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hello and welcome back to the nephrology
curriculum
today we're going to be talking about
nephritic syndromes nephritic syndromes
are part of the glomerular diseases and
i can say as a nephrologist they're
probably one of the most exciting
aspects of my job
so when we think about acute nephritic
syndrome it's characterized by five
different components
from the clinical standpoint this
includes hematuria of glomerular origin
that means that when i look at the urine
underneath a microscope
i can see what we call dysmorphic red
blood cells
that means that the red blood cell has a
funny shape to it
so if you look at the normal red blood
cell you can see that it's beautifully
shaped circular in appearance
but when you see a dysmorphic red blood
cell there are these little blebs
all over the membrane and sometimes they
even take on a mickey mouse
appearance it's not uncommon for us to
call them mickey mouse cells
we can also see red blood cell casts and
that means that these red blood cells
collect
in the tubule they bind with that tam
horsefall protein
and they form this beautiful cylindrical
cast
full of red blood cells with just a
slight reddish hue
we also see proteinuria in our nephrotic
patients and that protein area is
usually between 150 milligrams to three
and a half grams per day
so what we would term sub nephrotic
again we can have some patients who have
greater than three and a half grams of
proteinuria even though they have
nephritic syndrome
and these are typically patients who
have overlap syndromes that includes
membranoproliferative glomerulonephritis
and lupus nephritis which we're going to
be talking about today
azotemia also characterizes nephritic
syndrome
that means we have an elevated blood
urea nitrogen
typically that bun to creatinine ratio
is greater than 15.
and oligaria our patients are
classically oligaric meaning that they
make
less than 500 mils of urine per day
and finally hypertension patients who
have acute nephritic syndrome will
manifest
with higher blood pressures this is
typically because they are volume
overloaded
these patients are retaining sodium and
it's interesting because they actually
have suppression
of the renin-angioaldo system and
essentially
they have an increase in the sodium
potassium atpase at that principal cell
that's responsible for that sodium
uptake leading to volume overload
so when we think about the different
types of disorders that manifest as
acute nephritic syndrome they include
proliferative glomerulonephritis it's a
little bit difficult to say
so we like to abbreviate that as mpgn
there's iga nephropathy post-infectious
glomerular nephritis and some people
refer to that as
infection associated glomerular
nephritis
lupus nephritis and then there are the
rapidly progressive glomerular nephritis
and what that means is that patients
clinically have a rapid deterioration
in the renal function and
morphologically when we biopsy
these patients on pathology we see
something called necrosis
and crescents these include anti-gbm
disease good pasture syndrome if it
includes both lung
and kidney the immune complexes
diseases that i just spoke about that
includes lupus iga
post-infectious and mpgn if they
manifest with a rapid deterioration in
renal function and morphologically they
have crescents
and necrosis on pathology those patients
would be considered
uh in rpgn and finally the posse immune
glider nephrititis
and that includes our anchor associated
vasculities
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you