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hello
and welcome to the next lecture in your
nephrology curriculum
today we're going to be talking about
acute kidney injury
which is very near and dear to my heart
as a nephrologist because it's something
that i
see every day and it's something that
you're going to encounter
in your professional life as you take
care of patients
so acute kidney injury is defined by the
abrupt loss of kidney function
retention of urea and other nitrogenous
waste products
as well as the dysregulation of
extracellular volume and electrolytes
before we move on though there are some
important terms that i really want you
to understand so you can better
understand the cases that we're going to
be talking about
the first is creatinine creatinine is a
breakdown product of creatine phosphate
in muscle
it's filtered completely by the kidney
and it's not metabolized and therefore
is used to estimate kidney function
and filtration it does have an inverse
relationship to function meaning that
the higher the creatinine is the lower
the gfr or filtration rate is
you will also hear the word bun or blood
urea nitrogen
so urea nitrogen is formed from the
protein catabolism by the liver
it's filtered by the kidneys and it's
used as an additional measure of kidney
function
although a high bun generally reflects
lower filtration
there are some caveats when it comes to
bun and it can increase
independently of kidney function this
includes things like glucocorticoids or
steroids when our patients are on
steroids
tetracycline antibiotics or reabsorption
of blood from the gi tract
in each of those instances the bun may
rise and the creatinine might be normal
as well as kidney function so do keep
that in mind as we're talking about bun
oliguria is another important term to
know
our patients are commonly oligaric when
they develop acute kidney injury
and this really means that our patients
are producing less urine
typically it's defined as less than 500
ml of urine output within a 24
hours but do keep in mind there are a
few definitions that will define
oliguria as less than 400 mils
in a 24-hour period of time finally
there's aneurys
and urea anuria is defined by
less than 100 mils of urine output in a
24-hour period of time
and this is essentially one of the worst
signs of acute kidney injury
because our patients are essentially not
producing any urine
if you remember nothing else from this
lecture do remember that acute kidney
injury is significant
in our critically ill patients who
develop aki
their mortality is increased between 40
to 60 percent at 60 days
and their hospital stay is prolonged
part of the reason why
it's been so difficult in order to care
for and treat these patients
is because it took forever to develop
criteria in order to define
what aki is and to stage aki in order to
develop therapeutic targets in this
population
so finally in the early part of the
2000s the acute kidney injury network
came up with staging criteria
and this is based on absolute creatinine
a change in serum creatinine and
reduction in urine output
so beginning in stage one this
includes a creatinine increase of
greater than 0.3 milligrams per
deciliter
that's really significant because of the
fact that if you think about a patient
whose creatinine goes to 0.7 to just 1.0
that means that that patient has
developed aki and when you look at that
particular patient
their mortality is increased we also
look at the urine criteria as well
so less than 0.5 mils per kilo per hour
over a six hour period
of time stage two is an increase in
creatinine
of two to three times normal and then
again
a reduction in urine output over a 12
hour period of time
and finally stage 3 where patient's
serum creatinine is increased three to
four times that of normal
or a serum creatinine greater than four
milligrams per deciliter
with at least an acute increase of at
least 0.5 milligrams per deciliter
and these patients oftentimes are
aneuric
the higher the stage the worse the
outcome
so it's great that we have a staging
system however there are some caveats
that we need to think
of so despite having a consensus for
defining and grading aki
it still is based on serum creatinine
and urine output
and these two are really imperfect
biomarkers and again if i'm talking
about a biomarker i'm talking about a
biological
marker for organ injury why is this
because when the serum creatinine rises
or urine output decreases
already substantial injury has taken
place to that patient
it diminishes if you think about that
the ability to begin treatments aimed at
preventing the loss of renal function
and although we have had development of
novel biomarkers things like ngal
kidney injury molecule 1 or nag nag
they're not ready for prime time yet and
we're not using them
commercially in the u.s at this time
so let's kind of think about this in a
more conceptual fashion
if we have a patient that's coming in
but there's something about that patient
during this hospitalization that
increases their risk for acute kidney
injury
that makes them susceptible it might be
because they have
advanced age they might be hypovolemic
they might have diabetes mellitus or
they might be on medications like
non-steroidal anti-inflammatory drugs
which impair autoregulation
an insult occurs to that patient that
creates acute kidney injury
and this is where we should be looking
at our biomarkers to detect that
something's happened
but instead what happens it actually
takes a substantial amount of time for
gfr to decrease
and our patients really aren't
manifesting to us as being injured
until they already have kidney failure
so it's really
when they have complications of their
chronic kidney disease are they coming
to our attention
and you can see now how having
creatinine and urine output as
biomarkers
are just inadequate when it comes to
defining when
kidney injury happens so that we can
actually develop therapeutic targets
to help our patients at the time that
they need it rather than just taking
care of complications from their aki
so let's move on to thinking about the
etiologies of different types of acute
kidney injuries
and i think from our first year of
medical school everybody could really
think about the three main categories
that you've been taught since day one
which are really pre-renal this includes
things like volume depletion
and a decrease in effective arterial
blood volume intrinsic renal disease
and then this is separated or i'd like
to separate them by different
compartment compartments of the kidneys
this includes the tubules and
interstitium that includes acute tubular
necrosis
acute interstitial nephritis acute
tubular obstruction
the vascular compartment so any kind of
vascular disease
and of course my very favorite which is
glomerular disease
and then finally the post-renal category
which means that there's urinary
obstruction
anywhere from the renal pelvis to the
urethra
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you