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.
Students tend to get confused with uremia and azotemia.
Uremia is the clinical manifestations of renal failure
and I just gave you metabolic acidosis, hypocalcemia, so on, and so forth.
Whereas, azotemia is something that you could actually measure.
Azotemia, you need to think of this as being a disturbance in your BUN/Creatinine.
Azotemia is a clinically significant increase in the blood urea nitrogen, or BUN
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.
The big fat arrow that you see there in red is your blood urea nitrogen.
That little blue narrow arrow that you see there is referring to creatinine.
Okay, now, you tell me about the normal properties of your BUN/Creatinine.
Close your eyes. Both are arriving through the afferent arteriole to the glomerulus.
Will both of these be filtered? Yes, they both will be filtered.
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.
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.
Take a look at the right side here.
You see BUN over creatinine, and this is the ratio that you’re paying attention to.
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.
And what does this indicate to you? This is prerenal azotemia.
I told you this may lead into kidney damage.
Would you tell me what one of the most common causes are
of acute kidney injury, AKI, or acute renal failure? Ischemia.
So if there’s decreased cardiac output, doesn’t that mean decreased perfusion?
Doesn’t that mean ischemia? Of course, let’s move on.
So, continuation, let’s say that your patient has decreased cardiac output,
maybe hypovolemia, decreased perfusion to the kidney.
At some point, what’s gonna happen?
Oh, there’s going to be a kidney damage.
So one of the - you’ll see this and you read this, and you might be told this.
One of the most common causes of renal azotemia
which is my topic here is prerenal azotemia.
So now, say the perfusion as decreased,
you have ischemia who’s going to be affected? The tubular epithelial cells.
You focus on the filtrate please.
You see that? The filtrate, so acutely, are substances being filtered.
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.