What would be a good general
approach to a patient who has AKI?
We've talked about kind of different approaches
that are specific to each of our patients
but it's important to keep some general points in mind when
you're approaching a patient who's sitting in front of you.
Number one, look for episodes
of prolonged hypotension,
Was this patient perhaps on ICU?
Did they have septic shock?
Number two - has that patient have medications or
nephrotoxic exposures that can really induce a kidney injury?
Remember we talked about radiocontrast exposure
from CT scans or angiograms in a vulnerable population
Were they on medications like NSAIDS?
Remember how much nephrologists really are not the
friend of NSAIDS because of the fact in this case,
they can impair autoregulation, they can also cause
things like allergic interstitial nephritis.
We talked about how aminoglycosides and
amphotericin can actually cause tubular toxicity
and medications like acyclovir
can cause crystal precipitation.
And remember again as I mentioned, medications can
cause allergic interstitial nephritis like penicillin.
You want to do a good physical exam
so it's important to estimate volume status.
Let's look at the next things and
estimate patient's jugular venous pressure.
We can look at their skin turgor to tell us
a little bit more about their volume status.
It'd be important to look
for things like rashes.
In our patient who has AIN, they might
present with that exanthematous drug rash,
or livedo reticularis in the case of cholesterol
embolization or renal atheroembolic disease.
Imaging is gonna be
critical in this population.
An ultrasound is relatively cheap and
quick to get and that can rule out obstruction
in a large portions of patients who are
going to present with postrenal syndrome.
And of course, always look at the urine.
The urine holds clues
for just about everything .
So remember the importance of FENa that we talked
about to distinguish between prerenal disease and ATN.
Proteinuria and hematuria, if
we see that on a urine analysis,
that's really gonna point us to
the direction of glomerular diseases
and crystals can be seen with intertubular crystal
obstruction or nephrolithiasis or stone disease.
Sediment review is also critical and
that's probably my favorite part of the workup
so this is where I'm looking at
the urine directly under microscopy.
So if I see this beautiful picture over
here to the right which is muddy brown cast
in a patient who has ATN
from radiocontrast exposure
then I'm really really thinking about
ATN so I really want you to think about that
because that is going to show
up not only in your clinical practice
but you're gonna see that
in your board exams as well.
So muddy brown cast really are specific for ATN
White blood cell cast can be
suggestive of allergic interstitial nephritis.
And finally dysmorphic red blood cells - those are those
funny-shaped red blood cells seen in the urine sediment
or red blood cell cast as well as a couple of
white blood cell cast can be very suggestive
of rapidly progressive glomerulonephritis.
And of course, we want to do
renal biopsies in our selected cases.
So just some general
principles for you to think about
when it comes to the treatment of
your patient who has acute kidney injury
It's always important regardless of the etiology to
ensure that renal artery perfusion is maintained.
We want that mean arterial pressure to
be somewhere between 65 to 70 mmHg.
We want to avoid further nephrotoxic exposures
including NSAIDS or nephrotoxic medications.
If I know that my patient already has
AKI, I absolutely need to make sure
that nobody is gonna be giving them something like
ibuprofen or a medication that can cause tubular toxicity.
And I need to ensure that any renally
cleared medications are appropriately dosed
for the patient's renal function or GFR.
That's critical because remember, those
medications can build up to toxic levels
if we are not dosing them correctly
for our patient's renal function.
And finally, in coming to
treatment of our patients with AKI,
there's renal replacement
therapy with acute hemodialysis.
And this is really indicated in patients
who have complications of acute kidney injury
This would include somebody
who has refractory acidemia
meaning that they have a metabolic
acidosis that I can't treat medically,
or somebody that's so volume overloaded they're at risk
of pulmonary edema or if they're already ventilated.
They might be having increasing FiO2
requirements because they have so much volume.
Patients who are hyperkalemic that
again is refractory to medical treatment
and finally patients who develop uremic syndrome
particularly patients who have pericarditis.
That is an emergency for dialysis.
A couple of caveats that I'd like to mention about
renal replacement therapy with acute hemodialysis:
There’s no benefit to starting renal replacement
therapy early or before complications arise.
But it doesn't mean that we as nephrologist can't
individually tailor therapy for our specific populations.
I also want you to keep in mind that renal
replacement therapy doesn't hasten renal recovery
but it's certainly is gratifying to be able to provide
a therapy as a nephrologist that saves patient's lives.
And with that, this
concludes our AKI portion.