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Welcome to KD GO Conversations 
in Nephrology. 

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This episode titled How I Treat 
IGA Nephropathy Lessons from the

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Case Files is provided by KD Go 
and supported by Trevier. 

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Here's your host, Doctor Donna 
Rizik. 

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Hello and welcome to KD Co 
Conversations in Nephrology. 

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I'm Doctor Donna Rizik. 
I'm Professor of Medicine in the

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Division of Nephrology at the 
University of Alabama at 

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Birmingham, where I also serve 
as the Associate Dean for 

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Clinical Trial Research in the 
School of Medicine. 

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Joining me today to discuss IG 
and nephropathy treatment are 

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two distinguished guests, Doctor
Andrew Lazar and Dr. Gaya Kopoc.

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Doctor Kopuk is an Assistant 
Professor at the University of 

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Pennsylvania School of Medicine,
where she runs the Glomerular 

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Disease Clinical Trials Group, 
and her clinical and research 

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interests include 
immunomodulation in glomerular 

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diseases. 
Dr. Lazdar is the Clinical Trial

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Director at the University 
Hospitals of Cleveland, and his 

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clinical and research interests 
include glomerular diseases, 

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genetics in kidney diseases, and
the development of an 

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implantable dialysis device. 
Doctor Kobuk and Doctor Lazar, 

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welcome to the podcast. 
Thank you. 

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It's so great to be here. 
I really appreciate you having 

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me. 
Thank you. 

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Pleasure. 
So we have a nice conversation 

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ahead of us in light of the 
updated KD GO guidelines. 

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And as a reminder for perhaps 
our listeners, over the past two

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sessions, we reviewed some of 
the data behind the new KD GO 

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guidelines that were recently 
published and the IGN 

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nephropathy pathophysiology. 
So today we're hoping to 

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illustrate how we would apply 
these new guidelines to cases 

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that we see in our daily 
practices. 

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So I'm going to just share with 
you a couple of cases and see 

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how you would manage again in 
light of these new guidelines. 

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So let's start with a newly 
diagnosed case. 

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This is a 19 year old Caucasian 
man with a history of 

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depression, chronic Constipation
complicated by hemorrhoids, but 

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no history of inflammatory bowel
diseases who presents with 

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grossy materia around May of 
2025 after having a sore throat.

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At the time of resentation, his 
creatine was around 0.9 

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milligram per deciliter and his 
prior known baseline was about 

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0.7 and he was found to have 
quite a bit of hematuria with 

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more than 100 red blood cells 
per high power field and quite a

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bit of proteinuria with about 
2.3g per gram on a UPCR. 

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So evidently, he was referred 
for kidney biopsy that confirmed

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the diagnosis of IGA nephropathy
and his missed score that was 

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provided by the pathologist was 
M1E 1S1, T0 and C1O Gaia. 

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Let me start with you. 
How would you approach the 

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management of this patient? 
O you know, I think that this is

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a great example, maybe a classic
example of why we need to 

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address both immunologic and non
immunologic aspects of disease 

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in our patients with IGA 
nephropathy. 

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This one I think has a lot of 
features that would make us 

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concerned for immune activation,
including, you know, his young 

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age is hematuria, the higher 
grade proteinuria and then of 

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course the inflammatory changes 
on his mass C score, the M1, E 1

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and C1. 
And so I think this is a very 

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good example of somebody who I 
would quite early try to put on 

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HIT one targeting drug as well 
as HIT for targeting agents. 

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You know, in terms of what to 
choose for him for the HIT one 

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approach. 
You know, right now we're still 

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we're choosing often times 
between systemic steroids and 

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targeted release budesonide. 
This is a young person who has 

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relatively well preserved kidney
function and is a new diagnosis.

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And so just kind of to minimize 
toxicity and and hopefully 

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achieve good outcomes for him, I
think that targeted release 

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budesonide would be a good 
choice. 

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You know, with the systemic 
steroids, oftentimes it comes 

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with the prophylaxis and other 
pills. 

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And so especially for a young 
person, I think that that can be

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a little bit more of an 
overwhelming choice. 

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And then I like the data for 
targeted really speed us tonight

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efficacy. 
So that would probably be what I

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would choose for his hit one 
drugs. 

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That sounds great. 
Yeah. 

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And I guess if one doesn't have 
access to targeted release, the 

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desonide and systemic steroids 
at the low dose based on the 

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testing trial would be another 
option for sure. 

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So Andy, besides the immunologic
management of this patient, 

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would you consider any CKD 
management? 

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And if So, what would you start 
with? 

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I certainly would. 
I have a 19 year old, so I'm a 

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little bit afraid that I'm going
to bombard this young person 

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with a lot of drugs. 
So I know that we have to be a 

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little bit careful or will 
probably affect adherence, but I

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tell patients that I'm really as
much their cardiologist as I am 

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just about anything else. 
Any CKD patient including NYGIA,

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nephropathy patients, they are 
at greater cardiovascular risk, 

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certainly the worst their CKD 
is. 

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We know that they really have a 
shorter lifespan. 

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So very early on out of the gate
for this patient while we're 

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thinking about what can we do to
lower the chance hit one, hit 

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two, hit three at 4, we've got 
to think about we've got to get 

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blood pressure under control. 
We have data to show that these 

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patients probably should be in 
the less than 130 range and they

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often do have high blood 
pressure. 

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So certainly we want them on Ras
inhibitors. 

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But I think going to an 
endothelin antagonist early, you

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know, certainly if I can use a 
drug, maybe 1 drug to improve 

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adherence, where I can do Ras 
inhibition and I can do 

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endothelin antagonism should be 
something that we should think 

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about. 
We know when we add an 

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endothelin antagonist, we 
usually drop by about another 5 

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systolic, you know, So that's 
something I want to think about 

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in addition to that Ras 
inhibitor, Thinking about the 

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SGLT 2 inhibitors, we have a lot
of data now to show that we know

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they do lower proteinuria and 
that's something they want to do

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as fast as possible. 
The less amount of time that we 

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allow patients to be protein 
uric, we, we don't want that 

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proximal tubule to have all that
protein that it can take up, you

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know, and all the inflammation 
and the tubular interstitial 

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fibrosis that may follow. 
So we know that SGLT twos are 

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going to lower prognuria. 
We know it looks like they 

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probably save us EGFR maybe on 
the order of about 1mm per 

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minute per year. 
And when you look at trials like

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DAPA CKD where they had 270 such
patients, IGA patients, we know 

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that adding the SGLT 2 for these
pay that it did lower 

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cardiovascular events. 
You know you looked at 

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cardiovascular events last end 
stage and it lowered at about 

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70%. 
So I think pretty much out of 

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the gate I've got to think about
blood pressure, you know, so I'm

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going to think about Endofeon 
attacks them, the Ras inhibitors

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and I'm going to think about 
also LDL cholesterol that is 

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probably going to be next, you 
know, and we have data also I 

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gap patients LDL greater than 
100 are also a greater 

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cardiovascular risk and maybe 
even renal worsening. 

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But I'll be careful adding too 
many drugs too fast. 

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Yeah, I agree, especially with a
19 year old who was probably 

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healthy a week earlier prior to 
his biopsy. 

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So even though the guidelines do
recommend potentially starting 

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multiple agents at the same 
time, that doesn't mean we have 

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to start them all on one single 
day. 

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I totally agree with you. 
And you bring up and remind us 

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again of the cardiovascular risk
that's associated with kidney 

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disease, even in these young 
individuals. 

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So something to keep in mind and
definitely look for 

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hyperlipidemia. 
Vaping is a big deal. 

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I don't know about you guys, but
we see a lot of vaping now. 

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So you ask about smoking, they 
say no, I don't smoke. 

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So you have to specifically ask 
about vaping, which is another 

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risk factor. 
So, so guy, going back to you, 

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this gentleman had the C1 lesion
and you kind of alluded to the 

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fact that this is part of, you 
know, kind of your treatment 

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choice and you look at the 
inflammatory lesions. 

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Although of course, the 
guidelines could not have any 

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stand on the use of the mesc 
score for treatment choice, 

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simply because the data is not 
there. 

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All the trials did not take into
account, you know, athology 

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findings, but I think in 
practice we do look at these 

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lesions. 
So can you walk me a little bit 

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through what are your thoughts 
and how do you distinguish that 

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from a crescentic disease? 
Yeah. 

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I mean, I think crescents and 
IGA nephropathy are the very 

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murky space because we see 
crescents and nephrology and it 

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makes us quite alarmed. 
But of course, there is a 

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distinction particularly in 
these patients between an RPGN 

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and less than 25% of glomeruli 
with crescents, which is the C1 

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lesion. 
So with RPGN they fall outside 

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the KD GO guidelines because 
they're not well they're 

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addressed in the ego guidelines,
but they fall outside sort of 

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these new recommendations for 
management because people with 

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RPGN were excluded from clinical
trials. 

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And so we do tend to and I tend 
to still treat them sort of with

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the classic steroids and 
cyclophosphamide based approach 

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more like a traditional RPGN 
management. 

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However, this is this 
population, we see these people 

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with Crescent sometimes even 
with like minimal other 

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inflammatory changes in IGA 
nephropathy. 

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And I think the mess group 
updated their scoring system in 

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2017 to try to address these 
patients specifically. 

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But it's such a sort of sporadic
finding that the data have been 

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sort of a little bit hard to to 
classify. 

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And so you know, as you said, 
the messy score is more about 

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prognosis than it is about 
guiding management. 

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But I certainly with AC1 score 
would not put them into an RPGN 

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category. 
But my personal preference is to

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treat those people with 
immunosuppression. 

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Whereas in that higher grade, 
that RPGN category, more C2, I 

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treat them more aggressively. 
Their prognosis tends to be core

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regardless of treatment because 
it's a more inflammatory 

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subgroup. 
But we try very hard to do 

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everything we can to mitigate 
their disease. 

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Yeah, great point. 
And again, RPGN just to remind 

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the audience is a clinical 
diagnosis really. 

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So you just have to look at this
patient's trend in terms of 

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fries and serum creatinine. 
So and did the critical 

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guidelines mentioned the goal of
reducing galactose deficient 

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IGA, one that hit one that we've
been talking about and the 

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circulating immune complexes. 
So how do you in your clinic 

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when you're seeing patient, how 
do you operationally, how do you

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look at this at the time when we
really don't have the biomarkers

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at our fingertips? 
That's really a great question. 

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I think the three of us and I 
know a lot of the audience are 

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very excited about precision 
nephrology that we're trying to 

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head there. 
We don't want to put every 

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single patient on all the agents
that we have available to us. 

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So we are, you know, I hope that
we're nearing that time that 

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we'll have biomarkers, but 
looking at that table, you know,

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in the KD GO guidelines where 
they really prioritize thinking 

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about galactose division, IGA 1 
and circulating immune complex 

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complexes made me really happy. 
Hopefully, you know, in the not 

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so distant future, we'll be able
to look at GDIG A1 and as 

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probably a correlate to 
circulating immune complexes. 

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So, but the way that I 
prioritize it now or the way I 

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really operationalize it is I 
want to think about prioritizing

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agents that I know do lower GDIG
A1. 

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They have legitimized it you 
know in the guideline. 

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So we do know that TR budesonide
does lower GDIG A1, you know 

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maybe on the order of almost 
about 30%. 

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And we know that some of the B 
cell modulators that we will 

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have soon are the other agents. 
We know that to lower GDIG A1 

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and some of those the anti 
April's you know as well as the 

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anti bath slash April's I know 
have even looked. 

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They have also measured 
circulating immune complexes GD 

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IGA one in the accompanying IgG 
to it. 

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And so looking at being able to 
employ those drugs first are 

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what I'll be looking forward to 
doing. 

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I personally am also very 
excited about other biomarkers 

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coming. 
Looking at some of the soluble 

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CD163 data that you know is a 
marker of the M2 macrophage 

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activation, which looks like 
that's going to correlate maybe 

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with the inflammation of IGA 
nephropathy. 

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This is where I hope things are 
going, that we'll be able to 

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look at these biomarkers and 
choose drugs and then see what 

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happens to those biomarkers as 
we treat. 

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Yeah. 
I think people are working hard 

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to get these biomarkers to 
clinical practice. 

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And I would say to the audience 
to keep an eye out on some of 

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the exploratory studies that 
come out of the large clinical 

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trials because they will all be 
looking at different biomarkers 

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to hopefully guide treatment 
choice in the future. 

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So if you're just tuning in, 
you're listening to the KD Go 

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podcast on how I treat IGA 
nephropathy, lessons from the 

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case files. 
I'm Doctor Dana Rizik and it is 

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my pleasure today to be speaking
with Doctor Andrew Lazar and Dr.

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Gaya Kopak. 
So let's move on to our second 

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case. 
This is a little bit different 

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in that this is a prevalent case
that comes to your office. 

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A 34 year old Korean woman who 
has a history of obesity and 

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uveitis. 
She has had episodes of 

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synpharyngetic hematuria after 
strep infections as a child and 

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ultimately underwent 
tonsillectomy. 

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Since that time, she has not had
any more recurrences of her 

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grocery Victoria. 
She reports having had the 

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biopsy as a child but does not 
have access to the biopsy report

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she presents to your office. 
Refers from her primary care 

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physician with microscopic 
hematuria and proteinuria as 

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well as mild CKD with a 
creatinine of 1.4 milligram per 

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deciliter. 
Her UPCR was 2G per gram and her

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urine analysis was remarkable 
for not only proteinuria but 

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also hematuria with five to 10 
red blood cells per high power 

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field. 
She's already on the Ras 

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blockade for treatment of 
hypertension. 

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So you send her to have a repeat
kidney biopsy and again you 

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confirm the diagnosis of IGN 
nephropathy. 

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This time in this case, the mesc
score is M0E0S1T0 and C0. 

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So Andy, let me start with you 
in clinic. 

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Do you calculate the patient 
risk using the IGN prediction 

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tool at the time of a biopsy? 
And if you do, what do you do 

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with that information? 
I like to use the IGAN 

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prediction tool and I try to get
my fellows to use it also. 

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I do it because I can start to 
better communicate with the 

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patient regarding just how bad 
IGAN is and I do it. 

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This may sound funny, but I like
to do it also to remind myself 

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of how sick these people are. 
Because, you know, I trained 

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during those years where we 
didn't think. 

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Again, patients did that poorly,
but we didn't realize that 

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they're so young when we meet 
them. 

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And you know what? 
20 years may seem like a long 

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time, but it's not when you're 
30 years old and suddenly you're

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on dialysis or requiring 
transplant when you're only 50 

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years old. 
So I think that I'd like to do 

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that. 
You know, I'd like to be able to

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take clinical and look at that 
biopsy to use a validated tool 

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that I could sit with the 
patient to say you fall into 

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this low, medium or high risk. 
But what's funny is that a low 

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risk of 15%, let's say of a 50% 
drop in GFR or end stage kidney 

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disease at 5:00 or seven years, 
you know, it's still pretty darn

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high, you know, So I think it 
really instructs the patient. 

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It reminds me that wait a 
second, these patients really 

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are ill. 
What I like to do is do it at 

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the time of biopsy with the 
first two that have been 

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published and then consider 
about two years later, I'll use 

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the updated tool that was 
published maybe in 2022 that I 

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can do the math when a biopsy 
was done up to one to two years 

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prior. 
And I'll like to do the math 

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upfront, do the interventions we
do, and then do the math using 

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that updated tool two years out 
and see if we've moved that 

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needle. 
Yeah, hopefully the risk, you 

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know, is reduced by then. 
So you make a great point. 

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The tool can predict up to 5, up
to seven years maybe, which in 

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somebody's lifespan is not a 
long period of time, but it does

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really put in perspective 
sometimes how bad the prognosis 

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is. 
I totally agree with you. 

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So and then the older you get, 
the, you know, the more you feel

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like, oh, you know, 40 years 
old, 50 years old is nothing. 

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They still have a long time 
ahead of them. 

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00:17:28,720 --> 00:17:32,520
So Gaia, in this case, does the 
patient's racial background, so 

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the fact that she is Korean, 
change your approach to 

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management and if so, how? 
Yeah. 

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So, you know, the East Asian 
population, they tend to have 

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had a little bit more success 
with different immunosuppression

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options looking back 
historically at data. 

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And I think that has led to KD 
go including some alternative 

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therapies for these populations,
specifically cellcept or 

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mycophenolate moffatile we can 
use in East Asian patients. 

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Primarily it's indicating K 
digo. 

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00:18:04,480 --> 00:18:07,560
They referenced the Chinese 
population tonsillectomy, which 

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00:18:07,560 --> 00:18:12,200
this patient did have as a child
is also in the K digo guidelines

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for Japanese populations. 
And so although I mean that 

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comes from the evidence, but 
sometimes I think in East Asian 

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populations in general, I will 
sometimes try an alternative 

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agent even if they don't fit 
into the exact basket. 

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Just with the knowledge that 
those studies and in these 

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various ethnic groups have shown
some more efficacy than we've 

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seen, like in some European 
studies, for example, in terms 

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00:18:40,480 --> 00:18:43,680
of the newer agents, the 
targeted targeted release 

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00:18:43,680 --> 00:18:48,880
budesonide recruited very few 
Asians in their study, which is 

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00:18:48,880 --> 00:18:52,560
something to maybe consider when
you're trying to think about how

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00:18:52,560 --> 00:18:55,400
it may apply to our own patient 
populations. 

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00:18:55,720 --> 00:19:00,680
Systemic steroid trials actually
tended to recruit larger numbers

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00:19:00,880 --> 00:19:06,680
of of Asian populations. 
And so I think that has been not

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necessarily a criticism, but 
it's always something that's 

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looked at in clinical trials 
because we know this in our 

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00:19:12,600 --> 00:19:16,520
field that with patients with IJ
nephropathy, when you see a 

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00:19:16,520 --> 00:19:20,520
response to immunosuppression as
a reader, we always try to see, 

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00:19:20,520 --> 00:19:24,520
is this skewed by a population 
that tends to respond better to 

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00:19:24,520 --> 00:19:27,520
immunosuppression or does it 
have more of a global effect 

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00:19:27,520 --> 00:19:30,320
across different ethnic groups? 
And I think because this 

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00:19:30,320 --> 00:19:33,840
question comes up a lot, there's
a big focus in the newer 

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00:19:33,840 --> 00:19:38,080
clinical trials that are being 
published to have a good 

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00:19:38,080 --> 00:19:42,240
representation across diverse 
population so that they can try 

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00:19:42,240 --> 00:19:45,720
to answer more of these 
questions about like 

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00:19:45,720 --> 00:19:48,960
applicability and which of our 
patients might have a better 

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00:19:48,960 --> 00:19:50,920
chance of response. 
Yeah. 

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00:19:50,920 --> 00:19:54,160
And I think emerging data from 
these large clinical trials, at 

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00:19:54,160 --> 00:19:56,240
least the baseline 
characteristics that they're 

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00:19:56,360 --> 00:20:00,200
sharing publicly, does look like
they've achieved that goal of 

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00:20:00,200 --> 00:20:02,200
having this global 
representation, which is 

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00:20:02,200 --> 00:20:05,400
wonderful. 
So with that, I want to thank my

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guests, Doctor Andrew Lazar and 
Dr. Gaia Kopak for joining me 

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today. 
It was absolutely a great 

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00:20:11,640 --> 00:20:13,640
pleasure having you on the 
podcast. 

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Thank you so much. 
It's great. 

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Really appreciate you having me.
Thank you. 

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Thank you both. 
I am Doctor Dana Rizuk and to 

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access this and other episodes 
in our series, please visit 

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00:20:24,960 --> 00:20:29,520
kdgo.org/podcast and thank you 
so much for listening.