So we're now moving to our
vascular diseases of the kidney.
And there's three main broad categories I want you
to think about when it comes to vascular diseases.
The first is what we just talked about in
our case, which is renal atheroembolic disease.
So this typically occurs in patients who have
a very heavy atherosclerotic disease burden
and anytime they undergo something
that would involve manipulating the aorta,
or any of the large arteries, they will be at
risk for developing renal atheroembolic disease.
This includes things like coronary
angiography just as in the case of our gentleman,
and percutaneous coronary intervention, placing stents
or doing the angioplasty to any of those coronary arteries.
It also is going to involve anything
that will cause aortic manipulation
so for example if I have
a patient who's coming in
and they have an aortic aneurysm and
they're getting an endovascular aortic repair,
then that can also cause that
plaque burden to embolize distally.
Renal artery angioplasty and stent
placement is probably the worst culprit
when it comes to developing
renal atheroembolic disease
and you can think about
why that would happen.
I've got my renal artery here, I've got a very
heavy disease burden of atherosclerotic disease.
If I go in there and I try to
angioplasty or place a stent,
it's very easy for me to dislodge
those pieces of cholesterol
and have them embolize distally into
those small arterioles in the kidney.
So again, just as what we've been
talking about with each of these phenomena,
cholesterol plaque can break off after
that manipulation, it embolizes distally
and it then leads to partial or total occlusion of
multiple small arteries or glomerular arterioles.
So when that happens, what we typically
see is that serum creatinine serologically
that rise is gonna be more subacute.
It's happening over time because these pieces of
cholesterol tend to just embolize a little bit at a time.
So we will tend to see this phenomena somewhere
between 2-8 weeks following manipulation or procedure.
Again, let me go ahead and contrast this to
what we've talked about before in our ATN section.
So when we give radiocontrast and our
patients develop ATN from having radiocontrast,
that's that iodinated contrast
that causes tubular toxicity.
That rise in creatinine is really
gonna be more at 72 hours at most.
So they tend to get that injury right within
the first three days after contrast exposure.
When they have renal atheroembolic
disease, even though they're getting contrast,
that phenomena of those cholesterol emboli
that are embolizing to those distal arterioles,
that takes time for that to happen because
once they embolize, they cause ischemia,
they cause an inflammatory recruitment and that's
really more subacute in that 2-8 week time frame.
I really want you to understand the difference
between that because this is something clinically
that you're going to see and you're gonna
be able to better diagnose these two entities
and you're also gonna see it in your
licensure exam, so that's important.
So, the other thing with renal
atheroembolic disease serologically
is it's going to be associated with low complements in
the serum just as we saw in the gentleman in the case.
They tend to also get an eosinophilia
and a rash if we're lucky enough
to see it just as you can
see in this picture over here.
This is a rash that's representative
of livedo reticularis.
Okay, so that's renal atheroembolic disease.
Let's move to our next category of
vascular diseases, and that's vasculitis.
So vasculitis is inflammation and necrosis of
small to medium-sized arteries and arterioles
specifically in the kidney.
So this is going to include polyarteritis
nodosa which has an association with hepatitis B,
granulomatosis with polyangiitis formerly
known as Wegener's granulomatosis,
and then finally microscopic polyangiitis.
Now we're gonna talk about those latter
two which is GPA and microscopic polyangiitis
in our nephritic syndrome lecture.
And they are two of my favorite
entities to discuss, so stay tuned for that.
Okay, our third broad category of vascular diseases,
are the thrombotic microangiopathies or TMAs.
So what TMA refers to is any kind of injury
to the endothelial lining of the blood vessel,
then will result in platelet thrombi occluding
those small vessels and causing ischemia.
The way that TMA manifest clinically
is we will see thrombocytopenia,
meaning that we've got low platelets,
a microangiopathic hemolytic anemia, that
means that we have intravascular hemolysis
of these red blood cells in the circulation.
There's a couple of different entities that I
want you to think about when it comes to TMA.
So the first of these is thrombotic
thrombocytopenic purpura or TTP
and this is characterized by a pentad
of fever, neurological abnormalities,
renal failure and of course thrombocytopenia
and microangiopathic hemolytic anemia.
The next to think about is Shiga-toxin
mediated hemolytic uremic syndrome.
This is associated with Shiga
toxin-associated E. coli producing organisms,
formerly known as diarrhea-associated HUS.
When we think about Shiga-toxin mediated HUS, those
patients typically will present with the diarrheal prodrome.
The next is complement-mediated
TMA, formerly called atypical HUS.
Complement-mediated TMA is very interesting because these
patients tend to have genetic mutations in their complement system
or acquired autoantibodies that cause
constitutive activation of c3 convertase
and formation of the
The next to think about is drug-induced TMA.
So these are drugs like gemcytabine,
lincomycin, calcineurin inhibitors.
Those drugs actually cause injury to the endothelial
lining and that's what precipitates the TMA,
again manifesting with microangiopathic
hemolytic anemia and thrombocytopenia.
And finally our last category to think about when
it comes to the TMAs is malignant hypertension.
So patients who manifest with very high blood
pressures who typically have end-organ damage,
will have a renal-limited TMA.
They may not always manifest with microangiopathic
hemolytic anemia and thrombocytopenia,
but certainly the pathological
abnormalities are there on biopsy.