Diabetic nephropathy – Clinical presentation & treatment | NCLEX-RN | Khan Academy

Diabetic nephropathy – Clinical presentation & treatment | NCLEX-RN | Khan Academy

– [Voiceover] Diabetic nephropathy
is one of the most common and serious chronic complications associated with diabetes mellitus. In this tutorial, let’s
discuss how the mechanisms underlying diabetic nephropathy correlate with the clinical presentation as well as the treatment of the disease. Now fortunately the mechanisms underlying diabetic nephropathy, directly correlate with
the clinical presentation. And the first clinical
finding of the disease is somewhat paradoxically
an increased kidney filtration rate or
glomerular filtration rate. So, diabetic nephropathy,
if you break down the term into nephro and pathy literally means kidney
disease caused by diabetes. Now typically kidney disease is marked by a decreased filtration rate, so why is it that the first clinical stage of diabetic nephropathy is that of an increased glomerular
filtration rate? Well recall that the earliest mechanism contributing to diabetic nephropathy is an increased pressure
state, over here in blue. And this is due to hypertension and efferent vasoconstriction. So let’s use a common garden hose to help illustrate how this
increased pressure state will ultimately result in an increased glomerular filtration rate. So, imagine you have this garden hose and it has a small hole
in the middle of it. So first you’re gonna open up the spigot and increase the pressure
and flow through the hose. Intuitively, this is
going to increase the rate at which water is leaking
from the hole in the hose. Next, you partially kink off the end of the hose distal to the hole, and once again this is
gonna further increase the rate at which water
leaks from the hose. This is essentially what’s
occurring in the glomerulus with the hypertension representing the opening up of the spigot and increasing the pressure
before the glomerulus, in front of the glomerulus, and the efferent vasoconstriction representing the kinking off of the hose, which causes this back pressure. Both of which are going to
increase the filtration rate. This stage of diabetic nephropathy is most commonly asymptomatic, so it goes typically unnoticed. However, it’s going to set the stage for the next clinical step
of diabetic nephropathy; and that is detectable proteinuria. And what proteinuria is
is protein in the urine. So this increased pressure state causes trauma on the mesangium, in the middle of the glomerulus here and it results in mesangial expansion, which is this second mechanism
of diabetic nephropathy. Now as the mesangium expands, this also increases the
size of these fenestrations or spaces between the
podocyte foot processes, so let’s go back and look real closely at these fenestrations and
watch how they increase in size. Now, these podocyte
fenestrations are a component of the glomerular filtration mechanism. So, let’s think of these
podocyte foot processes as a coffee filter. A proper coffee filter is porous enough to allow for the water to flow through, but will retain the coffee
grounds within the filter. This is because the molecules of water are much smaller than the
size of the coffee ground, so over time the coffee pot is gonna fill just with the coffee
but no coffee grounds. Now imagine if the coffee filter was replaced with a cooking strainer, which has considerably larger pores. If you were to try and
use a cooking strainer as a coffee filter, when you
pour the hot water through, it’s not gonna work because the pores of this cooking strainer are much larger. Both the coffee as well as the grounds are gonna start to spill through and you’re gonna end up with
coffee grounds in your coffee. So in the glomerulus, the fenestrations between these podocyte foot processes are kind of like coffee filters and normally in the filtration of blood no proteins or large
molecules are allowed though. However, with mesangial expansion these fenestrations become much larger and when filtration
occurs they become leaky, and they allow for
molecules, such as proteins, to be spilled out into the urine. So this is what causes
the detectable proteinuria in diabetic nephropathy. One of these proteins is albumin. Urine tests are available to detect the presence of albumin in the urine, so frequently individuals with diabetes will have routine screening to test for this albumin or for
protein in their urine, which is a sign that they may be developing diabetic nephropathy or kidney disease due to diabetes. Then the next clinical stage
of diabetic nephropathy is that of a decreased
glomerular filtration rate. So you can see that we’ve gone from an increased glomerular filtration rate, then to a decreased
glomerular filtration rate. So what exactly causes this? Well, recall that part of the reason for this mesangial expansion is the release of cytokines
which cause inflammation and oxygen free radicals. Now, these cytokines
and oxygen free radicals damage the mesangium, resulting
in the mesangial expansion. However, they don’t just
damage the mesangium. They damage the cells
throughout the tubules as well as the vasculature
that supports the nephron. Now in addition to the cytokines
and oxygen free radicals, this vasculature is further damaged by this efferent vasoconstriction here. Which is one of the causes of
that increased pressure state. And this combination of damage from decreased blood flow and cytokines and oxygen free radicals results in ischemia and
atrophy of this vasculature. As this vasculature kind of dies off, it no longer can support
the tubules of the nephron, so the nephron itself
begins to die off as well, and so there’s a decreased
ability to filter the blood. Now initially this occurs
in just a small percentage of the nephrons in the kidney, and the kidney’s able to compensate, but eventually over time if
this diabetic nephropathy is not treated, a large enough number of nephrons throughout the
kidney are gonna die off, and it’s gonna be detected as
a decreased filtration rate. The kidney’s no longer able to keep up with the dying off of nephrons. If this is present, this
decreased filtration rate is present for more than
three months in a row, then it’s known as chronic kidney disease. As it continues to progress, eventually it will become
a permanent decrease, which is then known as
end-stage renal disease. Now that we have a better understanding of the mechanisms that
cause diabetic nephropathy and how they correlate with
the clinical presentation, let’s just briefly touch on how diabetic nephropathy is treated. This is, once again, gonna
be directly correlated to the underlying mechanisms. So, the most important thing
in diabetic nephropathy is to treat the underlying diabetes. This is because the hyperglycemia
associated with diabetes is the cause of this
increased pressure state, so if you can treat the diabetes, you can prevent the
increased pressure state, which will then prevent
the cascade of effects leading to diabetic nephropathy. However, if this increased pressure state does start to occur, the next step is to treat the pressure. And what I mean by that
is treat the hypertension. So if you can decrease the blood pressure, that goes into the
afferent arteriole here, you’ll decrease this
increased pressure state. In addition, one of the
most common medications to treat blood pressure are
known as ACE inhibitors. Now ACE inhibitors stands for angiotensin converting enzyme inhibitor and angiotensin is one of the hormones in that
renin-angiotensin-aldosterone system that results in the
efferent vasoconstriction. So by treating the blood
pressure with an ACE inhibitor, you’re also going to decrease
this vasoconstriction to further decrease this pressure state within the glomerulus. These two treatments should be occurring regardless of whether or not an individual with diabetes is in any of these clinical stages
of diabetic nephropathy. So these are not only treatments, but they’re also good for preventing the progression of diabetic nephropathy before someone even enters
this first clinical stage. However, if someone does
develop diabetic nephropathy and it unfortunately progresses far enough to have this decreased
glomerular filtration rate and they end up in
end-stage renal disease, unfortunately then there are
only two treatment options. The first is dialysis, in which the blood is filtered outside the body by a machine to kind of replace the
effect of the kidney. And the other is a kidney transplant. Fortunately though, like
most of the complications of diabetes mellitus, if
the underlying disease and its comorbidities,
such as hypertension, are properly treated, diabetic nephropathy can be a preventable complication
of diabetes mellitus.

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