Finerenone, marketed under the brand name Kerendia, has emerged as a notable treatment option in the management of heart failure and chronic kidney disease (CKD) associated with type 2 diabetes. Its introduction into clinical practice marked it as the first non-steroidal selective mineralocorticoid receptor antagonist. However, recent findings from the FINEARTS-HF trial have raised critical questions about its effectiveness, particularly regarding renal function in patients with heart failure exhibiting mildly reduced or preserved ejection fraction.
The FINEARTS-HF trial focused on a patient cohort that included individuals aged 40 and above, presenting symptomatic heart failure with an ejection fraction greater than or equal to 40%. These patients were selected based on their structural heart disease indicators and elevated natriuretic peptide levels. Crucially, the analysis encompassed over 6,000 participants with varying degrees of renal function as determined by baseline estimated glomerular filtration rate (eGFR).
Despite the intentions behind the trial, the findings revealed nuanced and, in some cases, disappointing results. A pivotal consideration was the incidence of a composite kidney outcome, which comprised significant declines in eGFR along with cases of kidney failure, which was notably greater among those treated with finerenone as opposed to a placebo group. This outcome calls into question the expected renal protective benefits attributed to finerenone, particularly for a demographic that was already deemed low-risk for adverse renal events.
The secondary analysis presented at the American Society of Nephrology Kidney Week highlighted that while finerenone did not demonstrate significant improvements in composite kidney outcomes, it did show efficacy in reducing the onset of micro- and macroalbuminuria. These findings suggest a potential benefit in albuminuria management, which could be important for cardiovascular health and renal prognosis. However, the larger implications for kidney function, particularly concerning eGFR, remain limited.
Disturbingly, the results indicated an acute decline in eGFR during the initial months of treatment with finerenone, contradicting the ultimate goal of maintaining or improving renal function in heart failure patients. Such an acute drop raises concerns regarding the drug’s short-term tolerability and longer-term efficacy in real-world clinical settings.
Heart failure with preserved or mildly reduced ejection fraction is often accompanied by CKD, affecting about half of this population, and is linked with increased morbidity and mortality. This paradox of having a treatment that potentially heightens renal risk in a population already predisposed to kidney complications is troubling. The presence and extent of albuminuria in patients with CKD serves as a powerful indicator of both cardiovascular and renal outcomes, adding another layer to the complexity of finerenone’s impact.
Experts emphasize the slow progression of CKD, suggesting that the relatively short follow-up period of the study may not have captured the full spectrum of treatment effects or potential benefits that could materialize over an extended timeframe. Ian de Boer, a researcher in this field, suggested the need for longer follow-up to assess whether albuminuria reduction could translate into sustained renal benefits.
While finerenone demonstrates potential in reducing albuminuria levels among patients with heart failure, the secondary analysis of the FINEARTS-HF trial unveils significant limitations in its renal protective capabilities. The overall incidence of kidney-related adverse events was higher with finerenone than placebo, complicating its clinical utility in this setting.
Moving forward, the medical community must navigate these findings with caution. Practitioners will need to consider patient-specific factors, including existing CKD status, when weighing the risks and benefits of finerenone. The evolving understanding of this medication’s effects underscores the necessity for ongoing research to clarify its role within heart failure therapies, ultimately aiming to enhance patient outcomes while minimizing the risks associated with renal dysfunction. The journey towards fully understanding finerenone’s place in treatment protocols continues, underscoring the importance of balancing innovative therapies with rigorous clinical evidence.
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