00:01
Hello, and welcome back to the nephrology curriculum.
00:03
Today, we're gonna be talking about nephritic syndromes.
00:07
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.
00:14
So, when we think about acute nephritic syndrome,
it's characterized by 5 different components from the clinical standpoint.
00:22
This includes hematuria of glomerular origin.
00:26
That means that when I look at the urine underneath the microscope,
I can see what we call dysmorphic red blood cells.
00:33
That means that the red blood cell has a funny shape to it.
00:36
So, if you look at the normal red blood cell,
you can see that it's beautifully shaped, circular in appearance.
00:41
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.
00:50
It's not uncommon for us to call them Mickey Mouse cells.
00:52
We can also see red blood cell cast and that means that these red blood cells collect in the tubule,
they bind with that Tamm-Horsfall protein,
and they form this beautiful cylindrical cast full of red blood cells with just a slight reddish hue.
01:07
We also see proteinuria in our nephritic patients
and that proteinuria is usually between 150 mg to 3.5 g per day.
01:17
So, what we would term sub-nephrotic.
01:20
Again, we can have some patients who have greater than 3.5 g of proteinuria
even though they have nephritic syndrome
and these are typically patients who have overlap syndromes.
01:31
That includes membranoproliferative glomerulonephritis and lupus nephritis
which we're gonna be talking about today.
01:37
Azotemia also characterizes nephritic syndrome.
01:41
That means we have an elevated blood urea nitrogen,
typically that BUN-to-creatinine ratio is greater than 15.
01:48
And oliguria, our patients are classically oliguric,
meaning that they make less than 500 mL of urine per day.
01:57
And finally, hypertension.
01:59
Patients who have acute nephritic syndrome will manifest with higher blood pressures.
02:03
This is typically because they are volume overloaded.
02:06
These patients are retaining sodium and it's interesting
because they actually have suppression of the renin-angio-aldo 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.
02:24
So, when we think about the different types of disorders that manifest as acute nephritic syndrome,
they include membranoproliferative glomerulonephritis.
02:33
It's a little bit difficult to say so we like to abbreviate that as MPGN.
02:38
There's IgA nephropathy, post-infectious glomerulonephritis
and some people refer to that as infection-associated glomerulonephritis.
02:48
Lupus nephritis and then there are the rapidly progressive glomerulonephritis.
02:54
And what that means is that patients, clinically, have a rapid deterioration in their renal function
and morphologically, when we biopsy these patients,
on pathology, we see something called necrosis and crescents.
03:09
These include anti-GBM disease, Goodpasture syndrome if it includes both lung and kidney.
03:15
The immune-complex diseases that I just spoke about.
03:19
That includes lupus, IgA, post-infectious, and MPGN.
03:24
If they manifest with a rapid deterioration in renal function
and morphologically, they have crescents and necrosis on pathology,
those patients would be considered in RPGN.
03:36
And finally, the Pauci-immune glomerulonephritis and that includes our ANCA-associated vasculitis.