Hello, and welcome back to the nephrology curriculum.
Today, we're gonna 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 5 different components from the clinical standpoint.
This includes hematuria of glomerular origin.
That means that when I look at the urine underneath the 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 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.
We also see proteinuria in our nephritic patients
and that proteinuria is usually between 150 mg to 3.5 g per day.
So, what we would term sub-nephrotic.
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.
That includes membranoproliferative glomerulonephritis and lupus nephritis
which we're gonna 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 oliguria, our patients are classically oliguric,
meaning that they make less than 500 mL 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-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.
So, when we think about the different types of disorders that manifest as acute nephritic syndrome,
they include membranoproliferative glomerulonephritis.
It's a little bit difficult to say so we like to abbreviate that as MPGN.
There's IgA nephropathy, post-infectious glomerulonephritis
and some people refer to that as infection-associated glomerulonephritis.
Lupus nephritis and then there are the rapidly progressive glomerulonephritis.
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.
These include anti-GBM disease, Goodpasture syndrome if it includes both lung and kidney.
The immune-complex 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 in RPGN.
And finally, the Pauci-immune glomerulonephritis and that includes our ANCA-associated vasculitis.