Okay, let's start with a clinical case. We have a 63-year-old gentleman.
He's noted to have microscopic hematuria and proteinuria on his recent laboratory data.
He has a history of hepatitis C, genotype 1a,
and he's planned by his hepatologist for direct-acting antiviral therapy.
On physical exam, his blood pressure is elevated to 150/88 mmHg, he has trace,
maybe 1+ lower extremity edema, otherwise, his exam his fairly unremarkable.
On laboratory data, his serum creatinine is slightly elevated at 1.3 mg/dL
and his urine analysis is positive for blood on the dipstick.
When you look at the urine sediment underneath the microscope,
it shows dysmorphic red blood cells, so those funny-shaped red blood cells
that we were talking about.
A few red blood cell casts and that spot urinary albumin-to-creatinine ratio is high at 1.2 g,
meaning that it estimates about 1.2 g in a 24-hour period of time.
When the blood studies, the serological studies, show a low complement C3 and C4.
So, the question is, what is the most likely etiology of this man's renal presentation.
Let's take a look through our history and our exam, and see if we can come to some clinical clues here.
So, I think importantly, our gentleman has microscopic hematuria
and proteinuria in the setting of hepatitis C.
That's important because there are only certain diseases
that are going to manifest with certain viral infections.
So, something like hepatitis C-associated MPGN might be coming to mind.
His exam definitely manifest with some of the features of nephritic syndrome that we talked about.
He has an elevated blood pressure, he's got some edema, proteinuria, and hematuria.
His laboratory data is also interesting.
We see an increase in his creatinine, we also see these dysmorphic red blood cells, and red blood cell cast.
That's a giveaway that there's something going on.
This is what we call an active sediment.
So, this is hematuria of glomerular origin and he also has subnephrotic range proteinuria.
The clincher in this case is that he has a low C3 and C4,
so complement is being activated through that classical pathway of activation.
Taken together with hepatitis C, this really is membranoproliferative glomerulonephritis
in association with hepatitis C.
We'll go over that so you'll understand that process.