In this lecture series, we will move away from glomerular damage
and take a look at other parts of the kidney in which our pathology is relevant.
Now, the first thing that you wanna do here is
well, anatomically locate yourself and this would be tubulointerstitial disease.
So this is not dealing with the glomerulus, this is dealing with the tubules
but keep in mind though, oftentimes, 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 go down to chronic renal failure,
well, we will then highlight as to what becomes important there.
So what kind of issues do you wanna keep in mind where the kidney
obviously and got hurt in acute nature and by acute,
what does that actually mean in reference to its timeline?
Clinical pathologic process of acute renal failure,
some of you have heard of it as such presenting as oliguria
and you must know that oliguria 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 tubular 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, meaning to say that endogenously,
there are certain substances that are being released maybe due to crush injury,
and as 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 hemolysis,
for example, paroxysmal 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 result in acute kidney injury.
Light chains, here, we’re thinking about monoclonal gammopathies
including your well, multiple myeloma and 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
so that you can give it that beautiful golden yellow color of a urine
that you’re all so familiar with
or you might then have conjugated bilirubin 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.
Aminoglycosides, the antibiotics notorious for 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 are you looking for?
Well, we’ll go through different phases here.
And 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.
Chronic renal failure, now that’s a 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, well go through maintenance phase and we’ll call something,
we’ll call a phase in which regeneration’s taking place as being recovery.
At first, you’ll have hypertension just like you would with the 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 angiotension II might play a role
and with your patient with acute kidney injury early on is going to present with hypertension.
Next, in addition, acute kidney injury in the early phase,
you are 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 are 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 meaning to say that now, your resting membrane potential is actually moving positive.
It’s becoming less negative and getting closer to threshold, be careful.
The pH here is the fact that now, you’re not able to properly hold on to the bicarbs,
so therefore, metabolic acidosis or not able to properly produce your ammonia
which takes place in the proximal convoluted 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, for one of the common causes of acute kidney injury in fact is ischemia
and you can only imagine that you’re not able to properly reabsorb the bicarb
and so therefore very much behaves like an RTA type two.
However, here it’s different because you’re also creating a type of metabolic acidosis
that would in fact be and an anion gap and that’s
because of organic acids, so you want to be careful.
Remember that RTA type two 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, just like chronic renal failure, take a look at this table.
This table kind of looks like what you'd expect to find in chronic renal failure.
Please be really careful.
Meaning to say that if you know that your patient is suffering form ischemia
and you know it’s acute kidney injury, early on, it could look like chronic renal failure.
Here, erythropoietin 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 nonhemolytic type of anemia, erythroblast decreased stimulation.
To continue our discussion, along with acute kidney injury, you will also have bone issues.
We’ll talk more about this in chronic renal failure.
You might have problems where you’re not able to properly reabsorb calcium
so you’ll 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 can now properly work on your kidney,
and so therefore, may result in renal osteodystrophy.
The phosphate would not be able to get rid of.
You have hyperphosphatemia.
The PTH as it just said here because you’re not able to properly reabsorb the calcium,
result in secondary hyperparathyroidism and calcitriol.
Well, it’s not present because if the PCT has been destroyed early on,
then you have decreased conversion
because of decreased 1-alpha-hydroxylase activity resulting in osteomalacia type.
As far as the calcium’s 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.
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
paying 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 will then be your hypocalcemia, secondary hypoparathyroidism,
hyperphosphatemia, the anemia, the metabolic acidosis, and the declining mental status.