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in this lecture series we
will move away from glomerular damage
and take a look at other parts of the
kidney
in which pathology is uh relevant
now the first thing that you want to do
here is
well anatomically locate yourself and
this would be two below interstitial
disease
so this is not dealing with the
glomerulus this is dealing with the
tubules
but keep in mind though often times in
order for you to cause damage to the
tubule you'll have to pass through the
glomerulus
we call this acute kidney injury aki
acute kidney injury
keep this separate from rpgn that we
talked about
and later on at some point when we get
into chronic renal failure
well we will then highlight as to what
becomes important there
so what kind of issues you want to keep
in mind where the kidney
awasan got hurt in an acute nature
and by acute what does that actually
mean in
the in reference to its timeline
clinical pathologic process of acute
renal failure
some of you have heard of it as such
presenting is aleguria
and you must know that allah gear refers
to less than 400 milliliters
of urine being produced in a day and
one of the most common causes of acute
kidney injury would therefore be
acute tuber necrosis now necrosis to you
should mean that the particular tissue
is not receiving oxygen
so therefore one of the most common
causes of acute tubular necrosis
in fact will be ischemia
we'll take a look at ischemic atn
nephrotoxicity
i mean to say that endogenously there
are certain substances that are being
released
maybe due to crush injury and so
therefore releasing myoglobin
resulting in damage to the kidney in an
acute nature
hemoglobin here you might be thinking
about what's known as intravascular
molecules
for example proxies of nocturnal
hemoglobinuria
in which upon destruction of the rbc
within the vasculature
is then going to release the hemoglobin
and this hemoglobin
as it passes through and filters through
the glomerulus may then cause damage and
cause
result in acute kidney injury light
chains here
thinking about monoclonal gammopathies
including your well multi-myeloma
company
in which kappa lambda chains may then
cause not only damage to the glomerulus
but may also cause damage to the tubules
and then bilirubin and remember that you
should normally have
urobilinogen in your kidney to so that
you can give it that
beautiful golden yellow color of a urine
that you're also familiar with
or you might then have conjugated
bilirubin
uh maybe due to hepatitis we talked
about that in
hepatobiliary or exogenous type of
damage that's taking place to the kidney
resulting in acute kidney injury
immunoglycosides antibiotics
are notorious for uh always making sure
that the renal function is
normal prior to administration heavy
metals lead poisoning
resulting in lead nephropathy sepsis
always worried about renal failure
other causes including volume depletion
urinary obstruction
rpgn and perhaps even acute interstitial
nephritis
ain but of all of the ideologies here
of acute kidney injury ischemic would be
the most common
now acute kidney injury what were you
looking for
well we'll go through different phases
here remember this is acute
which means that the patient if all goes
well
and is receiving proper treatment should
be able to recover the kidneys
you hear what i just said so this is not
chronic renal failure
failure chronic renal failure though
that's the point of no return and for
the most part
that patient it's just inevitable that
he or she is going to then be placed on
dialysis correct but then here
if it's acute we'll go through different
phases when the time is right
in which at first it very much behaves
like a dead kidney
then we'll go through maintenance phase
and we'll we'll call something we'll
call a phase in which uh
uh regeneration is taking place as being
uh recovery
at first you have hypertension just like
you would with chronic renal failure
what does that mean this means that
you're not able to properly filter your
plasma
and so therefore you are then holding on
to
fluid so your extracellular volume
increases
and maybe even perhaps angiotensin tube
might play a role in which you patient
with acute kidney injury
early on is going to present
hypertension
next in addition acute kidney injury in
the early phase you're not able to
properly filter so therefore you are
in a state of volume overload excess
water and
nacl accumulating in your
interstitium edema
just like in chronic renal failure which
is a very common cause of hyperkalemia
you're also going to find this early on
and what you're worried about
with hyperkalemia is the fact that the
heart
might be affected right so i mean to say
that now your resting membrane potential
is actually
moving positive it's becoming less
negative
getting closer to threshold be careful
the ph here is the fact that now you're
not able to properly
hold on to the bicarb so therefore
metabolic acidosis or
not able to properly produce your
ammonia
which is take which takes place at the
proximal cavity tubule
and these are some of the common places
think about your pct
extremely metabolic active remember that
discussion so lots of sodium potassium
pump activity a lot of atp
and so therefore if one of the common
cause of acute kidney injury in fact
is ischemia and you know you can only
imagine that you're not
able to properly reabsorb the bicarb and
so therefore very much behaves like a
rta type two however
here it's different because you're also
creating a
type of metabolic acidosis that would in
fact be
an anion gap and it's because of organic
acids
so you want to be careful remember that
rta type 2
is a metabolic acidosis but that is
absolutely
non-anion gap referring to well there's
no
gap in anions with rtas here however
there will be because of
increased organic acid that's important
what about erythropoietin
well i'll just say chronic renal failure
take a look at this table
stable kind of looks like what you'd
expect to find a chronic renal failure
please be really careful
i mean to say that if you know that your
patient is suffering from ischemia
and you know it's a acute kidney injury
early on it could look like chronic
renal failure
here the porting is not present because
of kidney damage so therefore
you would expect your bone marrow to not
function properly look for a type of
normocytic
non-hemolytic type of anemia orthoblast
decreased stimulation continuing our
discussion
along with acute kidney injury you will
also have bone issues we'll talk more
about this a chronic renal failure
you might have problems where you're not
able to properly uh
reabsorb calcium so you have
hypocalcemia may result in what's called
as
secondary hypoparathyroidism and
therefore resulting in
renal osteodystrophy but also at the
fact that maybe the pth cannot properly
work on your kidney
and so therefore may result in renal
osteodystrophy
the phosphate will not be able to get
rid of you have hypophosphatemia
the pth as i just said here because
you're not able to properly
absorb the calcium result in secondary
hypoparathyroidism
and calcitrio well it's not present
because
if the pct has been destroyed early on
then you have decreased uh conversion
because of decreased one off hydroxis
activity resulting in osteomalacia type
as far as the calcium is concerned it
will be hypocalcemic and the reason for
that as we said earlier
is because there is going to be
decreased production of calcitriol or
maybe perhaps decreased functioning
of your pth now this is acute acute
management is directed towards
correcting fluid overload
the hyperkalemia and signs of uremia
so at first everything that you're doing
here is very much
pay attention to that table and the
objective is to make sure that you take
care of that hypertension
hyperkalemia and those signs that we saw
earlier
uremia referring to your signs okay so
this would then be your
hypocalcemia secondary
hypoparathyroidism hyperphosphatemia the
the metabolic acidosis and and the
declining
mental status
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you