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Welcome to Katie. 
Go conversations in Nephrology. 

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This episode is titled benefits 
of rassi utilization. 

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For disclosure information. 
Please go to KD. 

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Go dot org slash podcasts here's
your host dr. 

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Roberto perk aphelion. 
Hello and welcome to the que 

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digo conversations in The 
Prodigy. 

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I am dr. 
Herbert Pavilions, senior 

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research, scientist at Arbor 
research collaborative for 

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health. 
Now professor of medicine at the

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pontifical Catholic University 
of paranoia joining me to 

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discuss the benefits of drugs, 
that block the reigning and to 

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Tenzin aldosterone system is dr.
Catherine Clays, dr. 

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Clays is a nephrologist and a 
professor of medicine at 

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McMaster, University in the 
editor-in-chief of the Canadian 

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Journal of Kidney Health and 
disease. 

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Katherine and I share the 
passion for this area of our 

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specialty and I had the 
privilege of co-chairing. 

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The que digo controversies 
conference on the management of 

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this Colony has in kidney 
disease with her Catherine. 

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Welcome to the program. 
Thank you, Roberto. 

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It's great to participate in 
this to be working with you 

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again and to participate in this
discussion on West blockade. 

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All right, so let's get started.
Seems like ass time goes by the 

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renin-angiotensin-aldosterone 
Inhibitors or rassi as I will 

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refer from. 
Now on in this episode are still

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very important Therapies in 
kidney and cardiovascular 

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disease. 
She's actually emphasized by the

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current revised guidelines in 
frolla G and Cardiology. 

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Now what's the main evidence 
based represents to the use of 

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rassi as a cardio? 
A protective therapy. 

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I think that's a great place to 
start with Ewing the randomized 

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evidence here. 
So when I think about the 

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strongest or perhaps the most 
prevalent indication or Reason 

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to use grassy, it would be 
cardiovascular protection in 

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people with cardiovascular 
disease or when people who have 

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diabetes and evidence of end 
organ damage. 

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So high risk vascular 
population. 

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Looking at a cardioprotective 
outcome and this goes back to 

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the Hope Study 20 years ago in 
which grassy would used major 

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cardiovascular. 
Switch. 

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I'm going to call him mace by 
three percent over five years. 

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So it's a large effect, high 
certainty directly applicable to

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people with CKD G1 G2 G3, who 
have established cardiovascular 

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disease, or high risk diabetes. 
So, in summary for cardio 

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protection, strong evidence, 
large effect. 

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This is a great summary about 
the benefits of rassi from a 

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general perspective. 
Now, it seems that there is also

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a robust evidence in heart 
failure. 

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Specifically. 
Right now, such guide. 

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So that evidence is actually our
ruined even more compelling. 

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It's specific to heart. 
Failure with wood used ejection 

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fraction and a good example here
would be say the save trial, 30 

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years ago and this trial where I
see reduced cardiovascular 

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events, but actually would use 
death for all causes by 5%, 

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which was a nominated tweet of 
20. 

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So that's really the strongest 
indication based on the 

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magnitude of the effect. 
And because we have here, Effect

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on all-cause mortality, which is
relatively unusual in Trials, 

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even Trials of cardiovascular 
outcomes. 

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Interesting. 
So can you go Revisited the raw 

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of rassi in patients with 
diabetic and non-diabetic kidney

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disease? 
There's something new in this 

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area when I think about this 
area, I'm really going back 

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again to evidence that was 
generated some time ago, think 

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about the gifts and study, I 
think about the prolific a 

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senior property study and 
fortunately There's a wonderful 

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meta-analysis that individual 
patient meta-analysis of those 

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studies. 
And what they show is that the 

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for people with put new a kidney
disease, there was a reduction 

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in kidney replacement therapy, 
that's dialysis or transplant. 

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That's the really clinically 
important outcome in this area. 

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But having said that, these were
Trials of Port Newark patients, 

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most of those studies. 
Had main put new at Baseline of 

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one gram a day or more and in a 
subgroup analysis within the 

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study, the benefit, in terms of 
kidney. 

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And Sarah P was limited to 
people who had waistline 

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proteinuria with more than 500. 
So that's why we have a 

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recommend, a strongest level of 
recommendation in the Katie go. 

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Blood pressure guidelines for 
2021, and this is why we think 

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that we have very clear evidence
to use, whereas inhibition to 

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prevent kidney failure in people
who have CK D & A 3 up in the 

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new area. 
In people with diabetes. 

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The evidence is comes from 
different trials. 

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Yes. 
But it's similar so we have id&t

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and we're now looking at people 
with microalbuminuria or case we

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as we call it now, looking at 
outcomes of doubling of 

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creatinine or kidney replacement
therapy, and then when we think 

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about people with diabetes and a
to album in your area or 

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microalbuminuria, we can go back
to the Hope Study and look at 

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the cardiovascular outcome, 
which was reduced. 

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So, for this reason, people with
a three-album Anew and CKD, Or a

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two of them in your area or 
above and diabetes. 

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These again are recommend when 
we look at the que digo 

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guidelines. 
So in this area of the block 

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pressure management and CKD, 
there has been some 

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controversies in the final 
report of the guidelines prepare

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by KD go, can you comment on the
decision? 

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Absolutely. 
So the biggest area of 

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controversy I think is the use 
of last blockade in people with 

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a CK D, we can say that somebody
with CKD and a 2 is at high 

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cardiovascular risk. 
We can say that most of these 

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patients or perhaps all of these
patients are at sufficiently 

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high risk that we should 
consider them like participants 

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in the Hope Study and that they 
should be taking last blockade 

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because of the cardiovascular 
benefit. 

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And I think that's a very good 
argument, but it's not the same 

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kind of directness of evidence 
that we have seen when we talked

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about the previous categories of
reasons. 

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To use last blockade when we 
look at the kidney progression. 

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Again, the data that we have on 
much less clear, we have some 

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evidence from the transcend, 
study some evidence from the 

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aask study. 
But again, we do not have that 

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consistency of direct evidence 
that leads to the highest level 

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of recommendation, and TD will 
reflect this controversy by 

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using the word suggests quite 
appropriately in my mind. 

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The other thing that Katie goes 
And with of course, is 

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hypertension in people who don't
have CKD or who have a one C KD 

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in that setting. 
It's not known really. 

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Whether there's a special role 
or a special benefit for us 

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blockade. 
But we can certainly work at 

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Nuys. 
That arsenic mission is going to

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be a useful tool in our toolbox.
When we're treating people with 

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hypertension, particularly when 
we start to apply the results of

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the Sprint study, we're looking 
at a blood pressure Target of 

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less than 120. 
Why are we doing that? 

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And because Cardiovascular 
outcomes were reduced by point 

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five percent in the Sprint 
study. 

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That's a number needed to treat 
a 200 bigger than the numbers. 

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We've talked about before but if
you and your patient come 

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together and make a 
patient-centered decision that 

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you're going to go for Sprint 
Target, the next thing that you 

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need to know is that that's 
going to take about 3 minutes on

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average rather than to meds and 
then we're using three different

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classes of medication having 
grasped locators. 

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One of those classes of 
medication is obviously going to

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be very useful. 
This further Evidence now about 

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a lower blood pressure Target 
from the recently published step

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study out of China. 
They have composite outcome of 

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maize, heart failure and atrial 
fibrillation, but they found 

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that over three years that was 
would use by fully 1% and kidney

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outcomes. 
Long-term kidney outcomes were 

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equivalent. 
So we now have two studies 

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pushing us towards that lower 
blood pressure Target. 

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And what I tend to do is 
approach this in a 

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patient-centered way, I tend to 
say you've prepared to take more

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drugs to have your blood 
pressure lower because Gets 

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better. 
Well, thanks for that Catherine.

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Let's change from the evidence 
and guidelines to the real 

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world. 
Clinical practice, always strike

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by the under utilization of 
Rossi that we see in different 

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real world, the cards. 
For instance, in the u.s. seems 

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like 50% of people. 
This continue rassi within five 

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years of starting. 
What do you think are the 

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challenges in applying this 
evidence? 

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I think that's really a very 
Important point that people are 

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starting and then they're 
stopping. 

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We know from a recent study that
when we look at prevalent 

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patients in the u.s. again, only
50% of people with putting your 

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ex e KD, for example, are 
actually actively on worse 

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inhibition. 
And when we look at the risk 

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factors for being in that 
situation, they are past Aki 

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past hyperkalemia and not being 
under the care of a 

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nephrologist. 
For those just tuning in, you 

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are listening to the key. 
Eagle conversations in frolla G.

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Our topic today is the benefits 
of Rossi utilization and October

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took the cloth video, and I'm 
speaking with dr. 

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Katherine Clays. 
Catherine, coming back to the 

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discussion about the under 
realization of Rossi in the real

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world. 
What do you think of the 

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Practical challenges of using 
this class of drugs in 2021? 

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The first thing to say is I 
don't think this is a knowledge 

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issue was just quoting some 
evidence that suggests that 

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though, only 50% of people. 
Well, with put new Acadia on 

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last blockade, 90% of been on in
the past. 

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I think that people have got the
message. 

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I think that there are 
challenges facing maintaining 

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people on West blockade, and 
those challenges are changes in 

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the creatinine levels, 
hyperkalemia and Aki. 

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So I'm going to start just by 
talking about hyperkalemia when 

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we look at while data only small
proportions of people develop 

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hyperkalemia, but in Clinical 
practice and routine care 

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studies. 
It tends to be higher. 

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So for example, in a Danish 
cohort 16% of people started on 

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grassy developed hyperkalemia. 
In the first six months, in five

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percent of people had Piper 
collinear greater than 6 and is 

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6% of people. 
There was recurrent 

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hyperkalemia. 
The other thing is that 

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potassium in patients at high, 
vascular risk seems to drift up 

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over time. 
So in the Queen's study for 

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example, when Most people would 
know, I think that in the 

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Queen's study people were 
optimized on West blockade at 

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Baseline. 
So this is a study of people who

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tolerate last locate the 
potassium level in Creedence 

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over the 42 months of the study,
just drifts up slowly by an 

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average of .3 millimoles per 
liter, which suggests that over 

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time, it may be harder to keep 
somebody on grass block head. 

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So what can we do about the 
problem of hyperkalemia, in the 

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context of us blockade, there 
are obvious things like looking 

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for Do non-prescribed 
supplements and salt 

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substitutions. 
Look at Co existing medications.

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Like potassium sparing are you 
addicts? 

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And look at Mrs. Unless they're 
being used for specific 

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indication and consider stopping
those things. 

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Very important to my mind is the
use of a diuretic in this 

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context. 
Usually I'll use it Loop 

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diuretic if the GFR is less than
30 and a thiazide. 

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If the GFR is above 30, I want 
to talk a bit about sigh aside 

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because I think the key there's 
a very strong evidence for 

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You're using thiazide in 
hypertension in general, we have

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meta-analyses showing reductions
in cardiovascular outcomes and 

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immortality. 
I also want to promote the use 

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of cloth valadon particularly in
this indication to lower 

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potassium. 
The blood pressure lowering was 

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closed. 
Saladin is superior to the blood

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pressure lowering of 
hydrochlorothiazide and so is 

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the potassium lowering. 
Probably by about point to 

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looked at another way. 
The odds ratio for hypokalemia 

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was 2.7 times that of 
hydrochlorothiazide in a u.s. 

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cohort so 2.7 times as much 
hypokalemia with close salad own

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as with Hydrochlorothiazide 
suggesting that it's a much more

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potent work when it comes to 
lowering potassium. 

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So whereas, this might be a 
caution for you, if you are 

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using it as monotherapy, when 
you are using it to reduce serum

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potassium chloride. 
Solid own is undoubtedly, a 

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better drug to use. 
The other thing is that for many

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A of these patients. 
If you're going for Sprint 

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Target, you're going to need to 
prescribe more than one 

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antihypertensive in any case. 
And in that case the combination

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of arson ambition with a 
thiazide diuretic is a very 

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useful and evidence-based, way 
to approach this. 

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And you'll notice that I'm 
coming to the whole question of 

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diet really right at the end 
because I think these other 

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things should be thought about 
first. 

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And the reason for that is 
because we don't really have 

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trials showing the effectiveness
of diet and we You actually have

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evidence showing that people's 
dietary potassium intake doesn't

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really call it with their 
levels. 

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However, using diet to using 
dietary restrictions to be 

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specific to control. 
Potassium is standard of care, 

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and moving away from this is 
going to be challenging and 

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needs to be done safely. 
So, what I'm doing is I'm 

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thinking very much about 
substituting vegetables, not 

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eliminating them, so the people 
can still have the health 

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benefits of eating vegetables 
and Yeti. 

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Eat vegetables that are lower in
potassium content. 

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I also talked about the meat 
content in the potassium content

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of meat as well. 
We know, for example, in 

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hemodialysis patients, that fall
out of the top five sources of 

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potassium in their diet are 
actually made products. 

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Even unprocessed made often 
contains injected additives and 

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processed meat is even worse. 
So, I would say, if you're 

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discussing diet to put the 
holder on the table, and not to 

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convey the impression that 
vegetables are particularly the 

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demons when it comes. 
To dietary content of potassium,

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right? 
Are there any developments here 

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that you would like to mention? 
What are your thoughts, for 

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example, and passing binders, 
quite well, most of our 

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listeners will be aware that 
there are new potassium, binders

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on the market. 
So, let's just talk about the 

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evidence base that we have here.
The first thing to say is that 

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for none of the potassium 
binders, do we have outcome 

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studies that include outcomes 
that are important to patients 

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or way. 
I used to cop clinically 

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important outcomes for our old 
binder, STS or kayexalate. 

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As it's often called, we have a 
small trial showing efficacy for

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potassium outcomes and then we 
have huge post-marketing 

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experience for homes. 
We have two very large 

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well-conducted, observation 
studies. 

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Looking at the magnitude of 
severe GI consequences of taking

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SPS and though it looks like 
there is a signal there. 

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My general take home from those 
studies is actually one of 

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reassurance. 
Because the absolute numbers are

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very small. 
We turn to the new binders, we 

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have a different situation. 
We have Trials of several 

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hundred patients. 
We don't have patient important 

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outcomes but we have lots of 
data showing, potassium outcomes

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and also showing non 
discontinuation of gasp. 

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Okay, that it's possible to keep
people on whereas blockade by 

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using these binders. 
We also know that the adverse 

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effects in those trials though 
they're not negligible or 

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probably acceptable. 
But of course what we don't have

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here is the face for experience 
that post marketing experience 

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about the way homes. 
So in my own practice, I 

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continue to use SPSS over time. 
I think we'll need to look at 

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the observational evidence, 
that's emerging about harms, and

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we'll also need to look at cost 
and cost Effectiveness. 

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So that's one new area. 
And then the other thing that I 

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find really exciting is 
literally just published this 

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month on sglt2 Inhibitors and 
I'm grateful to you for pointing

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this evidence out. 
Many populations that benefit 

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from u.s. inhibition of now 
being shown to also benefit from

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sglt2 Inhibitors ssion and the 
New Evidence is that in 

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Credence, at least with Canada 
Frozen. 

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There was a reduction in a 
variety of different potassium 

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related, adverse outcomes by 22 
to 34 percent. 

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So, that's quite a big risk 
reduction we're seeing in 

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potassium in a high potassium 
related outcomes. 

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An Really, you're not almost 
magically. 

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There's no difference in mean, 
potassium and there's no 

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increase in hypokalemia. 
So really, it's possible that 

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when we add an sglt2 Inhibitors,
and I wouldn't add it for 

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potassium alone, but if you add 
it, for one of the many 

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indications for sglt2 
inhibition, that that is going 

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to make it easier to avoid these
upwards. 

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Excursions of potassium that 
lead to a patient being 

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identified as hyperkalemic and 
that lead to as blockade. 

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Stop interesting to hear that 
there are multiple strategies 

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other than diet that we can use 
for controlling potassium. 

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I think our patients would also 
be happy to hear about that. 

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Are there any other particular 
challenges in keeping people on 

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00:17:40,800 --> 00:17:43,500
rassi? 
Yes, there are two other things 

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that I'd like to mention the 
first is acute kidney injury, so

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we aren't certain based on 
observational data when we have 

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an episode of acute kidney 
injury, We should restart people

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00:17:56,500 --> 00:18:00,900
aren't as blockade, but given 
this uncertainty and given the 

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00:18:00,900 --> 00:18:04,900
wealth of randomized evidence 
that we have for benefit in. 

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00:18:04,900 --> 00:18:09,500
Those specific situations, I was
talking about my personal 

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preference is to assess the risk
for recurrent Aki. 

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00:18:14,200 --> 00:18:18,400
If it's truly extreme, if a 
patient is coming into emergency

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with a high-output early ostomy 
and recurrent hypovolemic shock,

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then I might not restarted. 
But if there were 64, Aki are 

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the same as their risks for 
Progressive, kidney disease, and

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for cardiovascular disease. 
Then I do tend to restart West 

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located after Aki. 
The second issue is changing 

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creatinine, particularly 
changing creatinine with 

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00:18:40,000 --> 00:18:43,900
starting. 
We've all come to recognize that

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the idea that we should stop us 
blockade. 

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00:18:47,200 --> 00:18:50,000
If there's a change of more than
thirty percent is actually not 

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evidence based for sure a large 
Excursion in creatinine. 

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A large change in creatinine. 
Like, that is a bad prognostic 

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marker. 
Multiple studies show this. 

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But what we don't have is 
evidence that that change is 

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then associated with a reduced 
ability to benefit from the last

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00:19:06,900 --> 00:19:09,200
blockade itself. 
The other thing we know is that 

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in general for rasp locate 
Associated changes, when we 

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00:19:13,400 --> 00:19:17,600
repeat the creatinine in another
couple of weeks, it tends to go 

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00:19:17,600 --> 00:19:20,800
back towards Base Line and about
50%. 

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So unless the change in 
creatinine is truly extreme What

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00:19:24,800 --> 00:19:28,400
I suggest is following the 
trajectory stop the last 

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00:19:28,400 --> 00:19:31,400
placate, only if it's 
Progressive, and when you stop 

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00:19:31,400 --> 00:19:34,700
it, if the creatinine doesn't 
improve and your hypothesis, 

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00:19:34,700 --> 00:19:37,600
doesn't look as if it's correct,
then that's another great 

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00:19:37,600 --> 00:19:41,100
situation where you can 
consider, restarting grasp. 

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00:19:41,100 --> 00:19:44,800
Okay, it's a great Point. 
Catherine there, any final 

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00:19:44,800 --> 00:19:47,000
message you'd like to leave with
our listeners. 

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00:19:47,300 --> 00:19:50,400
I'd like to go back to when 
you're prescribing this. 

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00:19:50,400 --> 00:19:53,200
Think about what the indications
are the magnitude of the 

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00:19:53,208 --> 00:19:55,900
benefit. 
And remember that for many of 

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00:19:55,900 --> 00:19:58,900
the patients that were treating 
cardiovascular outcomes are more

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00:19:58,900 --> 00:20:02,300
numerous than kidney outcomes, 
even fun of artists. 

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00:20:02,700 --> 00:20:05,600
And then the second thing is to 
think about the residual risk, 

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00:20:05,600 --> 00:20:09,200
even though these are quite 
drugs and they would use risk, 

353
00:20:09,200 --> 00:20:13,000
consistently and biologic fact, 
we know the risk is still high 

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00:20:13,000 --> 00:20:16,400
for many patients and we now 
have strong evidence to use 

355
00:20:16,400 --> 00:20:21,000
additional therapies like, sglt2
Inhibitors, and Mrs, for many of

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00:20:21,000 --> 00:20:24,300
the same indications as well as 
see as add-ons Therapies. 

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So I'm always thinking about 
that. 

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It's a great way to round out 
our discussion today when you 

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think my guest dr. 
Katherine glaze for joining me. 

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Catherine was great. 
Having you on the program? 

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Thank you for having me. 
It's been an honor to 

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00:20:39,800 --> 00:20:41,400
participate. 
I am dr. 

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00:20:41,400 --> 00:20:45,500
Herbert I'll see you soon to 
access this and other episodes 

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00:20:45,500 --> 00:20:49,100
of the series. 
Visit Kate evil.org, Clash 

365
00:20:49,100 --> 00:20:54,100
podcast, thanks for listening. 
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366
00:20:54,100 --> 00:20:56,700
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367
00:20:56,700 --> 00:20:56,700
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