    2. It refers to the laboratory measurement of blood urea nitrogen.
    3. It is not useful for diagnosing disease of only the glomerulus.
    4. BUN:Cr ratio of 15 is approximately normal.
    5. It should only be used to assess acute kidney injury not chronic kidney failure.
    1. BUN:Cr ratio > 20-30
    2. BUN:Cr ratio 10-20
    3. BUN:Cr ratio can’t distinguish between pre-renal and intrinsic azotemia.
    4. BUN:Cr ratio ~ 1
    5. BUN:Cr ratio <15
    1. Creatinine is slightly secreted.
    2. Creatinine is completely reabsorbed.
    3. BUN is not freely filtered.
    4. BUN is never reabsorbed.
    5. BUN is slightly secreted.

    Author of lecture Disturbance of Acute Renal Failure

     Carlo Raj, MD

    Carlo Raj, MD


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