This is an important topic with the phases of acute kidney injury.
The fact that you’re even talking about phases automatically puts you in the realm of acute.
Keep in mind the timeframe, this is not RPGN,
this is not a chronic renal failure,
this is going to be beyond the three months, four months,
but this will be obviously less than years.
With acute kidney injury, what are the phases that we’re referring to?
At first, what you’re going to take a look at is literally the kidney is shocked.
Meaning to say, it is undergoing that initial inciting event of your acute kidney injury.
So this could include surgery, myocardial shock or cardiogenic shock, or hypovolemic shock,
so it’s many of those shocks that we’ve talked about
in which all of a sudden, the kidney is not functioning.
Next, urine osmolality here will be increased in prerenal
because aldosterone is removing and ADH is removing the fluid.
You expect your urine osmolality to be increased.
There’s a picture of prerenal.
Okay, let's say now the prerenal is causing intrinsic damage to the kidney,
you call this what? Renal azotemia.
If it’s renal azotemia, then you’re thinking about the phases that we just walked through.
The initial inciting event, that’s your initiation phase
and the maintenance phase kind of looks like chronic renal failure.
Now, what does this mean?
The tubular epithelial cells are dead, they’re not working properly.
These cells at some point maybe then start sloughing into the urine,
so you’re gonna find what kind of cast?
Good, you’re gonna end up having your tubular epithelial granular cast.
If it gets really bad, maybe muddy brown type of cast, correct?
If the tubular epithelial cells are not working properly,
then are you able to properly reabsorb urea? You cannot.
If you lose the numerator like crazy, then what then happens to the ratio?
Take a look please in acute renal failure or acute kidney injury,
and if it’s an intrinsic problem, you’ll find your BUN/Creatinine ratio,
the bottom row here being decreased less than 15.
I told you earlier that if you find your azotemia to be decreased,
I can guarantee you is that you do have kidney problems,
down or decreased BUN/Creatinine ratio, decreased kidney function.
Next, is that the most reliable? No, here, fractional excretion of sodium.
So now the tubular epithelial cells are not working properly
and so therefore, can the aldosterone properly work to remove the sodium?
No, it cannot.
And so therefore, what then happens to the fractional excretion of sodium?
You’ve lost a normal homeostatic mechanism reabsorption,
you’re gonna have an increase in fractional excretion of sodium.
The magic number? Greater than 2%.
Understand the concept and then, you take a look at the value and memorize.
Okay, now here, you’ll find an increase in urine sodium greater than 20,
the urine osmolality here, once again, you cannot properly concentrate the urine
because the tubular epithelial cells are dead
and therefore, it will be decreased urine osmolality.
So far, we have two phases.
Say that you’re able to properly take care of the perfusion as such
and you’re able to reestablish this, now what?
Well, that’s the question that you wanna ask.
Right before I go on, you’ll notice please at the bottom of this table
that I have not placed postrenal on purpose
because with postrenal, the symptoms will be obvious.
I gave you BPH, maybe there’s a kidney stone, whatnot,
and so therefore, they’ll be back up
and you can expect there to be perhaps hydroureters or hydronephrosis
and expect your BUN/Creatinine ratio to be elevated.
The only time that you’d find your BUN/Creatinine ratio to be decreased
would be with, good, renal or intrinsic azotemia.
Let’s go into its last little phase now.
Okay, so you reestablished your perfusion and now, well, the kidneys are regenerating.
Can they? Yes, you can.
Now, these are - your tubular epithelial cells are quiescent cells.
They’re quiet, stable cells.
When asked to be recruited,
they will move from G0 into the G1 phase of your cell cycle, won’t they?
Yes, they will.
So now, you’ve allowed for the cells to regenerate
and as they do so, guess what happens?
Oh my goodness gracious, your kidneys are so happy.
It’s like a dog walking through the wilderness and what is it doing?
Urinating everywhere, it’s marking its territory.
This is now welcome to your human marking.
So in other words, you’re going to have massive recovery phase.
If you had maintenance phase where in oliguria,
you weren’t producing as much urine and you had hypervolemia and hyperkalemia,
in the recovery phase, I’m so happy,
I’m urinating everywhere and you end up having hypovolemia, and you have hypokalemia.
Are we clear?
Once again, I don’t think I could be any more dramatic.
So you have increased urine volume during the recovery phase, look at this.
Three liters per day is how much you’re losing? That’s polyuria.
You have hypovolemia, hypokalemia,
compare this to the maintenance phase and restoration of renal function
but it’s very difficult for you to get back to 100%,
but pretty darn close, though, pretty darn close.
Now, the outcome depends on the underlying cause
so if there is let’s say your congestive heart failure and you give a positive inotropic agent,
you’re able to reestablish your profusion, guess what?
Hopefully, you’re able to catch your patient in acute kidney injury
and so therefore, reestablish and go through initiation phase,
maintenance phase, and recovery phase.
Treatment, rather supportive, meaning to say, dialysis,
and then here once again, we’ve gone through the table here of prerenal and renal azotemia.