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Katherine Tuttle, MD, joins Brendon Neuen, MBBS, PhD, and Shikha Wadhwani, MD, MS, to unpack new FIND-CKD finerenone analyses from ASN 2026.
Recording from ASN Kidney Week 2026 in Denver, Colorado, cohosts Brendon Neuen, MBBS, PhD, and Shikha Wadhwani, MD, MS, welcomed back Katherine Tuttle, MD, of Providence Inland Northwest Health and the University of Washington School of Medicine.
The group broke down new analyses from the FIND-CKD trial of finerenone in non-diabetic chronic kidney disease (CKD), presented during a dedicated finerenone session. Topics included combination therapy with SGLT2 inhibitors, hyperkalemia, IgA nephropathy, and outcomes across CKD severity.
FIND-CKD randomized 1584 patients with non-diabetic CKD, an eGFR of 25 to below 90 mL/min/1.73 m², and albuminuria on optimized renin-angiotensin system blockade to finerenone or placebo.¹ Finerenone slowed total eGFR decline by 0.7 mL/min/1.73 m² per year versus placebo over 32 months, and the effect was similar in the 17% of patients receiving an SGLT2 inhibitor at baseline (P for interaction = .71). The composite kidney-cardiovascular outcome was also reduced (hazard ratio, 0.77) regardless of SGLT2 inhibitor use.
00:05 - Welcome and episode overview
01:54 - Finerenone with and without SGLT2 inhibitors in FIND-CKD
03:38 - Hyperkalemia risk and management
07:01 - Finerenone in IgA nephropathy
13:31 - Cardiovascular risk and holistic care in IgAN
15:34 - Sequencing therapies for residual albuminuria
17:58 - Kidney injury biomarkers and innate immunity
22:07 - Finerenone effects across CKD severity
Tuttle called the consistency reassuring, noting the 2 drug classes act on different pathways. Neuen added time-updated analyses, accounting for SGLT2 inhibitor use increasing during the trial, showed the same pattern.
On hyperkalemia, Neuen noted potassium above 6.0 mmol/L occurred in about 4% of patients receiving finerenone compared with 2% with placebo, with few events leading to hospitalization or discontinuation. Across CKD severity, hyperkalemia rates ranged from 5.7% with finerenone vs 5.8% with placebo in the least severe group to 29.4% vs 20.6% in the most severe group.²
“So pay attention and manage it,” Tuttle said. “And most of the time, people can tolerate these therapies, and it’s worth it because these really are kidney, heart, and life-saving therapies.”
Of 1584 FIND-CKD participants, 416 (26%) had IgA nephropathy, and 93% had biopsy confirmation.³ Finerenone reduced urine protein-to-creatinine ratio (UPCR) by 51% versus placebo at month 12 and increased the likelihood of reaching UPCR below 500 mg/g (odds ratio, 6.8; 95% CI, 3.7–13.1).
The effect on total eGFR slope was similar in participants with and without IgA nephropathy (0.6 vs 0.7 mL/min/1.73 m² per year; P for interaction = .755).³ Finerenone did not reduce galactose-deficient IgA1 or other immunoglobulins but did lower kidney injury biomarkers, particularly KIM-1 and urinary MMP7.
Wadhwani said the ability to reach proteinuria targets without adding immunosuppression is meaningful, given many patients are diagnosed with advanced CKD. Tuttle pointed to cardiovascular disease, particularly heart failure, as the leading cause of death in this population.
Asked how to prioritize therapies, Tuttle advised letting residual albuminuria guide add-on treatment. She urged clinicians to “aspire to extinguish albuminuria even in people with IgA nephropathy, and not just to protect their kidneys, but protect the rest of them.” For patients at risk of heart failure, she said she would favor finerenone, while noting the opinion is not based on a head-to-head trial.
On the biomarker data, Tuttle said reductions in KIM-1 and MMP7 support a complementary mechanism targeting tubulointerstitial inflammation and fibrosis driven by innate immunity, which immunologic therapies leave unaddressed.
In an analysis presented by Tuttle, finerenone reduced the rate of eGFR decline and the composite kidney-cardiovascular outcome vs placebo irrespective of baseline eGFR and urine albumin-to-creatinine ratio.² Tuttle also described a pooled individual participant–level analysis of FIDELIO-DKD, FIGARO-DKD, and FIND-CKD showing consistent benefits, with greater kidney benefit in high-risk groups and greater cardiovascular benefit in lower-risk groups. She said the findings also carry a message for cardiologists, who often manage lower-risk patients, as finerenone can markedly reduce cardiovascular complications regardless of diabetes status.
“So no therapeutic inertia,” Tuttle said. “Initiate finerenone because it preserves kidney function in people with advanced CKD, where kidney failure is their most imminent risk.”
Editors’ note: Disclosures for Neuen include AstraZeneca, Bayer, Boehringer Ingelheim, Janssen, and others. Disclosures for Wadhwani include Boehringer Ingelheim, Calliditas Therapeutics, GSK, Otsuka Pharmaceutical Co., Travere Therapeutics, and others. Disclosures for Tuttle include Eli Lilly and Company, Boehringer Ingelheim, Astra Zeneca, Gilead, Goldfinch Bio, Novo Nordisk, Travere Therapeutics, and Bayer.
