hey everyone this lesson is on nephrotic syndrome and in this lesson were going to talk about what nephrotic syndrome is what
are some disease states that can cause nephrotic syndrome how do we treat
nephrotic syndrome and ultimately what are some of the health consequences of
having nephrotic syndrome so to begin nephrotic syndrome is
actually a glomerular inflammatory syndrome involving five different
aspects the first is excess proteinuria the second is hypoalbuminemia the
third is edema the fourth is hyperlipidemia and the fifth is
hypercoagulability i’m gonna show a picture of a glomerulus with a
glomerular basement membrane in a podocyte and we’re gonna talk about how
nephrotic syndrome and different diseases can affect different parts of
this glomerular apparatus and nephrotic syndrome exists on a spectrum on one end
of the spectrum we have high proteinuria with little hematuria and that’s known
as nephrotic syndrome on the opposite end of the spectrum we have high levels
of hematuria with very little proteinuria and that is nephritic syndrome and
different diseases exist on different parts of this spectrum
and at some point when we have high levels of protein in our urine or
proteinuria we consider that in a nephrotic syndrome and I’ll tell you what
that number is in the next slide so how does nephrotic syndrome present itself
clinically? I like to use the mnemonic HELP to help remember the clinical
presentation of nephrotic syndrome H E L P H stands for hypoalbuminemia and
hypercoagulability so a patient with nephrotic syndrome excretes excess of
amounts of protein in their urine and these proteins can include albumin,
protein C, protein s, and antithrombin 3 because they’re excreting so much albumin
in their urine they can become hypoalbuminemic and because they’re excreting
protein C, protein s and antithrombin 3 they can actually have an increased
risk of hypercoagulability. The next one is edema and edema is due
to that state of low albumin. If we have low levels of albumin we have decreased
oncotic pressure, we have a decreased ability to reabsorb some of that
interstitial fluid, leading to peripheral edema. The next one is lipid
abnormalities and generally with patients with nephrotic syndrome they
have an increased LDL cholesterol and they also have lipiduria or oval fat
bodies in their urine. And the last one is P for proteinuria and this is the
hallmark of nephrotic syndrome, and generally a level of 3.5 grams or
greater is necessary to consider a nephrotic syndrome. So, greater than 3.5
grams per 1.73 meter squared per day is the level of protein excretion in the
urine necessary for definition of the nephrotic syndrome and anything below
this with hematuria we would generally consider it a nephritic syndrome. So,
again to remember the clinical presentation remember HELP. H, E, L, P.
Hypoalbuminemia and hypercoagulability, edema, lipid abnormalities, and
proteinuria. So, nephrotic syndrome is not a disease state in of itself, but it can
be caused by other diseases, and there are about three to four different
diseases that can cause nephrotic syndrome.
The first one is minimal change disease. Minimal change disease is named minimal change disease because when we look at a glomerulus under a light microscope
there are minimal changes that are observed. So here’s a picture of a
glomerulus. It looks generally like a normal glomerulus – there are very little
changes if at all any when we look at it under light microscopy. Minimal change
disease primarily affects podocytes and what I want you to remember is that a majority of cases of nephrotic syndrome in children are due to minimal change
disease, especially children under the age of 10 years old. Other causes
of minimal change disease include drug use – so NSAIDs, lithium and ampicillin,
Hodgkin’s lymphoma, and atopic individuals also have a higher risk of
minimal change disease as well. The second disease is focal segmental
glomerulosclerosis or FSGS. Like minimal change disease, it primarily affects podocytes, but when we look at it microscopically we actually do see
significant changes – and in this image we see that there are collapses of
capillaries within the glomerulus. It is among the one of the most common causes
of idiopathic nephrotic syndrome in adults and generally it’s considered to
be about 35% of nephrotic syndrome. Some of the etiologies of FSGS include obesity,
infections with HIV and hepatitis B. Having sickle cell disease also
increases risk for FSGS, and heroin use. And the third disease is membranous
glomerulonephropathy and this involves glomerulus basement membrane thickening and autoantibodies to phospholipase A2 on podocytes. Here is an immunofluorescence image of
IgG antibodies to those podocytes. So some of the etiologies of membranous glomerulonephropathy include hepatitis b virus infection, lupus and thyroiditis. Some drugs can also lead to membranous glomerulonephropathy as well as exposure to
gold. So I know this is a lot of information! What I want you to remember
from these 3 disease states is the following… minimal change disease, minimal
changes on light microscopy It is the major cause of nephrotic
syndrome in children and remember NSAIDs, and Hodgkin’s lymphoma. For focal
segmental glomerulosclerosis – remember that it is a major
cause in adults remember obesity, hepatitis B, and heroin
and for membranous glomerulonephropathy remember there is basement membrane
thickening and it is again secondary to hepatitis B, lupus and thyroiditis and
you can also remember gold exposure for membranous glomerulonephropathy. Some of the other causes of nephrotic syndrome
include amyloidosis so there can be primary and secondary amyloidosis that
can lead to renal amyloidosis and for secondary amyloidosis this is often
associated with chronic inflammatory diseases such as rheumatoid arthritis
and osteomyelitis. And other causes of nephrotic syndrome – although these are
more likely to be an intermediate nephrotic syndrome, so they are kind of
in the middle of that spectrum that I showed you earlier – so there’s a mixture
of some nephrotic and nephritic components proteinuria and hematuria
we have membranoproliferazive glomerulonephritis. and So these can be
related to hepatitis C infections and monoclonal gammopathies And nodular glomerulosclerosis secondary to diabetic nephropathy so how
do we treat nephrotic syndrome? Treatment depends on the type of glomerulopathy if we have minimal change disease we use steroids if we have membranous
glomerulonephropathy we often want to reduce blood pressure and use steroids if we have FSGS we want to use
an ACE inhibitor or an ARB and steroids and for membranoproliferative
glomerulonephritis we want to use ASA and an ACE inhibitor for nodular
glomerulosclerosis we want to treat the underlying disease and that is often the
diabetes and in renal amyloidosis the treatment depends on if it’s primary or
secondary and I’m going to talk about that in a future lesson on amyloidosis so what are some of the health
consequences of nephrotic syndrome nephrotic syndrome increases a patient’s
risk for the following, an acute kidney injury so we can see an increase in the
level of creatinine so it can lead to kidney damage we can see an increased
risk of thromboembolism like I mentioned before patients with nephrotic syndrome
excrete a lot of protein C protein s antithrombin 3 this can lead to
hypercoagulability an increased risk of thromboembolism you can also increase
the risk of infection the mechanism by which this does this is not well known
but generally a patient with nephrotic syndrome has increased risk of
pneumococcal infections so having a pneumococcal vaccination is important
for these patients the fourth is a protein malnutrition there excreting
lots of lots of protein so they can actually be malnourished with regard to
protein in the last is hypovolemia so if they’re reducing a lot of their albumin
they become hypoalbuminemia hypo album anemic they can have an increased
diuresis and they can actually lose some of their this systemic volume becoming
hypovolemic and again the 5 health consequences of nephrotic syndrome are
aki thromboembolism infection protein malnutrition and hypovolemia anyways
guys take a breath that was a long lesson a lot of information I hope you
found this lesson helpful if you did please like and subscribe for more
lessons like this one and as always thank you so much for watching and I
hope to see you next time

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