So, when our patients present to us with a pre-renal
picture, we want to really be able to diagnose them.
We wanna be able to
do our diagnostic workup.
So, as a good detective as we are as internist, we're going
to want to take our patient history and chart review
and really look and see if that patient has had
any significant history consistent with this.
Have they been having emesis, diarrhea, things
that would make us think about a gastroenteritis,
any history of GI bleeding, or
do they have a known history
or are we diagnosing them with heart failure,
liver failure or portal hypertension and sepsis.
On physical exam, there's some signs
that can be very helpful to us.
Does our patient have orthostatic hypotension
or skin tenting, dry mucous membranes?
These tells us that the likelihood
of hypovolemia is very high.
How about our patients who have a low effective
arterial blood volume but their total ECF is expanded?
These are our edematous states.
This is a beautiful picture of
our patients, who have heart,
a patient with heart failure who has
an elevated jugular venous pressure.
That's really indicative of a patient
having something like heart failure.
So, how about a laboratory workup?
It's important for us to look, there are
some clues that are very simple on labs
that can help us to determine whether our
patient might be more suggestive of a pre-renal hit.
This includes looking at our BUN and
creatinine and the BUN to creatinine ratio.
So when we see a BUN to creatinine
ratio of greater than 20 to 1,
then that really indicates that perhaps
this patient has a pre-renal hit.
And a reason why that happens is
because remember, this is a reversible injury,
our tubules are still working.
And because you have a reduction
in GFR, you've got stasis of urine,
so you're really able to reabsorb more urea and so
you tend to have a higher BUN to creatinine ratio.
The urine osmolality tends to be
high - greater than 500 mosm/kg.
Why is this?
We just said that remember, autoregulation
is really helping us by enacting ADH.
We wanna conserve our
volume as much as possible.
So ADH is going to be active allowing us to
reabsorb waterin order to expand that vascular space
and in so doing, leaves us
with a very high urine osmolality.
Our urine sodium is going to be
very low as well as urine chloride.
Why is that?
Because remember, we just talked about how
the RAAS system, Renin-Angio-Aldo system is activated.
Angio II is activating not only
at the efferent arteriole but also,
it's having an effect on
increase in sodium reabsorption.
Aldosterone is being activated in
order to increase sodium reabsorption
and again we're doing this so that we
can really preserve our vascular volume,
leaving us with a very
low urine sodium chloride.
On urine analysis, we'll see a high specific
gravity, no protein or blood or white blood cells.
And as a nephrologist, when you
have me consult on your patient,
then I will actually look at the urinary sediment
and I will see that it shows nothing significant,
there are no casts and no cellular activity.
And just aside so you'd understand what that means is
that, when patients develop any kind of kidney injury,
it's important for a nephrologist to take a look at
that urinary sediment underneath the microscope.
There are so many different clues that are very helpful
on the diagnosis of a lot of different diseases.
So essentially, we take 10 ml of urine,
we spin it in a centrifuge at 3000 rpm,
we then take the supernatant, decant it and then
resuspend that pallet and using a transfer pipette,
we can look at that underneath the
microscope at both 10x and 40x magnification.
And there are many clues in
there whether they are casts or cells
that can lead us to a correct
diagnosis with our patients.
Another helpful test in the diagnosis
of our patients with pre-renal disease
is something called the fractional
excretion of sodium or FENa.
FENa measures the percent of
filtered sodium excreted in the urine
and it's really used to differentiate between
pre-renal disease and acute tubular necrosis.
And I wanna just take a moment to really
underscore that and say that one more time,
it's used to differentiate between pre-renal
disease and acute tubular necrosis.
It is not used to differentiate between pre-renal
disease and all intrinsic renal diseases or post-renal.
It is really just between pre-renal and ATN, so please
keep that in mind when you're using this formula.
It's estimated by simultaneously obtaining the urine
and plasma specimens of sodium and creatinine
and you can see the formula there in which
we use in order to actually obtain FENa.
But really what's important for you is to understand
that a FENa of less than 1% in pre-renal diseases
indicates that the patient most likely will be responsive
to volume or correcting their hypovolemic state.
A FENa that's greater than 2% is
going to be most common in ATN
and we're going to talk
about that in just a moment.
Another thing to keep in mind is that
this is best to use when patients are oliguric
because that's really what this test was
predicated on when it was first developed.
So, when our patient comes to us and we've
diagnosed them with pre-renal disease,
how do we treat our patients in order to
return their kidney function back to normal?
In a sense of true volume depletion,
it's fairly easy and intuitive.
We simply want a volume expand them and
we can do this if they have true volume depletion
with a crystalloid, something
that's isotonic to their osmolality.
So normal saline would be great or lactated
Ringer's which is a little bit more physiologic.
We can use both of those fluids
to correct their hypovolemia.
In a situation where our patient has a
decrease in effective arterial blood volume,
remember that's those edematous states
that we were talking about earlier.
It's really important to target
the underlying condition.
So in this situation of our
patient who has heart failure,
we really wanna correct their cardiac
hemodynamics and we can do this with diuretics
and if our patient is so volume
overloaded with their heart failure,
that they're off of the Starling curve,
the heart really can't pump effectively,
we can actually mobilize
volume off their body with diuretics
and we can actually get an
increase in the ejection fraction.
So that can be very helpful.
We wanna perhaps treat those patients
with vasodilators and afterload reducers.
And again, if our patient has an
organ perfusion that's impaired,
using something like inotropes
would be very important.
In our patients who have portal
hypertension and liver failure,
we wanna provide them with some
kind of oncotic pressure like albumin
in order to help again
with renal artery perfusion.
Because they have splanchnic dilatation and they
have a decrease in peripheral vascular resistance,
it's also important to use things like midodrine
or norepinephrine if our patients are in the ICU
and that really helps with
their systemic hemodynamics.
And then finally in our septic patients, we really
wanted to treat them with goal-directed therapy.
So we want to volume resuscitate them with crystalloid
usually at 30ml/kg within the first 3 hours
and then we want to use broad spectrum
antibiotics and vasopressor support
in order to again support their hemodynamics
and increase renal artery perfusion.
Okay, so we just finished pre-renal disease and
the take home points that I'd like you to remember
is that this is a reversible
injury that can get better
once you increase renal
perfusion back to the normal state
either with volume or by
correcting the underlying cause.