Hello and welcome to the general approach
to a patient with acute kidney injury.
Today we'll be discussing
an algorithm of acute kidney injury,
which really builds off our kidney lecture
so when our patient is sitting here before
us, how do we approach them?
And we think that they may have an acute
One of the first things
that we really have to ask ourselves
is, does this patient satisfy
one of the kidney disease improving global
outcomes or CODIGO criteria
for diagnosing acute kidney injury?
This includes an increase
in serum creatinine.
So believe it or not, an increase of just
0.3 milligrams per deciliter
or more within a 40 hour
period of time is suggestive of AKI,
as well as greater than 50% increase
in serum creatinine within seven days.
So looking at serum creatinine, it's
very important and knowing the time
course of which the patient is at risk.
Now, we also want to look at urine output
and having an acute decrease
in urine output of greater
than 0.5 milliliters per kilogram per hour
for greater than 6 hours
is also suggestive of A.I.
So it's important for us to both note
the serum creatinine as well as the urine
output in our patients in order to fully
be able to diagnose kidney injury.
Now, what is our next step
in looking at the patient?
This is a really fun part of medicine
because this is where we get to be
We're really looking at how
to take a good history in our patients.
So for example, if I'm thinking
my patient has an effective pre
renal state or pre renal as a team Mia,
I'm really looking for episodes where
they might have prolonged hypotension.
This means when they have a decrease
in perfusion to the kidneys and other
I might see this in patients
who are in shock, either basal dilatory
shock from sepsis or cardiogenic shock,
or perhaps in hemorrhagic shock after
I might see this in my patients
who have heart failure
or Cardiorenal syndrome,
and I may see this in patients
who are volume depleted when they're
just not getting enough intake
to actually perfused their vital organs.
I mean, I also see the situation
a bit because of medications
or neurotoxic exposures.
This would include things
like radio contrast exposure.
This is a type of media that we use in CT
scans or angiograms,
and it can be extremely toxic
to the tubular portion of the kidneys.
Now, we don't always see this acute
tubular necrosis for me,
a contrast exposure is somebody
who has underlying chronic kidney disease
or an elderly patient
who is coming in with volume depletion
or in a diabetic with underlying CKD
These patients are
at very high risk
when exposed to angiographic procedures
once the injecting ratio contrast
into the arterial circulation
and that will be toxic to the kidney.
It causes basal constriction
as well as tubular toxicity.
Acute tubular necrosis in our patients
We also discuss medications
being toxic as well.
These include things like aminoglycosides,
a very effective antibiotic,
but at the same time
it can cause acute tubular necrosis.
We see this with Amphotericin,
a very effective antifungal agent,
and we also see this with medications
such as NSAIDs,
which are infamous
for impairing auto regulation.
So it can turn a situation
that may have started out as an effective
pre renal state into something
that develops into tubular injury
because of the prolonged ischemia changes.
We can also see things like a
cycle of year that when given cause intra
tubular crystal precipitation or I.V.
methotrexate, where that medication again
and the volume depleted
patient can actually crystallize
within the tubules of the kidney
We call that intra tubular obstruction.
Now, I'm also looking for medications
that might be involved in the immune
response that the kidneys can see,
like an allergic interstitial nephritis
These include medications
and NSAIDs can cause this as well.
And I also see this
sometimes with proton pump inhibitors
these are medications
that when taken, patients
actually develop an immune response
that can manifest with the type one
or type four hypersensitivity reaction.
And when we end up with allergic
these patients oftentimes will manifest
with white cells in their urine.
And we'll be talking about
that a little bit later.
Now, the next thing we want to do
is do a physical exam and remember
how important physical exams are.
These are the signs that can really point
us to the right diagnosis.
So our patient oftentimes holds
all these answers.
The first thing I really like to do is to
estimate the volume status of my patient.
I look at things
like their neck in their face.
What does spectacular venous pressure
Do they have flat neck veins?
Do they have poor skin trigger,
or are they orthostatic
when they stand up,
or do they have hypertension?
This would lead me to believe
my patient is volume depleted
Do they have very plump neck veins
and elevated jugular venous pressure?
Do they have peripheral edema?
Am I thinking that my patient is
perhaps in heart failure?
That helped me to diagnose
maybe a Cardiorenal syndrome?
I also want to look for skin lesions
that can help me.
These include things like rashes
that we can often see
who have allergic interstitial nephritis.
Now, I'm not always lucky enough
to see that because of the full triad
interstitial nephritis, and the rash
only happens in about 10% of cases.
But if I see a drug reaction,
if I see a temporal correlation
with the drug and X and some of the drug
rash, perhaps peripheral eosinophilia
and a fever, I'm thinking about allergic
The other skin lesions that may help me
is the patient who has undergone
and aortic manipulation
or they've had some kind of procedure
where they have either injected dye
some kind of procedure to the aorta or
different arteries can actually dislodge
a large amount of cholesterol crystals
into their circulation.
So, for example, if my patient had
an endovascular repair of a triple AA,
then in that case
those adenomatous crystals or cholesterol
crystals cannibalized distally
and end up in the arterials
that cause renal disease just as they do
with glomerular circulation.
They can do the same in skin circulation.
So we may see skin lesions
that appear caused by
microvascular ischemic changes
from arterial occlusions
caused by these cholesterol crystals
that are embolization.
When I see that in the setting
of maybe four to six weeks ago,
my patient underwent in audit procedure.
This may guide my thinking.
Now, in addition to our physical exam,
for us to image our patients
so we can really see
what's going on in our patients
who have the acute kidney injury.
If I'm worried about my patient
having a post renal situation
where they have obstruction
of the urine, anywhere from the renal
pelvis to the urethra, then imaging can be
a very powerful tool
for me to really clinch that diagnosis.
I can do something
simple like an ultrasound
when I can actually define
the structural anatomy of the kidneys.
And if I see something like hyperhidrosis
where I see dilatation
of the pelvic system from urine
that's backing up into the renal pelvis
and actually the cortex,
this tells me I may have obstruction.
It could be from somebody
with an enlarged prostate like BPH
or it could be from an obstructive stone
or an obstructive lesion.
If I'm worried about
a stone disease in my patient,
I may want to get a non-contract CT scan
to actually look for that intense density
where I can actually see the obstruction
of urine outflow from a stone
or compression of the ureter from a tumor.
So imaging can be very powerful,
particularly in situations
where we're looking for post renal causes.
Now, the most important
thing is really looking at the urine
because oftentimes it holds
many of the answers one's looking for.
One of the first things I like to look at
for a patient when I'm considering,
does this patient have an effective pre
renal state or have they had
an episode of prolonged volume depletion
or they've developed ischemia?
The test that may help me is called a FINA
or fractional excretion of sodium.
It can be very helpful
because of what it tells us is
are the tubules intact
and are the T-bills able to function?
If we're an effective pre renal state,
remember, our body is trying to hold on
to all of the volume that it can in order
to produce the vitals.
The renin angiotensin system
is going to be activated
when RAAS is activated, we are going
to reabsorb every bit of sodium possible.
So we look at the fractional excretion
It should be extremely low.
It's less than 1% in
someone who is effectively pre renal
and trying to hold on to volume.
But the tubules are still functioning.
This tells me the state
my patient is in now.
Let's say my patient has a history
of an effective pre renal state,
but they have had volume depletion
and a prolonged hypertensive state
for such a long time that they've
now developed injury to the tubules.
They may now have ATN in that situation.
The Tubules are no longer
and even though the RAAS is trying to be
activated, it's not going to effectively
work on the kidneys.
And therefore I'll see sodium.
These tubules cannot reabsorb the sodium
because they're injured in this situation.
My figure is going to be greater than 2%.
And remember that less than 1%,
our patient is pretty renal.
They may be responsive to volume or we may
have to look at Cardiorenal syndrome.
We have to correct their
underlying cardiac function.
Now, in addition
to looking at the FINA, I really want to
look at the urine analysis.
The US or urine analysis are so important
because they tell us
whether there's protein
blood of cells in the urine.
So just getting a routine urinalysis,
either from a dipstick or from the lab,
I can see whether my patient
has proteinuria or hematuria.
If I see that I'm really thinking about
glomerular disease and nephritis syndrome.
If my patient has leukocyte estimates
or white blood cells or nitrates,
that's really helpful and suggestive
of a cute pyelonephritis
or some kind of urinary tract infection.
So even just looking at the dipstick
alone is very important
and can give me some answers.
Now, one of my favorite things to do
is actually look at the urine
underneath the microscope
because again, there's
so many different things in there that can
really help me clinch my diagnosis.
It's very satisfying,
and I know how to treat my patient,
like to do a microscopic exam, take ten.
Most of the patient's
urine, centrifuged it
at about 3000 RPMs for 5 minutes
and then decant the supernatant.
I can take an actual pellet
and resuspended that and look at that
on the slide underneath the microscope
at ten X or 40 X power.
When I do that, I see all sorts of things
that are help me to diagnose my patient.
If I see crystals such as uric acid
crystals, I might think my patient
has a gout nephropathy
or even something like tumor
lysis syndrome, where they just have
the rate that it's building
up, causing obstruction in the tubules
I may see calcium crystals in there
that would suggest that my patient
has a calcium oxalate stone,
which is one of the most common stones
seen in our patient population
or it could be something like ethylene
that leads to calcium
oxalate stones in the urine as well.
So again, you're very, very powerful
in these situations with this information.
Now, probably what I see most commonly,
it is going to be muddy
or evidence of acute tubular necrosis.
And this is exactly what it looks like,
these beautiful cylindrical shapes
Of course, regular pigmented casts,
also called Muddy Brown cast,
really represent what's happening
with acute tubular necrosis.
So think about this as the tubular
epithelium is getting injured.
It undergoes apoptosis or necrosis.
When those cells are apoptosis,
they get picked off
from the underlying basement
membrane and collect in the tubules
where they combine to form
this beautiful cylindrical cast
that is pigmented
with a granular appearance.
Those are then
degenerated tubular epithelial cells.
And when I see this in a patient,
I'm really thinking this patient has 18.
In my armament for diagnostic testing,
I may even be lucky enough
to see a free
floating, tubular epithelia cell intact.
And when I see that,
I'm really thinking about ATM.
we also see white cell casts.
if you look here at this picture,
you can see the beautiful
cylindrical shape here with the intact
white blood cells embedded
right into the cylinder or into the cast.
These are called white blood cell casts.
And again, what happens in patients
who have inflammatory lesions
such as allergic, interstitial nephritis
or even in pyelonephritis,
these white blood cells
will collect in the tubule and they can
bind with the urological protein
and we get these cylindrical shaped casts.
So in white blood cell carcinoma,
we can also see that in the urine,
I think about this
in the absence of bacteria.
But in the presence of bacteria,
I think of some sort of infection
or interstitial nephritis.
These are red blood
cell casts and dysmorphic red blood cells
in the left hand part of the slide.
So if you
look at the very left of the slide,
we have beautiful red blood casts.
This is going to occur
in the setting of nephrotic syndrome.
So again, red blood cells that collect
within tubule lumen will combine
with the urological proteins and form
these beautiful cylindrical casts.
You can see that
they have intact red blood cells
and a little bit of brownish red hue.
And that tipped me off
that this is in fact a red blood cell.
Sometimes I'm not lucky enough
to see these red blood cell casts,
but what I will see
are these dysmorphic red blood cells,
and that's pictured
in the middle of the slide.
And what happens is in these
nephrotic syndrome patients,
these red blood cells traverse
the glomerular basement membrane.
And as they do this, they become to form
and develop blood on their membrane.
This is what you can see here.
Now, interestingly, the top right corner,
you see what looks like a Mickey Mouse.
We sometimes refer to these affectionately
as Mickey Mouse cells
that we see in our patients
who have dysmorphic red blood cells.
this is suggestive of glomerular disease.
Now, finally, in some of our
we actually see white blood cell Cas.
I spoke about this when I was talking
about acute interstitial nephritis
or in the presence of a positive
bacterial culture pyelonephritis.
So finally, if we're looking at sediment
and we see isolated
white blood cells or pyrite,
we usually think about infection.
But this can also occur
in noninfectious cases, such
as a sterile culture,
a nitrate, negative dipstick.
And at this time, you want to think
about things like interstitial nephritis.
Now, if on the other hand,
I see a normal urinalysis with few cells
or no cars,
this is normally considered
boring for a nephrologist,
but probably better for the patient.
And with this,
there may be only a few cells here there,
but no real cellular casts or any true
In these cases, we think about pre
renal disease, urinary tract obstruction,
in hypercalcemia acute phosphate
nephropathy or myeloma cast nephropathy.
In certain cases, it may be necessary
to do a renal biopsy in these patients
to confirm your diagnosis.
And with that, you've made it
to the end of the lecture.