The American Society of Pediatric Nephrology Podcast
Sep 28, 2026 · 27 min · 9 segments
In this episode, Drs. Amirtha Chinnadurai and Jason Misurac are joined by Dr. Laurel Willig to discuss APOL1-mediated kidney disease in children. They discuss how to conceptualize APOL1 disease…
Laurel WilligGuest
Amirtha ChinnaduraiHost
Jason MisuracHost
So do you think this is going to be eventually thought of the way we think of FSGS, where we have like a primary and then secondary categories? Or do you think that it'll be thought of differently?
I think I wouldn't be surprised if we started classifying them as APOL1-mediated FSGS or APOL1-mediated hypertension or something to that effect, especially as the therapies develop further.
It will be important to label, I think, those diseases as being mediated by that.
But I do think they may be different enough physiologically that we may want to have subcategories within the big lump of APOL1-mediated kidney disease.
Right, because when it comes along with HIV or some other diagnosis, you're going to also always be treating the underlying diagnosis.
You wouldn't just treat the APOL1 side of things, but them having that high-risk APOL1 genotype means they're more likely to have a more rapid and severe course or progression than they otherwise would with whatever the other cause that they have of kidney disease would be.
And it might be sort of similar to like certain cancers, right? Where if you have this genotype in your cancer, you do X, Y, or Z treatment versus if you don't, you don't do that.
So, you know, if you're talking about like HIV nephropathy, you might have, this is APOL1 mediated HIV nephropathy, and you add as a therapy an APOL1 disease target.
But if you didn't, then you just treat it as... you would HIV nephropathy without the APOL1.
I mean, it's interesting that you, the way how you categorized it, I think that really resonated with like even nephrotic syndrome, for example.
I think patients who develop FSGS and then, you know, through the workup, we find out there's presence of APOL1 There is a notion to think about it as whether this is a genetic cause of FSGS as such to treat it like not needing immunosuppression as such, like congenital nephrotic syndrome, for example.
And, you know, which we're going to talk about in a minute about treatments.
Like I think like how it's not as dichotomous as how we look at it, because like even when we talk about FSGS and APOL1, And in our clinical notes, some are writing as genetic cause of nephrotic syndrome.
I guess like the documentation part of it also needs to reflect like what are we treating?
So do you think this is going to be eventually thought of the way we think of FSGS, where we have like a primary and then secondary categories? Or do you think that it'll be thought of differently?
I think I wouldn't be surprised if we started classifying them as APOL1-mediated FSGS or APOL1-mediated hypertension or something to that effect, especially as the therapies develop further.
It will be important to label, I think, those diseases as being mediated by that.
But I do think they may be different enough physiologically that we may want to have subcategories within the big lump of APOL1-mediated kidney disease.
Right, because when it comes along with HIV or some other diagnosis, you're going to also always be treating the underlying diagnosis.
You wouldn't just treat the APOL1 side of things, but them having that high-risk APOL1 genotype means they're more likely to have a more rapid and severe course or progression than they otherwise would with whatever the other cause that they have of kidney disease would be.
And it might be sort of similar to like certain cancers, right? Where if you have this genotype in your cancer, you do X, Y, or Z treatment versus if you don't, you don't do that.
So, you know, if you're talking about like HIV nephropathy, you might have, this is APOL1 mediated HIV nephropathy, and you add as a therapy an APOL1 disease target.
But if you didn't, then you just treat it as... you would HIV nephropathy without the APOL1.
I mean, it's interesting that you, the way how you categorized it, I think that really resonated with like even nephrotic syndrome, for example.
I think patients who develop FSGS and then, you know, through the workup, we find out there's presence of APOL1 There is a notion to think about it as whether this is a genetic cause of FSGS as such to treat it like not needing immunosuppression as such, like congenital nephrotic syndrome, for example.
And, you know, which we're going to talk about in a minute about treatments.
Like I think like how it's not as dichotomous as how we look at it, because like even when we talk about FSGS and APOL1, And in our clinical notes, some are writing as genetic cause of nephrotic syndrome.
I guess like the documentation part of it also needs to reflect like what are we treating?
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