@article{3033601,
    title = "Finerenone in Predominantly Advanced CKD and Type 2 Diabetes With or
Without Sodium-Glucose Cotransporter-2 Inhibitor Therapy",
    author = "Rossing, Peter and Filippatos, Gerasimos and Agarwal, Rajiv and Anker, and Stefan D. and Pitt, Bertram and Ruilope, Luis M. and Chan, Juliana C. N. and and Kooy, Adriaan and McCafferty, Kieran and Schernthaner, Guntram and and Wanner, Christoph and Joseph, Amer and Scheerer, Markus F. and Scott, and Charlie and Bakris, George L.",
    journal = "Kidney International Reports",
    year = "2022",
    volume = "7",
    number = "1",
    pages = "36-45",
    publisher = "EXCERPTA MEDICA INC-ELSEVIER SCIENCE INC",
    issn = "2468-0249",
    doi = "10.1016/j.ekir.2021.10.008",
    keywords = "albuminuria; chronic kidney disease; finerenone; sodium-glucose
cotransporter-2 inhibitors; type 2 diabetes",
    abstract = "Introduction: FIDELIO-DKD (Finerenone in reducing kiDnEy faiLure and
disease prOgression in Diabetic Kidney Disease) investigated the
nonsteroidal, selective mineralocorticoid receptor (MR) antagonist
finerenone in patients with CKD and type 2 diabetes (T2D). This analysis
explores the impact of use of sodiumglucose cotransporter-2 inhibitor
(SGLT-2i) on the treatment effect of finerenone.
Methods: Patients (N = 5674) with T2D, urine albumin-to-creatinine ratio
(UACR) of 30 to 5000 mg/g and estimated glomerular filtration rate
(eGFR) of 25 to <75 ml/min per 1.73 m(2) receiving optimized
reninangiotensin system (RAS) blockade were randomized to finerenone or
placebo. Endpoints were change in UACR and a composite kidney outcome
(time to kidney failure, sustained decrease in eGFR >= 40% from
baseline, or renal death) and key secondary cardiovascular outcomes
(time to cardiovascular death, nonfatal myocardial infarction, nonfatal
stroke, or hospitalization for heart failure) (ClinicalTrials.gov,
NCT02540993).
Results: Of 5674 patients, 259 (4.6%) received an SGLT-2i at baseline.
Reduction in UACR with finerenone was found with or without use of
SGLT-2i at baseline, with ratio of least-squares means of 0.69 (95% CI
= 0.66-0.71) and 0.75 (95% CI -= 0.62-0.90), respectively
(P-interaction = 0.31). Finerenone also significantly reduced the kidney
and key secondary cardiovascular outcomes versus placebo; there was no
clear difference in the results by SGLT-2i use at baseline
(P-interaction = 0.21 and 0.46, respectively) or at any time during the
trial. Safety was balanced with or without SGLT-2i use at baseline, with
fewer hyperkalemia events with finerenone in the SGLT-2i group (8.1%
vs. 18.7% without).
Conclusion: UACR improvement was observed with finerenone in patients
with CKD and T2D already receiving SGLT-2is at baseline, and benefits on
kidney and cardiovascular outcomes appear consistent irrespective of use
of SGLT-2i."
}