Song Guo, Yu Li
We therefore propose a proportionate strategy: allow a higher renal-risk band to prompt consideration of finerenone in suitable patients, resist equating a uniform relative risk with uniformly maximal absolute benefit or unchanged safety at very low eGFR, and escalate potassium monitoring in parallel with renal risk, especially at or beyond the trial's boundaries.
Chronic kidney disease has long been viewed as a reason for caution when prescribing mineralocorticoid receptor antagonists (MRAs) in heart failure (HF), a doctrine rooted in the safety record of the steroidal agents: in TOPCAT, drug discontinuation for adverse events rose steeply as kidney function declined. The prespecified kidney-risk analysis of FINEARTS-HF, which reported consistent relative benefit of the non-steroidal MRA finerenone across KDIGO risk bands with a non-significant interaction on the primary endpoint, is widely read as a mandate to treat higher-risk patients more readily. We welcome this move away from reflexive under-treatment, but argue that a careful reading supports a more qualified conclusion than "worse kidneys, therefore more finerenone." Two features deserve emphasis. First, the reassuring safety signal was generated within the trial's enrolment window, which excluded patients with an eGFR below 25 mL/min/1.73 m2 or a serum potassium above 5.0 mmol/L; extending "no excess hyperkalaemia" to the very-low-eGFR patients who most concern clinicians is an extrapolation, not a demonstrated finding. Second, absolute benefit did not increase smoothly with rising kidney risk: modelled absolute reductions were not largest in the highest-risk stratum, and a non-significant interaction test does not establish that the treatment effect is identical across strata. Earlier, larger falls in albuminuria among higher-risk patients are encouraging but remain a candidate intermediate endpoint rather than proof of durable cardiorenal gains. We therefore propose a proportionate strategy: allow a higher renal-risk band to prompt consideration of finerenone in suitable patients, resist equating a uniform relative risk with uniformly maximal absolute benefit or unchanged safety at very low eGFR, and escalate potassium monitoring in parallel with renal risk, especially at or beyond the trial's boundaries. The strongest inference is that finerenone is effective and well tolerated in patients with moderately advanced CKD, normal potassium, and close follow-up; its least secure inference is that the highest-risk patients are ipso facto the safest or most deserving recipients. Future work should define optimal monitoring for patients whose eGFR drifts very low during treatment.