FIDELIO..............................pdf

Key Findings from FIDELIO-
DKD: How Finerenone
Enhances Renal Outcomes
in T2D with CKD
PP-Fi-ID-0066-1

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➢ Bayer shall not assume any liability with respect to any damages caused by use of these slides or parts thereof
➢ Finerenone is currently approved in Indonesia to treat chronic kidney disease (with albuminuria) in adults with type
2 diabetes.
➢ This slide is unbranded, and the data presented in this deck do not endorse or recommend the use of Finerenone
in any country or for any indications that are not officially approved
Disclaimer

Mechanisms of MRA-Mediated Cardiovascular and Renal Protection
via Inhibition of Aldosterone-Induced MR Overactivation
Finerenone
Spironolactone Eplerenone
1st Generation 2nd Generation 3rd Generation
(1st Generation
of ns-MRA)
Generations of
MRAs
ns-MRA: non-steroidal Mineralocorticoid Receptor Antagonist
Curr Diab Rep. 2019 Jan 23;19(1):4.
Extracted from MA-M_FIN-ID-0088-1

To investigate the safety and
efficacy of finerenone, in addition to
standard of care, in reducing
cardiorenal mortality and morbidity
in patients with T2D and CKD
Bakris GL, et al. Am J Nephrol 2019;50:333–344

Eligible patients were those with CKD and T2D, treated
with a maximum tolerated dose of an ACEi or ARB
*Mean sitting SBP ≥170 mmHg or mean sitting DBP ≥110 mmHg at the run-in visit or mean sitting SBP ≥160 mmHg or mean sitting DBP ≥100 mmHg at the screening visit; #known significant non-diabetic kidney disease,
including clinically relevant renal artery stenosis
G1: high and optimal; G2: mild; G3a: mild to moderate; G3b: moderate to severe; G4: severe; G5: kidney failure
ACEi, angiotensin-converting enzyme inhibitor; ACS, acute coronary syndrome; ARB, angiotensin receptor blocker; CKD, chronic kidney disease; CV, cardiovascular; DBP, diastolic blood pressure; eGFR, estimated glomerular
filtration rate; GFR, glomerular filtration rate; HbA1c, glycated haemoglobin; NYHA, New York Heart Association; HFrEF, heart failure with reduced ejection fraction; SBP, systolic blood pressure; T2D, type 2 diabetes
1. Pitt B, et al. N Engl J Med 2021;385:2252–2263; 2. KDIGO. Kidney Int Suppl 2013;3:1–150
Aged ≥18 years
with T2D
On maximum
tolerated dose of
ACEi or ARB for
≥4 weeks
Serum [K+] ≤4.8 mmol/l
Diabetic
retinopathy for
patients with A2
albuminuria
HFrEF with
NYHA Class II–IV
HbA1c >12%
Uncontrolled
arterial
hypertension*
Other kidney
disease#
Key inclusion
criteria
Key exclusion
criteria
Albuminuria categories
(mg albumin/g creatinine)
A1
Normal to mildly
increased
A2
Moderately
increased
A3
Severely
increased
0–29 30–299 ≥300–≤5000
GFR
categories
(ml/min/1.73
m
2
)
G1 >90
G2 60–89
G3a 45–59
G3b 30–44
G4 15–29
G5 <15

eGFR and UACR categories Recruitment caps
*Recruitment cap: In FIDELIO-DKD, patients with moderately increased albuminuria and diabetic retinopathy were capped at 10% of all randomised patients and patients with severely increased albuminuria and eGFR 60–75
ml/min/1.73 m2 were capped at 10% of patients randomised with severely increased albuminuria
G1: high and optimal; G2: mild; G3a: mild to moderate; G3b: moderate to severe; G4: severe; G5: kidney failure
CKD, chronic kidney disease; eGFR, estimated glomerular filtration rate; UACR, urine albumin-to-creatinine ratio
A high proportion of eligible patients were those with
stage 3–4 CKD and severely increased albuminuria
Two pre-specified recruitment
caps closed per region limited the
randomisation patients
Patients with UACR
≥30–300 mg/g and
diabetic retinopathy
of all randomised
patients
Patients with UACR
≥300–≤5000 mg/g
and an eGFR 60–<75
ml/min/1.73 m2
of patients randomised
with severely increased
albuminuria
(~9% of all randomised patients)
25
75
≤4.8 mmol/l
at run-in and
screening visits
+ +
Albuminuria categories (mg albumin/g creatinine)
A1
Normal to mildly
increased
A2
Moderately
increased
A3
Severely
increased
0–29 30–299 ≥300–≤5000
GFR
categories
(mL/min/1.73
m
2
)
G1 >90
G2 60–89
G3a 45–59
G3b 30–44
G4 15–29
G5 <15
10%
*
9%*
~10% ~10%
[K+]

*Up-titration of study drug from 10 to 20 mg od was encourage from Month 1 provided serum potassium ≤4.8 mmol/l and was eGFR stable; down-titration of study drug from 20 to 10 mg od was permitted at any time after
start of treatment; #ESKD or sustained eGFR <15 ml/min/1.73 m2; ‡confirmed by two eGFR measurements ≥4 weeks apart
ACEi, angiotensin-converting enzyme inhibitor; ARB, angiotensin receptor blocker; CV, cardiovascular; eGFR, estimated glomerular filtration rate; ESKD, end-stage kidney disease; HF, heart failure; MI, myocardial
infarction; od, once daily; R, randomisation
Bakris GL, et al. N Engl J Med 2020;383:2219–2229
FIDELIO-DKD was a double-blind, randomised,
placebo-controlled trial
2.6 years’ median
follow-up
Placebo
+SoC
10 mg od (if eGFR 25–<60 ml/min/1.73 m2)
20 mg od (if eGFR ≥60 ml/min/1.73 m2)
R
Screening
Run-in
5734 patients
randomised
4–16 weeks
Optimisation of ACEi/ARB therapy
Primary endpoint
Kidney composite:
time to kidney failure#, sustained
≥40% decrease in eGFR from
baseline‡, or kidney death
Key secondary endpoint
CV composite:
time to CV death, non-fatal MI,
non-fatal stroke, or hospitalisation
for HF
Finerenone*
+SoC
13,911 patients
enrolled

Summary of Baseline characteristics
ACEi, angiotensin-converting enzyme inhibitor; ARB, angiotensin receptor blocker; CKD, chronic kidney disease; UACR, urine albumin-to-creatinine ration
Median follow-up was 2.6 years
At baseline, patients had
advanced CKD, with a
mean eGFR of 44 ml/min/1.73m2
and a median UACR of 852 mg/g
98% and 99% of patients
were treated with a
maximum tolerated dose
of an ACEi or ARB,
respectively
Adherence to treatment was high
(~92% in the finerenone and
placebo groups)
Cumulative treatment duration
and number of permanent
discontinuations were similar
between finerenone and placebo

Kidney failure*, sustained ≥40% decrease in eGFR from baseline, or renal death#
On top of maximum tolerated RAS therapy, finerenone
significantly reduced the primary kidney outcome by 18%
*ESKD or an eGFR <15 ml/min/1.73 m2; #Events were classified as renal death if: (1) the patient died; (2) KRT had not been initiated despite being clinically indicated; and (3) there was no other likely cause of death;
‡number of patients with an event over a median of 2.6 years of follow-up
CI, confidence interval; eGFR, estimated glomerular filtration rate; ESKD, end-stage kidney disease; HR, hazard ratio; NNT, number needed to treat; RAS, renin–angiotensin system
Bakris GL, et al. N Engl J Med 2020; 383:2219–2229
No. at risk
Finerenone 2833 2607 1808 787 83
Placebo 2841 2586 1758 792 82
Time to first event (months)
Cumulative
incidence
(%)
0
0
6 12 18 24 30 36 42 48
10
20
30
40
HR=0.82; 95% CI 0.73–0.93
p=0.001
Placebo
Finerenone 504/2833 (17.8%)‡
600/2841 (21.1%)‡
18%
RRR

Finerenone had consistent effects on the components
of the primary kidney-specific composite outcome
Outcome
Finerenone
(n=2833)
Placebo
(n=2841) HR (95% CI)
p-
value
n (%)
n per
100 PY
n (%)
n per
100 PY
Primary composite kidney
outcome
504 (17.8) 7.59 600 (21.1) 9.08 0.82 (0.73–0.93) 0.001
Kidney failure* 208 (7.3) 2.99 235 (8.3) 3.39 0.87 (0.72–1.05) –
End-stage kidney disease 119 (4.2) 1.60 139 (4.9) 1.87 0.86 (0.67–1.10) –
Sustained# decrease in eGFR
to <15 ml/min/1.73 m2 167 (5.9) 2.40 199 (7.0) 2.87 0.82 (0.67–1.01) –
Sustained# ≥40% decrease in
eGFR from baseline
479 (16.9) 7.21 577 (20.3) 8.73 0.81 (0.72–0.92) –
Renal death 2 (<0.1) – 2 (<0.1) – – –
0,50
Favours finerenone Favours placebo
1.00 2.00
According to N Engl J Med policy p-values are not reported for components of composite outcomes; *Kidney failure defined as either ESKD (initiation of chronic dialysis for ≥90 days or kidney transplant) or sustained
decrease in eGFR <15 ml/min/1.73 m2; #confirmed by two eGFR measurements ≥4 weeks apart; CI, confidence interval; eGFR, estimated glomerular filtration rate; ESKD, end-stage kidney disease; HR, hazard ratio;
PY, patient-years; Bakris GL, et al. N Engl J Med 2020; 383:2219–2229

Primary kidney outcome components: The incidence of kidney
failure was numerically lower with finerenone vs placebo
*Kidney failure defined as either ESKD (initiation of chronic dialysis for ≥90 days or renal transplant) or sustained decrease in eGFR <15 ml/min/1.73 m2;
#number of patients with an event over a median of 2.6 years of follow-up
CI, confidence interval; eGFR, estimated glomerular filtration rate; ESKD, end-stage kidney disease; HR, hazard ratio
Cumulative
incidence
(%)
2833 2733 2658 2506 1932 1393 897 510 104
2841 2741 2645 2508 1911 1390 892 513 103
No. at risk
Placebo
Finerenone
208/2833 (7.3%)#
235/2841 (8.3%)#
HR=0.87; 95% CI 0.72–1.05
0 6 12 18 24 30 36 42 48
Placebo
Finerenone
0
10
20
30
Incidence of kidney failure*
13%
RRR

Primary kidney outcome components: Finerenone reduced
the incidence of a sustained ≥40% decrease in eGFR* by 19%
vs placebo
*From baseline and sustained over ≥4 weeks; #number of patients with an event over a median of 2.6 years of follow-up
CI, confidence interval; eGFR, estimated glomerular filtration rate; HR, hazard ratio
2833 2703 2606 2396 1808 1275 788 442 83
2841 2722 2588 2379 1758 1249 793 453 82
479/2833 (16.9%)*
577/2841 (20.3%)*
Cumulative
incidence
(%)
No. at risk
Placebo
Finerenone
HR=0.81; 95% CI 0.72–0.92
0
10
20
30
40
0 6 12 18 24 30 36 42 48
Placebo
Finerenone
Sustained ≥40% decrease in eGFR
19%
RRR

Time to CV death, non-fatal MI, non-fatal stroke or HHF
On top of max tolerated RAS therapy, finerenone significantly
reduced the risk of the key secondary CV outcome by 14%
*number of patients with an event over a median of 2.6 years of follow-up
CI, confidence interval; CV, cardiovascular; HHF, hospitalisation for heart failure; HR, hazard ratio; MI, myocardial infarction; RAS, renin–angiotensin system
2841 2653 1969 951 115
2833 2688 2017 984 111
Cumulative
incidence
(%)
No. at risk
Placebo
Finerenone
HR=0.86; 95% CI 0.75–0.99
p=0.03
0
0
6 12 18 24 30 36 42 48
10
20
15
25
5
Placebo
Finerenone
367/2833 (13.0)*
420/2841 (14.8%)*
14%
RRR

Finerenone had consistent effects on cardiovascular death,
myocardial infarction and hospitalisation for heart failure
Outcome
Finerenone
(n=2833)
Placebo
(n=2841) Hazard ratio (95% CI)
p-
value
n (%)
n per
100 PY
n (%)
n per
100 PY
Key secondary CV outcome* 367 (13.0) 5.11 420 (14.8) 5.92 0.86 (0.75–0.99) 0.03
CV death 128 (4.5) 1.69 150 (5.3) 1.99 0.86 (0.68–1.08) –
Non-fatal MI 70 (2.5) 0.94 87 (3.1) 1.17
0.80
(0.58–1.09)
–
Non-fatal stroke 90 (3.2) 1.21 87 (3.1) 1.18
1.03
(0.76–1.38)
–
Hospitalisation for HF 139 (4.9) 1.89 162 (5.7) 2.21
0.86
(0.68–1.08)
–
According to N Engl J Med policy p-values are not reported for components of composite outcomes
*Composite of CV death, non-fatal MI, non-fatal stroke or HF hospitalisation
CV, cardiovascular; HF, heart failure; HR, hazard ratio; MI, myocardial infarction
0,5 1 2
Favours finerenone Favours placebo

FIDELIO-DKD Subanalysis: Finerenone Consistently
Improves Kidney and CV Outcomes in Asians and ROW
Koya D et al. Am J Nephrol. 2023;54(9-10):370-378
15%
RRR
≥40% eGFR composite includes outcomes of kidney failure, a sustained decrease of at least 40% in eGFR from baseline, or death from renal causes. ≥57% eGFR
composite includes outcomes of kidney failure, a sustained decrease of at least 57% in eGFR from baseline, or death from renal causes. CI, confidence interval; eGFR,
estimated glomerular filtration rate; PY, patient-years; CV, Cardiovascular; ROW, Rest of the World
30%
RRR

0,2
0,4
0,6
0,8
1,0
1,2
0 4 12 24 36
Finerenone reduced UACR by 31% between
baseline and month 4 vs placebo*
UACR
LS
mean
ratio
to
baseline
#
Bakris GL, et al. N Engl J Med 2020. doi: 10.1056/NEJMoa2025845
31% in 4
months
A lower mean UACR with finerenone versus placebo was maintained throughout the study
UACR
LS
mean
ratio
to
baseline
#
Geometric mean (gSD) UACR at baseline:
Placebo: 814.7 (2.67)
Finerenone: 798.7 (2.65)
(-34.7%)
(-4.7%)
(-41.3%)
(-3.0%)
(-39.9%)
(-2.0%)
(-29.3%)
(4.1%)
Placebo
Finerenone
Months since randomisation
Ratio of LS mean 0.69; 95% CI 0.66–0.71
0,2
0,4
0,6
0,8
1,0
1,2
0 4 12 24 36
Geometric mean (gSD) UACR at baseline:
Placebo: 814.7 (2.67)
Finerenone: 798.7 (2.65)
(-34.7%)
(-4.7%)
(-41.3%)
(-3.0%)
(-39.9%)
(-2.0%)
(-29.3%)
(4.1%)
Placebo
Finerenone
Ratio of LS mean 0.69; 95% CI 0.66–0.71
Data in parentheses are mean change from baseline; *Full analysis set. Mixed model with factors treatment group, region, eGFR category at screening, type of albuminuria at
screening, time, treatment time, log-transformed baseline value time as covariate. Separate unstructured covariance patterns are estimated for each treatment group; #Data are LS
mean/95% CI. CI, confidence interval; eGFR, estimated glomerular filtration rate; gSD, geometric standard deviation; LS, least-squares; UACR, urine albumin-to-creatinine ratio;
SoC, Standard of Care (well controlled BP and blood glucose)

SGLT-2i use at baseline
Reduction in UACR (%) with finerenone vs placebo*
*Ratio of LS mean change assessed in the full analysis set, using a model with factors for treatment group, region, eGFR category at screening, type of albuminuria at screening, time, treatment*time,
log-transformed baseline value nested within type of albuminuria at screening, and log-transformed baseline value*time as covariates. Gmean, geometric mean; LS, least-squares.
Rossing P, et al. ADA 2021; poster 14-LB.
Peter Rossing et al. Kidney International Reports (2022) 7, 36–45
In FIDELIO-DKD, Finerenone improved UACR in patients
with CKD and T2D irrespective of SGLT-2i use at baseline
0
200
400
600
800
1000
No baseline SGLT-2i Baseline SGLT-2i
UACR
(mg/g)
Low patient numbers and event rates meant that it was not possible to make meaningful conclusions
on the effects of combination therapy on kidney and composite endpoints
–32%
–25%
SGLT-2i at baseline (n=259)
No SGLT-2i at baseline
(n=5415)
Baseline Gmean
816 mg/g
Baseline Gmean
630 mg/g
pinteraction=0.31
259 (4.6%) patients
on an SGLT2-i
Modified from MA-M_FIN-ID-0114-1

*Mixed model analysis of eGFR over time. Full analysis set; #LS mean change in eGFR slope from baseline to month 4; ‡LS mean change in eGFR slope from month 4 to the permanent
discontinuation or end-of-study visit
CI, confidence interval; eGFR, estimated glomerular filtration rate; LS, least-squares
Bakris GL, et al. N Engl J Med 2020;383:2219–2229
The acute effect of finerenone is a drop in eGFR but the
long-term effect is a slowing of eGFR decline*
8 12 16 20 24 28 32 36 40 44
Acute change in eGFR,#
ml/min/1.73 m2 (95% CI):
Finerenone: –3.18 (–3.44 to –2.91)
Placebo: –0.73 (–1.03 to –0.44)
4
Chronic annualised change in eGFR,‡
ml/min/1.73 m2/year(95% CI):
Finerenone: –2.66 (–2.96 to –2.36)
Placebo: –3.97 (–4.27 to –3.66)
Acute Chronic
-16
-14
-12
-10
-8
-6
-4
-2
0
2
eGFR
LS
mean
change
(ml/min/1.73
m
2
)
Mean eGFR at baseline (ml/min/1.73 m2):
Finerenone: 44.4±12.5 Placebo: 44.3±12.6

Cardiorenal protective drugs, including RAASi,
SGLT2i, and nsMRAs, may initially reduce
eGFR by 5-30% when treatment begins1
Practice Point 2.1.4: Among people with
CKD who initiate hemodynamically active
therapies, GFR reductions of >30% on
subsequent testing exceed the expected
variability and warrant evaluation2.
❖ Acute rises in SCr (or declines in eGFR) of <20%–30% are
expected and do not warrant changes in therapeutic agents,
which may be important for cardio- and kidney-protective effects in
the long term2.
❖ A significant drop in eGFR (>30%) while initiating antihypertensive
agents, RASi, MRA, or SGLT2i should prompt a review into other
causes and warrants close monitoring. However, healthcare
providers should avoid the urge to stop these kidney-protective
agents, particularly because these earlier “dips” are typically
reversible and not an indication of drug toxicity2.
1. Bakris GL, Weir MR. Am J Nephrol 2022;53:513–515; 2. Kidney International (2024) 105 (Suppl 4S), S117–S314
RAASi, renin–angiotensin–aldosterone system inhibitors; SGLT2i,
Sodium-glucose cotransporter-2 inhibitors; nsMRA, nonsteroidal
mineralocorticoid receptor antagonist

AE, adverse event; SAE, serious adverse event; Bakris GL, et al. N Engl J Med 2020;383:2219-2229
Treatment-emergent adverse events, n (%) Finerenone (N=2827) Placebo (N=2831)
Any AE 2468 (87.3) 2478 (87.5)
AE related to study drug 646 (22.9) 449 (15.9)
AE leading to treatment discontinuation 207 (7.3) 168 (5.9)
Any serious AE 902 (31.9) 971 (34.3)
Serious AE related to study drug 48 (1.7) 34 (1.2)
Serious AE leading to treatment discontinuation 75 (2.7) 78 (2.8)
The overall incidence of treatment-emergent adverse events was similar
between the finerenone and placebo groups
Treatment-emergent adverse events, n (%) Finerenone (N=2827) Placebo (N=2831)
Kidney-related AEs
Acute kidney injury 129 (4.6) 136 (4.8)
Hospitalisation due to acute kidney injury 53 (1.9) 47 (1.7)
Treatment discontinuation due to acute kidney injury 5 (0.2) 7 (0.2)
Hospitalisation due to acute renal failure* 70 (2.5) 71 (2.5)
Treatment discontinuation due to acute renal failure* 31 (1.1) 36 (1.3)
Reproductive system and breast disorders
Breast hyperplasia 0 3 (0.1)
Gynaecomastia 6 (0.2) 6 (0.2)
Acute kidney injury, acute renal failure and gynaecomastia were balanced between groups

*Investigator-reported AEs using the MedDRA preferred terms ‘hyperkalemia’ and ‘blood potassium increased’. AE, adverse event; SAE, serious adverse event
Although investigator-reported hyperkalaemia was
increased, the clinical impact was minimal
There were no deaths due to hyperkalaemia,
and the incidences of treatment discontinuation or hospitalisation due to hyperkalaemia were low
516
(18,3%)
333
(11,8%)
64
(2,3%)
44
(1,6%)
40
(1,4%) 0
(0%)
255
(9,0%)
135
(4,8%
25
(0,9%)
12
(0,4%)
8
(0,3%)
0
(0%)
0
5
10
15
20
25
Any Related to study
drug
Leading to
permanent
discontinuation
SAE Leading to
hospitalisation
Leading to death
Patients
with
a
treatment-emergent
AE
(%)
Placebo (n=2831)
Finerenone (n=2827)
Any treatment-emergent AE Treatment-emergent AE with clinical consequences
Investigator-reported AEs relating to hyperkalaemia*
Leading to permanent
discontinuation
Any Related to
study drug
Serious AE Leading to
hospitalisation
Leading to
death

The maximum difference in mean serum [K+] between groups was 0.23 mmol/l at month 4*
Finerenone had a predictable impact on serum potassium
Numbers in parentheses show change from baseline; error bars show standard deviation
*Based on a mean change of 0.25 mmol/l in the finerenone and 0.02 mmol/l in the placebo group
3,6
3,8
4,0
4,2
4,4
4,6
4,8
5,0
5,2
5,4
0 4 8 12 16 20 24 28 32 36 40 44
Mean
serum
K+
(mmol/l)
Mean baseline
serum [K+]
Finerenone: 4.37±0.46
Placebo: 4.37±0.46
(0.25)
(0.02)
(0.24)
(0.04)
(0.20)
(0.21)
(0.21)
(0.05) (0.07) (0.07)
2827
2831
2708
2709
2600
2596
1872
1865
882
862
344
348
N
Finerenone
Placebo

The difference in mean SBP between groups was -2.9 mmHg at month 1 and -3.0 mmHg at month 12#
110
120
130
140
150
160
0 4 8 12 16 20 24 28 32 36 40 44
Mean
SBP
(mmHg)
Finerenone had a modest impact on blood pressure
Numbers in parentheses show mean change from baseline; error bars show standard deviation
*Analysis of safety set; #mean change from baseline systolic blood pressure from baseline to month 1 and month 12 was –3.0 and –2.1 mmHg with and –0.1 and 0.9 mmHg with placebo, respectively. SBP, systolic blood pressure
Patients (n):
Finerenone
Placebo
2826
2831
2746
2751
2628
2636
1906
1895
902
884
348
353
Mean SBP
at baseline (mmHg):
Placebo: 137.98 ±14.42
Finerenone: 138.02 ±14.31
(-3.20) (-2.13) (-1.83) (-2.58) (-2.84)
(0.87) (-0.12) (-0.08)
(0.68) (0.38)

Finerenone had no effect on HbA1c
Numbers in parentheses show mean change from baseline; error bars show standard deviation
HbA1c, glycated haemoglobin
4
5
6
7
8
9
10
0 4 8 12 16 20 24 28 32 36 40 44
Mean
HbA1c
(%)
Mean HbA1c
at baseline (%):
Finerenone: 7.66±1.33
Placebo: 7.69±1.36
(0.05) (0.08) (0.07) (0.05)
(0.02)
(0.07) (0.14) (0.16) (0.09)
(0.03)
2821
2828
2697
2694
2605
2610
1889
1871
893
870
346
349
Patients (n):
Finerenone
Placebo

Finerenone, one of the pillars of treatment in patients with CKD
and T2D in reducing the risk of CV events and progression of CKD1-9
• To optimise risk reduction, 3-pillar pharmacotherapy should be combined with glycaemic control, blood pressure control, lipid
control, smoking cessation, proper nutrition and regular exercise9
1. Mancia G, et al. J Hypertens. 2023 Dec 1;41(12):1874-2071; 2. Marx N, et al. Eur Heart J. 2023 Oct 14;44(39):4043-4140; 3. McDonagh TA, et al. Eur Heart J. 2023 Oct 1;44(37):3627-3639; 4. de Boer IH, et al. Diabetes Care.
2022 Dec 1;45(12):3075-3090; 5. Sarafidis P et al. Clin Kidney J. 2023 Jun 24;16(11):1885-1907; 6. Kidney Disease: Improving Global Outcomes (KDIGO) Diabetes Work Group, Kidney Int. 2022 Nov;102(5S):S1-S127; 7. ElSayed
NA et al. Diabetes Care 2023;46(Suppl. 1):S191–S202; 8. Blonde L et al. Endocr Pract. 2022 Oct;28(10):923-1049; 9. Blazek O & Bakris GL. Am Heart J Plus 2022;19:100187
CKD, chronic kidney disease; T2D, type 2 diabetes; RASi, renin–angiotensin system inhibitor; SGLT2is, sodium-glucose co-transporter-2 inhibitors; nsMRA, non-
steroidal mineralocorticoid receptor antagonist

*HRs adjusted for HbA1c, SBP, UACR at baseline (log-transformed), and eGFR at baseline. pinteraction values are based on a stratified Cox proportional hazards model including treatment, subgroup,
and treatment by subgroup interaction; #Composite of CV death, non-fatal MI, non-fatal stroke, or HHF; ‡Kidney failure (ESKD or eGFR <15 mL/min/1.73 m2),
a sustained ≥57% decrease in eGFR from baseline (equivalent to a doubling of serum creatinine) for ≥4 weeks, or renal death; §Kidney failure (ESKD or eGFR <15 mL/min/1.73 m2), a sustained
≥40% decrease in eGFR from baseline maintained for ≥4 weeks, or renal death
1. Rossing P, et al. Diabetes Care 2022;45:2991–2998; 2. Rossing P, et al. ASN Kidney Week 2021; oral presentation SA-OR22
The Kidney and CV Benefits of Finerenone on top of RASi, Remain
Consistent Regardless of Baseline SGLT-2 Inhibitor Use1,2
Endpoint Finerenone
n/N (n/100 PY)
Placebo
n/N (n/100 PY)
HR (95% CI) Adjusted HR
(95% CI)*
pinteraction*
CV composite#,1
0.46
No SGLT-2i 786/6081 (4.4) 887/6068 (5.1) 0.87 (0.79–0.96)
SGLT-2i 39/438 (3.0) 52/439 (4.1) 0.67 (0.42–1.07)
HHF1
0.18
No SGLT-2i 246/6081 (1.4) 303/6068 (1.7) 0.80 (0.68–0.95)
SGLT-2i 10/438 (0.7) 22/439 (1.7) 0.44 (0.19–0.99)
eGFR 57% kidney composite‡,1
0.29
No SGLT-2i 351/6081 (2.1) 448/6068 (2.6) 0.80 (0.69–0.92)
SGLT-2i 9/438 (0.7) 17/439 (1.4) 0.42 (0.16–1.08)
eGFR 40% kidney composite§,2
0.59
No SGLT-2i 818/6081 (5.0) 961/6068 (5.9) 0.84 (0.76–0.92)
SGLT-2i 36/438 (2.9) 34/439 (2.8) 0.70 (0.41–1.21)
0,125 0,25 0,5 1 2
Favors finerenone Favors placebo
Extracted from MA-M_FIN-ID-0120-1

1. FIDELIO-DKD study shows that on top of standard of care, Finerenone provides dual cardiorenal
benefit by significantly delayed CKD progression by 18% and reduced the risk of cardiovascular
events by 14% compared to placebo.
2. Finerenone also reduced UACR by 31% from baseline to month 4.
3. FIDELIO-DKD sub-analysis for the Asian population demonstrated consistent cardiorenal benefits
with Finerenone.
4. No deaths from hyperkalemia occurred in the Finerenone group, with low rates of treatment
discontinuation or hospitalization due to hyperkalemia.
5. Finerenone is one of the key pillars of treatment for patients with CKD and T2D, helping to lower the
risk of CV and CKD progression.
Summary

FIDELIO..............................pdf

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