Latest news with #Finerenone
Medscape
a day ago
- Health
- Medscape
Benefits of HF Drug May Weaken Soon After Withdrawal
TOPLINE: Finerenone, a third-generation nonsteroidal mineralocorticoid receptor antagonist, showed promise in reducing the incidence of cardiovascular events in patients with heart failure (HF). However, its abrupt withdrawal after long-term use was associated with an increased incidence of serious adverse events (related to the heart, leading to death approximately 30 days after withdrawal of treatment. METHODOLOGY: Guidelines recommend lifelong use of therapies for HF due to their presumed lasting benefits; however, clinicians and patients frequently question whether such treatments can be safely stopped once the disease becomes stable. Researchers conducted a secondary analysis of the FINEARTS-HF trial to assess the cardiovascular effects of discontinuing finerenone after long-term use of the drug. The FINEARTS-HF trial included 6001 patients with symptomatic HF and left ventricular ejection fraction of at least 40% who were randomly assigned to receive either finerenone (mean age, 71.9 years; 45.1% women) or placebo (mean age, 72 years; 45.9% women) for a median duration of 2.6 years. After the treatment phase ended, 3742 surviving patients (1852 on placebo and 1890 on finerenone) were withdrawn from the interventions; the patients remained blinded to the treatment and withdrawal. Adverse events were assessed approximately 30 days after the withdrawal, focusing on serious cardiovascular episodes or any event resulting in death. TAKEAWAY: Before the withdrawal, patients receiving finerenone vs placebo experienced fewer serious cardiovascular adverse events or adverse events leading to death (6.0 vs 9.2 per 100 patient-years). The withdrawal of finerenone was associated with a 2.8-fold increase in the incidence of cardiovascular events or adverse leading to death, a pattern not observed after the withdrawal of placebo (time period-treatment P for interaction = .006). Most of the cardiovascular events in the withdrawal period were related to HF; withdrawal of finerenone vs placebo was associated with more HF-specific serious events or adverse events leading to death (time period-treatment P for interaction = .012). IN PRACTICE: 'Global implementation efforts are needed to promote long-term MRA [mineralocorticoid receptor antagonist] therapy persistence to maximize treatment potential. Minimal changes in serum potassium or kidney function during MRA therapy should not automatically lead to treatment interruption,' the researchers wrote. SOURCE: This study was led by Muthiah Vaduganathan, MD, MPH, of Harvard Medical School in Boston. It was published online on July 28, 2025, in the Journal of the American College of Cardiology. LIMITATIONS: Patients assigned to receive finerenone or placebo may no longer have been directly comparable years after randomization. Clinical events during the withdrawal period relied on reporting of adverse events without adjudication. Fewer than 50 clinical events were recorded during the short withdrawal period, reducing the precision of the estimates. DISCLOSURES: The FINEARTS-HF trial was funded by Bayer. Several authors reported serving on advisory boards, having speaker engagements, receiving research support, and having other financial ties with multiple pharmaceutical, biotechnology, and healthcare companies. Three authors reported being employees of Bayer. This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.
Medscape
18-07-2025
- Health
- Medscape
Jul 18 2025 This Week in Cardiology
Please note that the text below is not a full transcript and has not been copyedited. For more insight and commentary on these stories, subscribe to the This Week in Cardiology podcast , download the Medscape app or subscribe on Apple Podcasts, Spotify, or your preferred podcast provider. This podcast is intended for healthcare professionals only. In This Week's Podcast For the week ending July 18, 2025, John Mandrola, MD, comments on the following topics: Finerenone, what not to consider when choosing treatment of AS, brain health after atrial fibrillation ablation, early rhythm control for AF, and Watchman reimbursement cuts. I received an email from an academic EP who is involved with regulation, regarding my coverage of pulmonary embolism (PE) devices two shows back. He clarified my thoughts on the 510(k) approval pathway where devices get approved by being similar to an already approved device. I called it extremely problematic and called for FDA to reform it. My colleague writes that it's not up to FDA to reform the program. The 510(k) pathway and the rules around substantial equivalence are in federal law and Congress would need to change these rules. Speaking of 510(k) pathway, he agrees it can be problematic. It works well for devices like blood pressure (BP) cuffs and diagnostic EP catheters, in which the underlying technology is well established. It's harder in things like artificial intelligence or machine learning-based devices or anything that is sort of—but not completely—new. He said we spend a lot of time on these, often focused on whether the intended use is the same, whether we have enough bench and clinical data, etc. And, he writes, 'substantial equivalence' means we need to be assured that the device performs as well as the predicate and that often requires clinical data. I have come to really appreciate listener feedback because it is so instructional. I did not know that Congress has to change the 510(k) pathway. Keep coming with the listener feedback. Finerenone FDA Widens Indication of Finerenone for Heart Failure Patients Medscape news has a good summary of the FDA approval of finerenone. It's actually an expansion of the indication of the nonsteroidal mineralocorticoid receptor antagonist (MRA). The FDA initially approved finerenone in 2021 to reduce the risk for cardiovascular death heart failure hospitalization (HHF), myocardial infarction (MI), and kidney complications in adults with chronic kidney disease (CKD) associated with type 2 diabetes—a rather specific indication. The new expansion will be for patients with heart failure (HF) and left ventricular ejection fraction (LVEF) of at least 40%. This is based on the FINEARTS-HF trial published in New England Journal of Medicine in 2024. This was a big 6000+ patient trial comparing finerenone to placebo in patients with heart failure with preserved ejection fraction (HFpEF). Mean age 72, LVEF 53%, most with NYHA Class 2 and 3 HF. The primary endpoint was a composite of total worsening HF events (HHF or urgent visit) and CV death. Follow-up was 2.5 years. There was a 16% reduction in the primary endpoint. The hazard ratio was 0.84 and confidence intervals were significant. The absolute risk reduction (ARR) was 2.8%, or a number needed to treat (NNT) of 35. The primary composite was driven almost completely by HF events as there was no statistical difference in CV death or all-cause death. This came at a cost of more increases in creatinine and potassium. High potassium more than 6 was 3.0% vs 1.4%. FINEARTS-HF is fine. It was a positive trial. My criticism of the trial and finerenone use in HFpEF centers on three main issues. First issue: Wrong comparator. Finerenone should have had to beat spironolactone. I say that because the Americas part (US, Canada, Brazil, Argentina) of the TOPCAT trial clearly show that spironolactone improved outcomes in HFpEF. Of course it does. MRA drugs as a class help in HFrEF and likely do in HFpEF. The question facing clinicians is which MRA to start—one that costs pennies, spironolactone, or one that will surely cost bunches, finerenone. The lack of head-to-head comparison is what we get when we let industry control regulatory trials. If I were at FDA, I would have pushed for a spironolactone arm. The second issue was that the benefit from finerenone was modest. Despite enrolling 6,000 patients, there were only 200 fewer events in the finerenone arm, and no difference was seen in cardiovascular death. The 16% reduction in the primary endpoint was driven solely by heart failure events, not mortality. Finerenone is a diuretic after all. HFrEF patients have 4 classes of 'disease-modifying' drugs. Finerenone cannot be called disease-modifying. The third issue I have with FINEARTS is that the authors surely have — but don't share — the effect on total hospitalizations. As I have shown in other HFpEF trials, most hospitalizations in these patients is not HF. So, if a drug or device reduces one type of hospitalizations (here for HF), but this type is only a small fraction of the total burden of hospitalizations, the patient does not win. HHF are a reasonable surrogate in HFrEF, because in those patients a weak LV is the primary issue. But in HFpEF, these patients are older and burdened with much higher co-morbidity, so HHF becomes a weak surrogate measure. I don't have a problem with FDA approving the drug for this indication. But they should have been stronger in the regulatory input regarding the seminal trial. Drug companies will jump over the bar we set for them. We help them when we set the bar low. For clinicians, we shall see what the cost of this drug is. I still believe we start with spironolactone and keep finerenone in the bullpen for relief when the first line fails. One of the most common decisions in the field of valvular HD is whether to do transcatheter aortic valve implantation (TAVI) or surgical aortic valve replacement (SAVR) in patients with severe aortic stenosis (AS). There are obvious cases when patients are clearly poor surgical candidates. TAVI is the choice. There are also obvious surgical choices when the patient is very young or has the need for concomitant surgical procedures, such as left atrial (LA) ablation, mitral disease, or coronary artery disease (CAD) requiring revascularization. Then SAVR. For the large number in the middle, patients and doctors have to translate the nuances of the PARTNER, EVOLUT, Notion 1 and 2, DEDICATE, and UK-TAVI trials. You could have day-long conferences on sorting through the details of these trials. Ultimately, there is a tension between the much lower burden of TAVI vs its long-term durability relative to SAVR. Editors of the European Heart Journal and authors, mostly from Columbia University, tempt us to consider another factor in the decision: the carbon footprint of the two procedures. I kid you not. EHJ has the top impact factor of all cardiology journals, and it has now published a comparison of the carbon footprint of 10 patients who had SAVRs and 20 patients who had TAVIs (10 in the OR and 10 in the cath lab). They used a model that measured the kilograms of CO 2 equivalents based on the primary data, such as the materials, procedures, energies, in the preoperative, operative, and postoperative setting. TAVI used less CO 2 equivalents than SAVR (about half less). The numbers were 300 kg of CO 2 equivalents in TAVI vs 600 kg of CO 2 equivalents in SAVR. Postoperative intensive care unit and floor care accounted for the largest portion of the carbon footprint. The intraoperative footprint of SAVR was driven by biological waste, postoperative length of stay, and inhaled anesthetic gases. The authors concluded: The carbon footprint of SAVR is about twice as high as those from OR–TAVI or CATH–TAVI. These findings should potentially be considered when making population level decisions and guidelines moving into the future. I don't know what is happening to us as a field. The authors write this in the discussion: While carbon emissions should not be the deciding factor in the treatment strategy for individual patients, relative emissions should play a role in the future when deciding between different treatment options. I did a simple Google search on carbon emissions. Even if we accept their calculations, the difference was about 300 kg of CO 2 equivalents. To fly across the US is 1000 kg of CO 2 equivalents per passenger. So if you take your family of 4 that's like 13x more than the difference in these two procedures. Walk through Atlanta, Dulles, Newark, or LAX airports and just eyeball the number of people flying. I am all for climate stewardship. I ride a bike to work. I live close to everything in town. I don't litter. I like European hotels that minimize wasteful energy use. But my friends, the role of carbon footprint should have exactly zero influence on medical decisions such as TAVI vs SAVR. Number 1, it is miniscule relative to other human activities, and number 2, we take care of patients not the environment. Public health should have no bearing on individual decisions. Finally, I used to think coffee, blueberry, and quinoa studies were the most wasteful of time and effort. Now I think studying the carbon footprint of two medical procedures may have earned top honors in the most useless and wasteful studies. Come on you all. Post-Ablation Visual Auras a Sign of Transient Brain Injury? The group of Dr Greg Marcus at UCSF continue to do interesting work in EP. Their latest, led by fellow Adi Elias, investigated the possible association of a transseptal puncture during catheter ablation for ventricular arrhythmias with post-procedural visual auras. As well as to assess the relationship between occipital and parietal lobes acute brain emboli and migraine-related visual auras. The questions are important because it goes to the health of the brain during left-sided ablation, which is undergoing a massive increase due to the use of pulsed-field ablation (PFA) in the left atrium (LA). This work is actually an observational substudy of a recent randomized controlled trial called TRAVERSE. I will discuss both because both papers are making the rounds in the EP. Note also that this isn't just an EP topic because visual auras and micro-emboli to the brain also occur with coronary angiography, percutaneous coronary intervention (PCI) and valvular procedures. Let's talk first about the TRAVERSE trial, published in Circulation , in February 2025, first author Greg Marcus. TRAVERSE randomized only 146 patients who were to have a left sided ventricular tachycardia (VT) ablation to either retrograde aortic (RA) approach vs transseptal approach. The primary endpoint was an acute brain lesion on MRI. The main result: in the retrograde aortic approach, 28 of 62 (45%) exhibited an acute brain lesion compared with 19 of the 69 (28%) of those randomized to a transseptal puncture ( P = .036). No differences in clinically manifest complications or procedural efficacy were observed. No patient had a clinical stroke. Notable in the study was 10% of patients did not get an MRI—which means that they did not have a primary endpoint measured. The authors conclude from this data that: A transseptal approach may be the more favored strategy over a retrograde aortic approach for catheter ablation of endocardial left ventricular arrhythmias to reduce brain injury. The heightened risk of new brain lesions detected using MRI without overt clinical manifestations in the retrograde aortic arm may suggest a higher risk of other organ damage that is not immediately clinically occult. It is possible other procedures conventionally performed through a retrograde aortic approach might incur similar harms, and that novel transseptal approaches may yet prove beneficial. The first thing to say is that they have convinced many in the EP world that transseptal is the preferred approach to the LV. I sent a message to private EP group about access for a VT case and the overwhelming answer was transseptal and [quote] 'I am impressed by the UCSF data.' Well, my friends, I like many of the authors of this multicenter trial, but the trial is a mess, and it does not tell us the best approach. The first thing to say is that there were only 47 primary outcome events, and the primary outcome events were white spots on an MRI that disappear and have no know permanent sequalae. So even if there were a statistically robust difference, would it be clinically significant? I am not sure, and likely neither are you. I put the numbers into a Fragility Index calculator, which tells us how many non-events or events in each group would have been required to make the results nonsignificant or greater than P value of .05. The Fragility Index is 1. If one more patient in the transseptal group had a white spot, then the trial is negative. That is not a statistically robust finding. Not at all. What's even worse is that 10% of patients did not have an MRI. So the missing data is 10x the Fragility Index. The authors acknowledge this limitation but soft roll it. The academic editorialists don't mention the fragility of the data, nor the massive missingness. I think it is an existential problem with this study. We simply do not know. Imagine a drug or device outcome trial where 10% of the patients did not have a primary outcome measured. My final take of this study is that EP doctors might spend less time destroying LA during AF ablation and more time learning to look at evidence. TRAVERSE was a good effort, but its internal validity issues, small differences in a surrogate outcome and no difference in stroke tells us near zero about what approach to use when ablating LV sources of arrhythmia. To me, the doctor should choose the approach most likely to achieve success. Retrograde aortic access is clearly superior to transseptal for some areas of the V. TRAVERSE should not discourage them from using it. In the meantime, the question of best approach is an answerable question: it simply requires a larger study with more primary outcome events and less loss to follow-up. The second paper, first author fellow Adi Elias, was published in Heart Rhythm last week. This observational study asked two questions: (a) did the access site (RA vs transseptal) affect visual auras and (b) was there an association between occipital and parietal white spots and migraine-related visual auras. In total, 121 patients of the 146 had assessment of visual auras. A total of 18 reported a visual aura in the first month after the procedure and 103 did not. Pause there. Because the authors will soon be making conclusions about 18 reported visual auras. This paper also suffers from serious missingness, as 15% of those in the transseptal arm and 21% of those in the RA arm did not complete the 1-month questionnaire about having a visual aura, which was the primary endpoint. The first main result was that there was no difference between post-ablation visual auras observed between transseptal (16% of 63) and retrograde aortic approaches (14% of 57; P = .78). The second main result was that more participants with acute brain emboli in the occipital or parietal lobes experienced migraine-related visual auras (38% vs. 11%; P = .014). The actual numbers are 7 of 18 of those with occipital/parietal lesions vs 12 of 103 patients without parietal/occipital lesions. I calculated the Fragility Index on this difference, and it was 2. If 2 of the 103 without a white spot in the occipital/parietal area had a visual aura, then the association is non-significant. And again, recall that loss to follow-up was more than 15% in both groups. The authors make positive conclusions from this fragile data. Transseptal puncture was not associated with visual auras, however acute brain emboli involving the visual cortex was associated with such symptoms. These data suggest that transseptal punctures are not causal in migraine-related visual auras and that post-procedure acute brain emboli are apparently not always clinically silent. They then double down in their interviews on Medscape. Marcus says, 'These findings demonstrate that, contrary to a long-held belief that these post-ablation MRI-detected small brain lesions are asymptomatic — in fact, they are often referred to as 'asymptomatic cerebral emboli' or 'ACEs' — these small acute brain lesions actually can, and perhaps often do, manifest in clinical symptoms.' Dr Elias, too, is too strong. He says, 'The data show that these post-ablation brain lesions are not clinically silent. It may be the case that we haven't known what to look for and assessed for symptoms immediately without enough time for the subsequent visual auras that would occur.' Again, maybe they are correct, but the data is not statistically robust. They're making big conclusions based on 18 MRI scans and nearly 1 in 10 patients did not have an MRI and 1 in 5 patients did not have an assessment for visual auras. Only 2 events would change the conclusions. The data, therefore, do not support their conclusions. I would conclude only that there may be a signal, but we need more data to understand the relationship of postprocedure brain emboli and visual auras. Finally, my criticism of these studies is not meant to downplay the issue of brain emboli after procedures. These are potentially quite serious because even if the effect size on cognition is small, the large numbers of procedures being done means there could be a huge public health crisis in the future. As it is in all of medicine: everything turns on patient selection. When we do TAVI in an older person who has less than 6 months to live due to severe AS, and he or she gets asymptomatic brain emboli, we worry a little. In contrast, when we blast a 50-year-old with persistent AF with PFA, ablating the pulmonary veins, posterior wall and God knows what else, creating oodles of microbubbles that then cause multiple brain lesions, we should worry a lot. The best way to avoid brain emboli is to avoid procedures. That's not happening now. The reverse is. Early AF ablation is a money maker for doctors and hospitals. PFA lowers the threshold for doing AF ablation because it's faster and less likely to cause catastrophic complications. But our profession should be wise enough to be concerned about these observations. We should demand better data on brain MRIs as well as cognitive testing, especially with the advent of PFA. A small harm could turn into a huge problem. European Heart Journal has published a rapid communication from EAST-AFNET authors, regarding the short-term benefit of early rhythm control (ERC) vs rate control. To briefly review, NEJM published EAST-AFNET 5 years ago in 2020. About 2800 patients with newish AF were randomized to two strategies: early rhythm control (mostly with antiarrhythmic drugs) vs rate control. The primary endpoint was a composite of CVD, stroke, heart failure hospitalization, or acute coronary syndrome. The 5-year trial found a 21% statistically significant reduction in the primary endpoint. The primary safety endpoint did not differ. However, the authors combined death and stroke as both primary efficacy and safety endpoints. If you don't double count stroke and death, there were nearly 3x more safety events (68 vs 19) in the early rhythm control group (ERC) vs rate control. A couple notables: EAST-AFNET was not an ablation trial. Less than 1 in 5 patients in the ERC had ablation. So you have to posit that antiarrhythmic drugs (AAD) reduced hard outcomes—a first for sure. Another notable, there was only a 20% difference in the presence of sinus rhythm (80% vs 60%) at 2 years. So you also have to posit that a difference in sinus rhythm of only 20% drove hard outcomes. I am pretty sure — no, highly sure — that the better outcomes in EAST-AFNET were just performance bias, in that the ERC transmitted ECGs with symptoms had many, many more interactions with their clinicians. I am not against ERC, and do it often, but I oppose the use of EAST-AFNET to foster lucrative early AF ablations. I believe strongly that patients with AF who do not have HF or decompensation should be treated slowly and given a chance to let nature (or natural history) or risk factor modification help with their AF. One more thing about EAST-AFNET: the Kaplan-Meier curves for the primary endpoint do not separate for about 1.5 to 2 years , which is what you expect with patients with new AF. If there is a benefit of SR or enhanced medical interactions, it should take time to reduce cardiac outcomes. Now to the rapid communication of a post-hoc study. Here the EAST-AFNET authors look specifically at outcomes in the first 30 days both in the overall population and in the subset with HF. First result: A primary outcome event occurred in 9 of the 1400 patients randomized to early rhythm control and in 21 of the 1400 patients in the usual care group hazard ratio (HR) 0.43, 95% CI, 0.20–0.93). Second result: Deaths in first 30 days were observed in 1 of 1400 patient randomized to early rhythm control and in 4 of the 1400 patients randomized to usual care (HR 0.25, 95% CI, 0.03–2.24). The third result involved HF patients in EAST-AFNET 4. Slightly less than one third of all patients had prevalent heart failure, of which 400 patients were randomized to early rhythm control therapy and 400 to usual care. Within 30 days after randomization, a primary outcome occurred in 3 vs 14 patients with prevalent heart failure randomized to early rhythm control vs rate control, respectively (HR 0.22, 95% CI, 0.06–0.77; Figure 1). The authors concluded that: This exploratory analysis suggests immediate beneficial effects of early rhythm control therapy within 30 days after randomization, including a lower incidence of the primary outcome, fewer deaths, and a reduced composite of death or heart failure hospitalization—in both the overall population and in those who have HF at baseline. This supports its early implementation in patients at risk of heart failure or with acute and advanced heart failure. Again, I offer no malice to the authors, but this is a really problematic study. The numbers are tiny. I don't care what the P value or confidence interval say. EAST-AFNET was powered to tell differences over many years , not 30 days. So small are the differences in the first year, the Kaplan-Meier curves do not separate at all in the main paper. I am not sure why the authors set out to look at a comparison with so few events, or why the EHJ published something so unhelpful. But it depresses me to see stuff like this. Not only does it not help us , the small numbers of events (9 vs 21, for instance, in a study of 3000 patients) is more likely to deceive us . EAST-AFNET was a great effort. Strategy trials are hard; they are noisy. Performance bias was likely. But looking at 30 days with its few events only adds more noise to a noisy piece of evidence. I will close on a positive note. Our government, and likely yours too, makes a lot of mistakes. We should celebrate when government does something smart. This week, the Centers for Medicare & Medicaid Services announced that reimbursement will be cut by 27% for percutaneous LAAO. Since I strongly believe there is little to no benefit for these procedures—perhaps even a net harm—I consider this a positive. Better would have been zero reimbursement unless the patient is in a trial. Then we would have an idea of whether this procedure works. Keep in mind, my friends, that the PROTECT AF trial of warfarin vs Watchman did not pass FDA scrutiny due to internal validity issues. PREVAIL missed its first primary endpoint of stroke, systemic embolism, or CV death. Watchman did not meet noninferiority vs warfarin. Most patients having left atrial appendage occlusion (LAAO) would not have been included in the regulatory trials. And no clear data exist comparing LAAO to direct oral anticoagulants or no anticoagulation. Also, a note to my enthusiastic EP colleagues. Go ahead. Keep posting on Twitter that you can do LAAO or AF ablation in 6.5 minutes. We get that you are fast. Do you think that payers don't follow you on social media? Finally, I am still trying to understand the new National Coverage Determinations (NCD) criteria for tricuspid transcatheter edge-to-edge repair (T-TEER). The matter in question is the coverage with evidence criteria wherein patients having T-TEER have to be enrolled in a proper study. I don't know of one of those but will continue searching.
Time of India
26-05-2025
- Health
- Time of India
How can people with diabetes effectively prevent kidney disease?
Kidney disease affects more than one third of people with diabetes and is the most common cause of renal failure on a global scale. People with diabetes can get kidney disease as result of poor control of glucose levels or other secondary causes like infections, autoimmune diseases, harmful medications etc. Preventing diabetic kidney disease needs a proactive approach with optimal management of lifestyle, medications to control the risk factors, and regular screening. Lifestyle changes are key in control of the metabolic risk factors for the kidney disease. Portion control of carbohydrates with increasing the vegetables, and lean proteins is important for good glycemic control. Eliminate simple carbs and processed sugars. Salt restriction is necessary for control of hypertension. A physical activity schedule involving aerobic and resistance training with at least 150 minutes of moderate activity is necessary. Weight loss of even 5% can improve the insulin sensitivity and reduce the blood pressure. Adequate hydration is important for renal health. People with diabetes are at a higher risk for urinary infections. It is important to screen and treat the urinary infections promptly as ascending infections often cause renal dysfunction. Especially people with additional risk factors like urinary stones, phimosis, and urethral strictures etc. need to be extra cautious. Medications such as NSAIDs, antifungals, and antibiotics which can potentially lead to renal injury should be used cautiously under medical supervision. When choosing the medications in patients with diabetes, the risk for kidney disease needs to be considered. We have medications like SGLT2 inhibitors, and GLP1 receptor agonists which can reduce the progression of kidney damage independent of the glucose control they provide. For patients with early signs of renal damage like proteinuria, these medications can delay and potentially prevent the onset of kidney disease. In addition, we need to control the cholesterol levels to optimal targets for reduction of cardiovascular events in addition to renal protection. Medications used for control of blood pressure like ACE inhibitors and ARBs also reduce the proteinuria and help in prevention of progression of the kidney disease. We have a new class of medications called non-steroidal MR blockers e.g. Finerenone which also reduce the proteinuria and prevent kidney disease progression. With the help of lifestyle measures and appropriate medications, we should target optimal glucose levels with Hba1c <7% for most adults and to keep the blood pressure < 130/80 mm Hg. Regular screening for kidney disease helps in early detection. Annual screening for proteinuria (using urine albumin to creatinine ratio) and estimated glomerular filtration rate (calculated based on serum creatinine level) is imperative for people with type 2 diabetes. Timing of the intervention plays an important role in prevention of kidney damage. Educating the patients about complication screening during clinic visits for diabetes helps a lot. At a community level educating the public with collaboration of dieticians, primary care physicians, endocrinologists, and nephrologists is imperative in spreading the awareness. Promoting widespread access to screening tests boosts efforts in early diagnosis and prevention. We need to think of primordial prevention. Identifying the people with metabolic risk factors, and preventing diabetes, and hypertension through lifestyle measures will have a greater impact than interventions at a later stage. To summarize, prevention diabetic kidney disease revolves around improvement of lifestyle, optimization of the metabolic risk factors through medications, and regular screening to diagnosed the kidney disease in a very early stage. With early diagnosis and optimal management, we can preserve the renal health and improve the quality of life for people with diabetes. Dr. Varun Suryadevara, Endocrinologist, MBBS MD Internal Medicine DM Endocrinology, Apollo Hospitals, Bangalore One step to a healthier you—join Times Health+ Yoga and feel the change
Yahoo
30-04-2025
- Health
- Yahoo
Finerenone continues to impress in diabetic kidney disease
In a recent study conducted by Sankar D Navaneethan and colleagues and published in the International Society of Nephrology, the cardiovascular and kidney benefits of Bayer's Kerendia (finerenone) are maintained regardless of acute changes in estimated glomerular filtration rate (eGFR) following treatment initiation in patients with chronic kidney disease (CKD) and type 2 diabetes (T2D). Leading data and analytics company GlobalData believes that this comprehensive analysis will reassure nephrologists about prescribing finerenone to patients with CKD and T2D, even if initial eGFR declines are observed. The consistent efficacy across eGFR change subgroups, combined with a manageable safety profile, supports the use of finerenone as an important therapeutic option for this high-risk patient population. Finerenone is a nonsteroidal mineralocorticoid receptor antagonist (MRA). Compared to steroidal MRAs, finerenone has a shorter half-life and a more balanced distribution between the heart and the kidney. The study included an analysis of the prespecified FIDELITY trial, a pooled individual-level analysis of two major Phase III clinical trials: FIDELIO-DKD and FIGARO-DKD. This new analysis addressed an important clinical concern, specifically the hesitancy to prescribe or continue medications associated with acute eGFR decline. The study demonstrated that finerenone consistently reduced composite cardiovascular outcomes across all eGFR change subgroups, with hazard ratios of 0.74 (95% confidence interval 0.61-0.90) for patients with more than 10% eGFR decline, 0.87 (0.73-1.04) for >0-10% eGFR decline, 1.06 (0.87-1.28) for 0-10% eGFR increase, and 0.78 (0.61-0.99) for more than 10% eGFR increase. While there was a numeric interaction (p=0.048), the interaction was not significant (p=0.58) when modelled as a continuous variable. Similarly, finerenone reduced composite kidney outcomes across all eGFR change categories, with hazard ratios of 0.67 (0.53-0.85) for more than 10% eGFR decline, 0.78 (0.61-1.01) for >0-10% eGFR decline, 0.56 (0.40-0.77) for 0-10% eGFR increase, and 0.75 (0.50-1.14) for more than 10% eGFR increase. The interaction was not significant (p=0.23 for categories, p=0.36 for continuous modelling). These findings provide reassurance for nephrologists who may be hesitant to prescribe medications associated with initial eGFR reductions. Kerendia received US Food and Drug Administration approval in July 2021 to reduce the risk of sustained eGFR decline, end-stage kidney disease, cardiovascular death, nonfatal myocardial infarction, and hospitalisation for heart failure in adults with CKD associated with T2D. "Finerenone continues to impress in diabetic kidney disease" was originally created and published by Clinical Trials Arena, a GlobalData owned brand. The information on this site has been included in good faith for general informational purposes only. It is not intended to amount to advice on which you should rely, and we give no representation, warranty or guarantee, whether express or implied as to its accuracy or completeness. You must obtain professional or specialist advice before taking, or refraining from, any action on the basis of the content on our site. Sign in to access your portfolio
