2f:I[703058,["/_next/static/immutable/chunks/3bhq_5eh1d760.js","/_next/static/immutable/chunks/1855-ogyi8eh4.js","/_next/static/immutable/chunks/2pfsjpn6k6zlg.js","/_next/static/immutable/chunks/26c7v3_3uwnwu.js","/_next/static/immutable/chunks/25a3ozcrvi1ff.js","/_next/static/immutable/chunks/2r4wx50nvjh_4.js","/_next/static/immutable/chunks/23fsw06hsi5b1.js","/_next/static/immutable/chunks/06_yt270h41rg.js","/_next/static/immutable/chunks/3ezsiz-7shkna.js","/_next/static/immutable/chunks/20x2y96ldu5wx.js","/_next/static/immutable/chunks/2lxntcm3pd1_h.js","/_next/static/immutable/chunks/00dgco8irq3jw.js","/_next/static/immutable/chunks/00nwe-kq0rboc.js","/_next/static/immutable/chunks/2051ffx3xzio9.js"],"PaperListPageClient"] 30:T6e8,The renin-angiotensin-aldosterone system (RAAS) plays a central role in regulating renal hemodynamics, sodium and water balance, and cardiovascular homeostasis. Chronic RAAS activation contributes to hypertension, proteinuria, inflammation, fluid overload, and fibrosis, making RAAS blockade (RAASb) a cornerstone therapy across the kidney life cycle. Over the past decades, ACE inhibitors, angiotensin receptor blockers, direct renin inhibitors, and mineralocorticoid receptor antagonists have demonstrated substantial benefits in slowing chronic kidney disease (CKD) progression, reducing proteinuria, and lowering cardiovascular risk. However, the efficacy and safety of RAASb vary according to the kidney life cycle. Evidence supports its use in proteinuric CKD and even in advanced stages, whereas the benefit in non-proteinuric disease remains limited. Novel non-steroidal mineralocorticoid receptor antagonists such as finerenone further enhance renal and cardiovascular protection, particularly in persons with diabetes and CKD. In dialysis populations, RAASb may preserve residual kidney function improve cardiac structure/function, although the benefit of steroidal MRAs remains uncertain. In kidney transplantation, RAASb appears safe and may improve long-term graft and patient survival, particularly when initiated early. The emergence of SGLT2 inhibitors and GLP-1 receptor agonists has reshaped therapeutic strategies, with accumulating evidence supporting complementary rather than competing roles with RAASb. This review synthesizes current evidence on RAAS modulation across the kidney life cycle from primary prevention to advanced CKD, dialysis, and transplantation, highlighting both established benefits and areas of current clinical uncertainty.31:T72c,ABSTRACT The renin–angiotensin–aldosterone system (RAAS) plays a central role in regulating renal hemodynamics, sodium and water balance, and cardiovascular homeostasis. Chronic RAAS activation contributes to hypertension, proteinuria, inflammation, fluid overload, and fibrosis, making RAAS blockade (RAASb) a cornerstone therapy across the kidney life cycle. Over the past decades, ACE inhibitors, angiotensin receptor blockers, direct renin inhibitors, and mineralocorticoid receptor antagonists (MRAs) have demonstrated substantial benefits in slowing chronic kidney disease (CKD) progression, reducing proteinuria, and lowering cardiovascular risk. However, the efficacy and safety of RAASb vary according to the kidney life cycle. Evidence supports its use in proteinuric CKD and even in advanced stages, whereas the benefit in non-proteinuric disease remains limited. Novel non-steroidal MRAs such as finerenone further enhance renal and cardiovascular protection, particularly in persons with diabetes and CKD. In dialysis populations, RAASb may preserve residual kidney function and improve cardiac structure/function, although the benefit of steroidal MRAs remains uncertain. In kidney transplantation, RAASb appears safe and may improve long-term graft and patient survival, particularly when initiated early. The emergence of SGLT2 inhibitors and glucagon-like peptide-1 receptor agonists has reshaped therapeutic strategies, with accumulating evidence supporting complementary rather than competing roles with RAASb. This review synthesizes current evidence on RAAS modulation across the kidney life cycle from primary prevention to advanced CKD, dialysis, and transplantation, highlighting both established benefits and areas of current clinical uncertainty.25:[[["$","script","0",{"type":"application/ld+json","dangerouslySetInnerHTML":{"__html":"{\"@context\":\"https://schema.org\",\"@type\":\"CollectionPage\",\"name\":\"Mineralocorticoid Receptor Antagonist: modality Research & Clinical Takeaways\",\"description\":\"Explore peer-reviewed papers on Mineralocorticoid Receptor Antagonist (modality). Clinician-written summaries and actionable practice insights. 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The authors apply sensitivity analyses but the assumption remains a key limitation.","value_numeric":null},{"paper_doi":"10.1016/j.jchf.2026.103295","tag_type":"warning","value":"Treatment rates sourced from Epic Cosmos may reflect a health-system-biased sample and may not generalize to uninsured or underserved populations.","value_numeric":null}],"summaries":{"what_studied":"This population-level decision analytic modeling study estimated the number of U.S. adults with HFrEF eligible but not receiving quadruple GDMT (ARNI, beta-blocker, MRA, SGLT2 inhibitor), and projected deaths and hospitalizations preventable with optimal implementation over 12 months, using 2022–2025 national data sources.","key_result":"Only 18.2% of an estimated 2.76 million eligible U.S. HFrEF adults received quadruple GDMT. Optimal implementation was projected to prevent ~113,747 deaths (95% UI: 90,173–149,875) and ~357,332 HF hospitalizations annually.","limitations":"Estimates rely on modeled assumptions and trial-derived NNTs applied to real-world populations, which may not fully reflect comorbidity burden or contraindication rates. Treatment rates from Epic Cosmos may not represent all U.S. practice settings. Aggregate death estimates assume independent, additive benefits across drug classes.","practice_takeaway":"More than 1.5–1.8 million HFrEF patients remain untreated for each individual GDMT class — closing these gaps could prevent over 100,000 deaths per year. Clinicians should systematically audit HFrEF patients for GDMT eligibility and prioritize initiation of ARNIs and SGLT2 inhibitors, where gaps are largest."}},{"doi":"10.1016/j.jacc.2026.06.018","pmid":"42494134","title":"Management of Heart Failure With Preserved Ejection Fraction: 2026 ACC Expert Consensus Decision Pathway","journal_title":"JACC","journal_issn":"0735-1097","published_at":"2026-07-23T00:00:00.000Z","url":"https://doi.org/10.1016/j.jacc.2026.06.018","source_score":100,"is_retracted":false,"is_open_access":null,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":false},"created_at":"2026-07-26T13:44:37.835Z","updated_at":"2026-07-26T13:44:37.835Z","tags":[{"paper_doi":"10.1016/j.jacc.2026.06.018","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1016/j.jacc.2026.06.018","tag_type":"category","value":"Cardiac & Cardiovascular Systems","value_numeric":null},{"paper_doi":"10.1016/j.jacc.2026.06.018","tag_type":"condition","value":"Heart Failure With Preserved Ejection Fraction","value_numeric":null},{"paper_doi":"10.1016/j.jacc.2026.06.018","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1016/j.jacc.2026.06.018","tag_type":"level_of_evidence","value":"7","value_numeric":null},{"paper_doi":"10.1016/j.jacc.2026.06.018","tag_type":"modality","value":"Angiotensin Receptor Blocker","value_numeric":null},{"paper_doi":"10.1016/j.jacc.2026.06.018","tag_type":"modality","value":"Angiotensin Receptor-Neprilysin Inhibitor","value_numeric":null},{"paper_doi":"10.1016/j.jacc.2026.06.018","tag_type":"modality","value":"Diuretic","value_numeric":null},{"paper_doi":"10.1016/j.jacc.2026.06.018","tag_type":"modality","value":"GLP-1 Receptor Agonist","value_numeric":null},{"paper_doi":"10.1016/j.jacc.2026.06.018","tag_type":"modality","value":"Mineralocorticoid Receptor Antagonist","value_numeric":null},{"paper_doi":"10.1016/j.jacc.2026.06.018","tag_type":"modality","value":"SGLT2 Inhibitor","value_numeric":null},{"paper_doi":"10.1016/j.jacc.2026.06.018","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1016/j.jacc.2026.06.018","tag_type":"study_design","value":"Expert Consensus / Clinical Practice Guideline","value_numeric":null},{"paper_doi":"10.1016/j.jacc.2026.06.018","tag_type":"warning","value":"Level of evidence assigned as '7' (expert consensus/opinion) because this is a guideline/pathway document, not a primary research study.","value_numeric":null},{"paper_doi":"10.1016/j.jacc.2026.06.018","tag_type":"warning","value":"Only the publisher landing page and partial full text were available; specific trial names, drug dosages, and individual recommendation grades cited in the document could not be fully extracted.","value_numeric":null},{"paper_doi":"10.1016/j.jacc.2026.06.018","tag_type":"warning","value":"The document is dated July 23, 2026 — it is a 'Just Accepted' publication and may not yet reflect final copyedited content or supplemental appendix details.","value_numeric":null}],"summaries":{"what_studied":"This 2026 ACC Expert Consensus Decision Pathway (ECDP) updates the 2023 version, providing practical guidance on the diagnosis and management of HFpEF, including optimal medical therapy (SGLT2 inhibitors, nonsteroidal MRAs, incretin-based therapies, ARNIs, ARBs), nonpharmacologic strategies, device therapy, and comorbidity management.","key_result":"Key updates emphasize SGLT2 inhibitors, nonsteroidal mineralocorticoid receptor antagonists, and incretin-based therapies (GLP-1 receptor agonists) as central pillars of optimal medical therapy in HFpEF, reflecting recent favorable trial data; HFpEF now accounts for >50% of all HF cases with outcomes comparable to HFrEF.","limitations":"This is a consensus/expert opinion document, not a systematic review or RCT; recommendations are derived from committee deliberation and may lag behind the most recent published trials. The pathway is primarily focused on the ambulatory setting and may not fully apply to acute inpatient care.","practice_takeaway":"Clinicians should prioritize SGLT2 inhibitors, nonsteroidal MRAs, and incretin-based therapies in eligible HFpEF patients, while also screening for and managing key comorbidities (obesity, diabetes, CKD, hypertension, atrial fibrillation, CAD). Use structured diagnostic scoring tools (HFA-PEFF, H2FPEF, HFpEF-ABA) to confirm diagnosis and exclude mimics before initiating therapy."}},{"doi":"10.1001/jamacardio.2026.2104","pmid":"42418169","title":"Finerenone and Blood Pressure in Heart Failure With Mildly Reduced or Preserved Ejection Fraction","journal_title":"JAMA Cardiology","journal_issn":"2380-6583","published_at":"2026-07-08T00:00:00.000Z","url":"https://eprints.gla.ac.uk/view/journal_volume/JAMA_Cardiology.html>,","source_score":50,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-08-17T13:33:01.465Z","updated_at":"2026-08-17T13:33:01.465Z","tags":[{"paper_doi":"10.1001/jamacardio.2026.2104","tag_type":"age_group","value":"older_adult","value_numeric":null},{"paper_doi":"10.1001/jamacardio.2026.2104","tag_type":"brand","value":"Kerendia","value_numeric":null},{"paper_doi":"10.1001/jamacardio.2026.2104","tag_type":"category","value":"Cardiac & Cardiovascular Systems","value_numeric":null},{"paper_doi":"10.1001/jamacardio.2026.2104","tag_type":"condition","value":"Heart Failure With Mildly Reduced Ejection Fraction","value_numeric":null},{"paper_doi":"10.1001/jamacardio.2026.2104","tag_type":"condition","value":"Heart Failure With Preserved Ejection Fraction","value_numeric":null},{"paper_doi":"10.1001/jamacardio.2026.2104","tag_type":"condition","value":"Hypertension","value_numeric":null},{"paper_doi":"10.1001/jamacardio.2026.2104","tag_type":"generic","value":"finerenone","value_numeric":null},{"paper_doi":"10.1001/jamacardio.2026.2104","tag_type":"impact_flag","value":"confirms_prior","value_numeric":null},{"paper_doi":"10.1001/jamacardio.2026.2104","tag_type":"level_of_evidence","value":"2","value_numeric":null},{"paper_doi":"10.1001/jamacardio.2026.2104","tag_type":"modality","value":"Mineralocorticoid Receptor Antagonist","value_numeric":null},{"paper_doi":"10.1001/jamacardio.2026.2104","tag_type":"sample_size","value":"n=5999","value_numeric":5999},{"paper_doi":"10.1001/jamacardio.2026.2104","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1001/jamacardio.2026.2104","tag_type":"study_design","value":"Randomized Controlled Trial","value_numeric":null},{"paper_doi":"10.1001/jamacardio.2026.2104","tag_type":"warning","value":"Multiple authors have financial relationships with Bayer AG, the trial sponsor, which funded the study and was involved in study supervision and data collection.","value_numeric":null},{"paper_doi":"10.1001/jamacardio.2026.2104","tag_type":"warning","value":"The brand name 'Kerendia' is assigned based on known finerenone branding; the paper itself does not mention a brand name.","value_numeric":null},{"paper_doi":"10.1001/jamacardio.2026.2104","tag_type":"warning","value":"This is a prespecified secondary/subgroup analysis of the FINEARTS-HF trial, not the primary trial report — causal mediation estimates should be interpreted cautiously given wide confidence intervals crossing zero.","value_numeric":null}],"summaries":{"what_studied":"This prespecified secondary analysis of the FINEARTS-HF RCT examined the blood pressure (BP) effects of finerenone vs placebo in 5,999 adults with HFmrEF/HFpEF (mean age 72 years, 45% female, mean baseline SBP 129 mmHg), and whether baseline BP or BP reduction mediated finerenone's cardiovascular benefits over up to 36 months.","key_result":"Finerenone produced an early, sustained SBP reduction (overall placebo-adjusted mean: −3.1 mmHg; 95% CI, −3.6 to −2.6; P<.001), consistent across all baseline SBP categories. Cardiovascular death and total HF events were reduced irrespective of baseline SBP or DBP (P for interaction .96 and .83, respectively), and causal mediation analysis showed only ~7.4% of finerenone's benefit was mediated by SBP change (95% CI, −0.7 to 27.0).","limitations":"- No 24-hour ambulatory BP monitoring, limiting BP characterization.\n- Exclusion of patients with symptomatic hypotension or uncontrolled SBP ≥160 mmHg (or ≥180 mmHg) may limit generalizability to extreme BP ranges.\n- Industry-sponsored trial (Bayer AG) with multiple author conflicts of interest.","practice_takeaway":"Finerenone lowers BP modestly but its cardiovascular benefit in HFmrEF/HFpEF is not driven by BP reduction — clinicians can use it across a broad baseline BP range without concern that only hypertensive patients benefit. The ~1.6–2.0× higher odds of SBP <100 mmHg events with finerenone vs placebo were consistent across BP subgroups, so monitoring for hypotension remains relevant regardless of baseline BP."}},{"doi":"10.1093/eurheartj/ehag450","pmid":"42390477","title":"Brain mineralocorticoid receptor activation and antagonism in heart failure with preserved ejection fraction: a hypothesis","journal_title":"European Heart Journal","journal_issn":"0195-668X","published_at":"2026-07-02T00:00:00.000Z","url":"https://doi.org/10.1093/eurheartj/ehag450","source_score":27,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-07-09T13:36:07.499Z","updated_at":"2026-07-09T13:36:07.499Z","tags":[{"paper_doi":"10.1093/eurheartj/ehag450","tag_type":"category","value":"Cardiac & Cardiovascular Systems","value_numeric":null},{"paper_doi":"10.1093/eurheartj/ehag450","tag_type":"condition","value":"Heart Failure With Preserved Ejection Fraction","value_numeric":null},{"paper_doi":"10.1093/eurheartj/ehag450","tag_type":"impact_flag","value":"limited_evidence","value_numeric":null},{"paper_doi":"10.1093/eurheartj/ehag450","tag_type":"level_of_evidence","value":"7","value_numeric":null},{"paper_doi":"10.1093/eurheartj/ehag450","tag_type":"modality","value":"Mineralocorticoid Receptor Antagonist","value_numeric":null},{"paper_doi":"10.1093/eurheartj/ehag450","tag_type":"study_design","value":"Hypothesis / Narrative Review","value_numeric":null},{"paper_doi":"10.1093/eurheartj/ehag450","tag_type":"warning","value":"No patient data, sample size, or clinical outcomes are reported — this is a mechanistic hypothesis paper only. Tags for sample size, sex, and age group are omitted accordingly. Study design label reflects the conceptual/opinion nature of the publication.","value_numeric":null}],"summaries":{"what_studied":"This paper proposes a hypothesis about the role of brain mineralocorticoid receptor (MR) activation and its antagonism in the pathophysiology and treatment of heart failure with preserved ejection fraction (HFpEF).","key_result":"The authors hypothesize that brain MR activation contributes to the neurohormonal dysregulation seen in HFpEF, and that MR antagonism may exert beneficial effects partly through central nervous system mechanisms, beyond its known peripheral actions.","limitations":"This is a hypothesis paper, not an interventional or observational study — no clinical outcome data or patient cohort is presented. The proposed central MR mechanisms in HFpEF remain largely untested in humans.","practice_takeaway":"While MR antagonists are used in heart failure, this hypothesis suggests their brain-mediated effects may be an underappreciated therapeutic mechanism in HFpEF — clinicians should watch for emerging trial data testing this concept."}},{"doi":"10.1093/ndt/gfag150","pmid":"42360710","title":"Systolic blood pressure and albuminuria reduction mediate cardiovascular benefits of finerenone in T2 diabetes and CKD","journal_title":"Nephrology Dialysis Transplantation","journal_issn":"0931-0509","published_at":"2026-06-26T00:00:00.000Z","url":"https://doi.org/10.1093/ndt/gfag150","source_score":10,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-07-01T13:27:18.784Z","updated_at":"2026-07-01T13:27:18.784Z","tags":[{"paper_doi":"10.1093/ndt/gfag150","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1093/ndt/gfag150","tag_type":"brand","value":"Kerendia","value_numeric":null},{"paper_doi":"10.1093/ndt/gfag150","tag_type":"category","value":"Urology & Nephrology","value_numeric":null},{"paper_doi":"10.1093/ndt/gfag150","tag_type":"condition","value":"Cardiovascular Disease","value_numeric":null},{"paper_doi":"10.1093/ndt/gfag150","tag_type":"condition","value":"Chronic Kidney Disease","value_numeric":null},{"paper_doi":"10.1093/ndt/gfag150","tag_type":"condition","value":"Type 2 Diabetes","value_numeric":null},{"paper_doi":"10.1093/ndt/gfag150","tag_type":"generic","value":"finerenone","value_numeric":null},{"paper_doi":"10.1093/ndt/gfag150","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1093/ndt/gfag150","tag_type":"level_of_evidence","value":"2","value_numeric":null},{"paper_doi":"10.1093/ndt/gfag150","tag_type":"modality","value":"Mineralocorticoid Receptor Antagonist","value_numeric":null},{"paper_doi":"10.1093/ndt/gfag150","tag_type":"sample_size","value":"n=12143","value_numeric":12143},{"paper_doi":"10.1093/ndt/gfag150","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1093/ndt/gfag150","tag_type":"study_design","value":"Causal Mediation Analysis","value_numeric":null},{"paper_doi":"10.1093/ndt/gfag150","tag_type":"warning","value":"Sex breakdown of the FIDELITY pooled cohort is not specified in the abstract; 'mixed' sex tag is inferred from prior FIDELITY publications.","value_numeric":null},{"paper_doi":"10.1093/ndt/gfag150","tag_type":"warning","value":"The joint mediation CI of 21–100% is very wide; the upper bound of 100% should not be interpreted as near-certainty of complete mediation.","value_numeric":null},{"paper_doi":"10.1093/ndt/gfag150","tag_type":"warning","value":"The study design is a post-hoc causal mediation analysis of pooled RCT data (FIDELITY), not a prospectively powered mediation trial — the 'level 2' evidence rating reflects the RCT origin of the data, but mediation estimates carry additional analytical assumptions.","value_numeric":null}],"summaries":{"what_studied":"Causal mediation analysis of FIDELITY pooled data (n=12,143 adults with T2D and CKD) to quantify how much of finerenone's long-term cardiovascular benefit (CV death, nonfatal MI, nonfatal stroke, HF hospitalization) is mediated by 4-month changes in UACR, SBP, body weight, and serum potassium.","key_result":"Early reductions in UACR (−32.2%) and SBP (−3.6 mmHg) together mediated 50% (95% CI 21–100%) of finerenone's cardiovascular benefit; UACR alone mediated 39% (95% CI 7–71%) and SBP alone 21% (95% CI 3–40%). Body weight (−0.23 kg) and serum potassium (+0.19 mEq/L) changes did not mediate cardiovascular outcomes.","limitations":"- Wide confidence intervals (e.g., joint mediation 21–100%) reflect residual uncertainty about the true mediated fraction.\n- Mediation analysis assumes no unmeasured confounding of the mediator–outcome relationship, which cannot be fully guaranteed.\n- All data derive from a single pooled trial program (FIDELITY), limiting external generalizability.","practice_takeaway":"In patients with T2D and CKD on finerenone, early drops in UACR and SBP at 4 months are meaningful signals of cardiovascular efficacy — not just renal markers. Monitoring both within the first few months can help confirm the drug is working as intended."}},{"doi":"10.1038/s41581-026-01098-6","pmid":"42343109","title":"Benefits of finerenone treatment across chronic kidney disease aetiologies","journal_title":"Nature Reviews Nephrology","journal_issn":"1759-5061","published_at":"2026-06-24T00:00:00.000Z","url":"https://doi.org/10.1038/s41581-026-01098-6","source_score":8,"is_retracted":false,"is_open_access":false,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-06-29T13:22:45.392Z","updated_at":"2026-06-29T13:22:45.392Z","tags":[{"paper_doi":"10.1038/s41581-026-01098-6","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1038/s41581-026-01098-6","tag_type":"brand","value":"Kerendia","value_numeric":null},{"paper_doi":"10.1038/s41581-026-01098-6","tag_type":"category","value":"Urology & Nephrology","value_numeric":null},{"paper_doi":"10.1038/s41581-026-01098-6","tag_type":"condition","value":"Chronic Kidney Disease","value_numeric":null},{"paper_doi":"10.1038/s41581-026-01098-6","tag_type":"condition","value":"Glomerular Disease","value_numeric":null},{"paper_doi":"10.1038/s41581-026-01098-6","tag_type":"generic","value":"finerenone","value_numeric":null},{"paper_doi":"10.1038/s41581-026-01098-6","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1038/s41581-026-01098-6","tag_type":"level_of_evidence","value":"2","value_numeric":null},{"paper_doi":"10.1038/s41581-026-01098-6","tag_type":"modality","value":"Mineralocorticoid Receptor Antagonist","value_numeric":null},{"paper_doi":"10.1038/s41581-026-01098-6","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1038/s41581-026-01098-6","tag_type":"study_design","value":"Research Highlight / Clinical Trial Summary","value_numeric":null},{"paper_doi":"10.1038/s41581-026-01098-6","tag_type":"warning","value":"Level of evidence is assigned based on the underlying RCT design described; the highlight itself is a secondary summary and does not constitute primary evidence.","value_numeric":null},{"paper_doi":"10.1038/s41581-026-01098-6","tag_type":"warning","value":"Study design tag reflects that this article summarizes two primary RCTs (FIND-CKD and a glomerular disease substudy); it is not itself an original trial report.","value_numeric":null},{"paper_doi":"10.1038/s41581-026-01098-6","tag_type":"warning","value":"The brand name 'Kerendia' was inferred from known finerenone branding; it is not explicitly stated in this article.","value_numeric":null},{"paper_doi":"10.1038/s41581-026-01098-6","tag_type":"warning","value":"This is a research highlight/editorial summary, not the full FIND-CKD trial report — quantitative primary endpoint results (e.g., hazard ratios, absolute risk reductions) are not available from this text alone.","value_numeric":null}],"summaries":{"what_studied":"This research highlight summarizes findings from the FIND-CKD trial (presented at the 63rd European Renal Association Congress) evaluating finerenone, a nonsteroidal mineralocorticoid receptor antagonist, in people with CKD **without** diabetes — extending prior evidence beyond the diabetic CKD population. A second referenced study examined finerenone specifically in CKD due to glomerular diseases.","key_result":"Finerenone demonstrated kidney and cardiovascular protective benefits in people with CKD without diabetes. Hyperkalaemia occurred in 17% of treated patients vs. 13.3% on placebo, with a modest mean serum potassium increase of 0.12 mmol/L between groups; the drug was overall safe and well tolerated.","limitations":"This is a brief research highlight, not the full trial report — specific primary endpoint data, effect sizes, and sample sizes are not provided. Full details require access to the primary publications in NEJM and JAMA.","practice_takeaway":"Finerenone may benefit patients with CKD regardless of diabetes status, including those with glomerular disease. Monitor serum potassium closely — hyperkalaemia rates were higher with treatment (17% vs. 13.3%), though the absolute potassium rise was small (0.12 mmol/L)."}},{"doi":"10.2215/cjn.0000001158","pmid":"42335037","title":"A Framework for Risk-Based Implementation of Combination Therapy in CKD","journal_title":"Clinical Journal of the American Society of Nephrology","journal_issn":"1555-9041","published_at":"2026-06-23T00:00:00.000Z","url":"https://doi.org/10.2215/cjn.0000001158","source_score":16,"is_retracted":false,"is_open_access":false,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-06-25T13:25:28.659Z","updated_at":"2026-06-25T13:25:28.659Z","tags":[{"paper_doi":"10.2215/cjn.0000001158","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.2215/cjn.0000001158","tag_type":"category","value":"Urology & Nephrology","value_numeric":null},{"paper_doi":"10.2215/cjn.0000001158","tag_type":"condition","value":"Chronic Kidney Disease","value_numeric":null},{"paper_doi":"10.2215/cjn.0000001158","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.2215/cjn.0000001158","tag_type":"level_of_evidence","value":"6","value_numeric":null},{"paper_doi":"10.2215/cjn.0000001158","tag_type":"modality","value":"GLP-1 Receptor Agonist","value_numeric":null},{"paper_doi":"10.2215/cjn.0000001158","tag_type":"modality","value":"Mineralocorticoid Receptor Antagonist","value_numeric":null},{"paper_doi":"10.2215/cjn.0000001158","tag_type":"modality","value":"SGLT2 Inhibitor","value_numeric":null},{"paper_doi":"10.2215/cjn.0000001158","tag_type":"study_design","value":"Review / Framework Paper","value_numeric":null},{"paper_doi":"10.2215/cjn.0000001158","tag_type":"warning","value":"Age group defaulted to 'adult' as CKD combination therapy trials predominantly enroll adults; pediatric applicability is not discussed.","value_numeric":null},{"paper_doi":"10.2215/cjn.0000001158","tag_type":"warning","value":"No sample size is applicable as no primary patient data are reported.","value_numeric":null},{"paper_doi":"10.2215/cjn.0000001158","tag_type":"warning","value":"Sex distribution of the underlying evidence base is not described in the abstract.","value_numeric":null},{"paper_doi":"10.2215/cjn.0000001158","tag_type":"warning","value":"This is a framework/opinion-style review paper, not an original trial or meta-analysis — level of evidence is expert consensus/narrative review.","value_numeric":null}],"summaries":{"what_studied":"This paper proposes a risk-based framework for implementing combination therapy in CKD, integrating SGLT2 inhibitors, non-steroidal MRAs, and GLP-1 receptor agonists, guided by albuminuria and validated risk equations.","key_result":"Evidence from large RCTs and meta-analyses shows that SGLT2 inhibitors, non-steroidal MRAs, and GLP-1 receptor agonists provide independent and additive kidney and cardiovascular benefits, with select combinations also improving safety profiles.","limitations":"This is a framework/review paper without original trial data; specific combination regimen evidence is still emerging and not yet fully established from dedicated combination therapy trials.","practice_takeaway":"Use albuminuria level and validated risk scores to guide how many and which agents to combine in CKD — higher-risk patients warrant earlier initiation of multidrug regimens. Watch for upcoming single-pill combinations and adaptive trial data that may further streamline clinical decision-making."}},{"doi":"10.1093/eurheartj/ehag426","pmid":"42284132","title":"Albuminuria and heart failure","journal_title":"European Heart Journal","journal_issn":"0195-668X","published_at":"2026-06-12T00:00:00.000Z","url":"https://doi.org/10.1093/eurheartj/ehag426","source_score":26,"is_retracted":false,"is_open_access":false,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-06-22T13:24:08.577Z","updated_at":"2026-06-22T13:24:08.577Z","tags":[{"paper_doi":"10.1093/eurheartj/ehag426","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1093/eurheartj/ehag426","tag_type":"category","value":"Cardiac & Cardiovascular Systems","value_numeric":null},{"paper_doi":"10.1093/eurheartj/ehag426","tag_type":"condition","value":"Albuminuria","value_numeric":null},{"paper_doi":"10.1093/eurheartj/ehag426","tag_type":"condition","value":"Chronic Kidney Disease","value_numeric":null},{"paper_doi":"10.1093/eurheartj/ehag426","tag_type":"condition","value":"Heart Failure","value_numeric":null},{"paper_doi":"10.1093/eurheartj/ehag426","tag_type":"condition","value":"Hypertension","value_numeric":null},{"paper_doi":"10.1093/eurheartj/ehag426","tag_type":"condition","value":"Type 2 Diabetes","value_numeric":null},{"paper_doi":"10.1093/eurheartj/ehag426","tag_type":"generic","value":"finerenone","value_numeric":null},{"paper_doi":"10.1093/eurheartj/ehag426","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1093/eurheartj/ehag426","tag_type":"level_of_evidence","value":"5","value_numeric":null},{"paper_doi":"10.1093/eurheartj/ehag426","tag_type":"modality","value":"Mineralocorticoid Receptor Antagonist","value_numeric":null},{"paper_doi":"10.1093/eurheartj/ehag426","tag_type":"modality","value":"Renin-Angiotensin System Inhibitor","value_numeric":null},{"paper_doi":"10.1093/eurheartj/ehag426","tag_type":"modality","value":"SGLT2 Inhibitor","value_numeric":null},{"paper_doi":"10.1093/eurheartj/ehag426","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1093/eurheartj/ehag426","tag_type":"study_design","value":"Narrative Review","value_numeric":null},{"paper_doi":"10.1093/eurheartj/ehag426","tag_type":"warning","value":"No specific patient-level sample size applies to this review article; the sample_size tag has been omitted accordingly.","value_numeric":null},{"paper_doi":"10.1093/eurheartj/ehag426","tag_type":"warning","value":"This is a narrative review; conclusions on UACR as a modifiable target are based on association data from clinical trials, not direct causal evidence. The impact_flag 'practice_changing' reflects the review's call for routine UACR screening not yet universally adopted in HF guidelines, which may be aspirational rather than established practice.","value_numeric":null}],"summaries":{"what_studied":"This review evaluates the role of albuminuria (measured by urinary albumin-to-creatinine ratio, UACR) as a risk marker and potentially modifiable factor in heart failure — covering its prevalence, prognostic value, measurement approaches, guideline recommendations, and the effect of HF therapies on UACR.","key_result":"Albuminuria is present in nearly half of all HF patients and is an independent risk marker for incident HF and worse outcomes in pre-existing HF. Reductions in UACR with guideline-directed therapies (RAASi, SGLT2 inhibitors, finerenone) are associated with lower cardiovascular, HF, and CKD event rates.","limitations":"This is a narrative review, so it does not provide new primary data or meta-analytic pooling. Causal directionality of UACR reduction on outcomes remains uncertain — albuminuria may be a marker rather than a proven modifiable target.","practice_takeaway":"Consider routine UACR screening in HF patients, as it identifies high-risk individuals who may benefit from targeted therapy. SGLT2 inhibitors and finerenone reduce UACR and may offer dual cardiovascular and renal protection in this population."}},{"doi":"10.1001/jamacardio.2026.1552","pmid":"42268625","title":"Cost Offset With Quadruple Therapy for Heart Failure","journal_title":"JAMA Cardiology","journal_issn":"2380-6583","published_at":"2026-06-10T00:00:00.000Z","url":"https://pmc.ncbi.nlm.nih.gov/articles/PMC13254798/","source_score":47,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-08-17T13:33:00.507Z","updated_at":"2026-08-17T13:33:00.507Z","tags":[{"paper_doi":"10.1001/jamacardio.2026.1552","tag_type":"age_group","value":"older_adult","value_numeric":null},{"paper_doi":"10.1001/jamacardio.2026.1552","tag_type":"brand","value":"Entresto","value_numeric":null},{"paper_doi":"10.1001/jamacardio.2026.1552","tag_type":"category","value":"Cardiac & Cardiovascular Systems","value_numeric":null},{"paper_doi":"10.1001/jamacardio.2026.1552","tag_type":"condition","value":"Heart Failure With Reduced Ejection Fraction","value_numeric":null},{"paper_doi":"10.1001/jamacardio.2026.1552","tag_type":"generic","value":"sacubitril-valsartan","value_numeric":null},{"paper_doi":"10.1001/jamacardio.2026.1552","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1001/jamacardio.2026.1552","tag_type":"level_of_evidence","value":"4","value_numeric":null},{"paper_doi":"10.1001/jamacardio.2026.1552","tag_type":"modality","value":"Angiotensin Receptor-Neprilysin Inhibitor","value_numeric":null},{"paper_doi":"10.1001/jamacardio.2026.1552","tag_type":"modality","value":"Beta-Blocker","value_numeric":null},{"paper_doi":"10.1001/jamacardio.2026.1552","tag_type":"modality","value":"Mineralocorticoid Receptor Antagonist","value_numeric":null},{"paper_doi":"10.1001/jamacardio.2026.1552","tag_type":"modality","value":"SGLT2 Inhibitor","value_numeric":null},{"paper_doi":"10.1001/jamacardio.2026.1552","tag_type":"sample_size","value":"n=50598","value_numeric":50598},{"paper_doi":"10.1001/jamacardio.2026.1552","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1001/jamacardio.2026.1552","tag_type":"study_design","value":"Economic Evaluation / Cost Analysis","value_numeric":null},{"paper_doi":"10.1001/jamacardio.2026.1552","tag_type":"warning","value":"Full text is under embargo until June 10, 2027; analysis is based on the abstract and results section only—some methodological details may not be fully captured.","value_numeric":null},{"paper_doi":"10.1001/jamacardio.2026.1552","tag_type":"warning","value":"Level of evidence assigned as 4 (modeling/economic study using registry + RCT inputs); this is not a prospective trial.","value_numeric":null},{"paper_doi":"10.1001/jamacardio.2026.1552","tag_type":"warning","value":"The ARNI component is implied but not explicitly named in the abstract; sacubitril-valsartan (Entresto) is tagged as the canonical ARNI for HFrEF based on standard guidelines.","value_numeric":null},{"paper_doi":"10.1001/jamacardio.2026.1552","tag_type":"warning","value":"The wide drug-cost range ($1,223–$16,136/year) reflects multiple pricing sources and formulary scenarios, meaning real-world net cost will vary substantially by payer and formulary.","value_numeric":null}],"summaries":{"what_studied":"This economic evaluation estimated the 1-year health care cost offset and net cost of implementing quadruple GDMT (ARNI + β-blocker + MRA + SGLT2i) at discharge in adults ≥65 years hospitalized with HFrEF, using Medicare-linked GWTG-HF registry data from 2016–2020 (n=50,598).","key_result":"Mean 1-year costs were $41,802/patient, with $25,172 driven by hospitalizations. Quadruple GDMT was modeled to reduce all-cause hospitalization costs by $9,780/patient/year (95% CI, $7,900–$11,660). With annual drug costs ranging $1,223–$16,136, net costs ranged from **$8,556 in savings to $6,347 in net cost**, with most regimens yielding net savings.","limitations":"Treatment effects were modeled multiplicatively from separate pivotal RCTs rather than a single head-to-head trial of all four agents together; the cohort is limited to Medicare patients ≥65 years, limiting generalizability to younger adults; drug costs varied widely across pricing sources, creating a broad range of net-cost estimates.","practice_takeaway":"For older adults hospitalized with HFrEF, starting full quadruple GDMT at discharge will often pay for itself by cutting rehospitalization costs—ask about formulary options to keep drug acquisition costs below the ~$9,800 hospitalization savings threshold. Prioritizing generic or lower-cost formulations of each drug class can tip most patients into net savings territory."}},{"doi":"10.1001/jama.2026.9923","pmid":"42246414","title":"Finerenone in Patients With Chronic Kidney Disease Due to Glomerular Diseases","journal_title":"JAMA","journal_issn":"0098-7484","published_at":"2026-06-05T00:00:00.000Z","url":"https://doi.org/10.1001/jama.2026.9923","source_score":202,"is_retracted":false,"is_open_access":false,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-06-10T14:23:40.857Z","updated_at":"2026-06-10T14:23:40.857Z","tags":[{"paper_doi":"10.1001/jama.2026.9923","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1001/jama.2026.9923","tag_type":"brand","value":"Kerendia","value_numeric":null},{"paper_doi":"10.1001/jama.2026.9923","tag_type":"category","value":"Medicine, General & Internal","value_numeric":null},{"paper_doi":"10.1001/jama.2026.9923","tag_type":"condition","value":"Chronic Kidney Disease","value_numeric":null},{"paper_doi":"10.1001/jama.2026.9923","tag_type":"condition","value":"Focal Segmental Glomerulosclerosis","value_numeric":null},{"paper_doi":"10.1001/jama.2026.9923","tag_type":"condition","value":"Glomerular Disease","value_numeric":null},{"paper_doi":"10.1001/jama.2026.9923","tag_type":"condition","value":"IgA Nephropathy","value_numeric":null},{"paper_doi":"10.1001/jama.2026.9923","tag_type":"condition","value":"Membranous Nephropathy","value_numeric":null},{"paper_doi":"10.1001/jama.2026.9923","tag_type":"generic","value":"finerenone","value_numeric":null},{"paper_doi":"10.1001/jama.2026.9923","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1001/jama.2026.9923","tag_type":"level_of_evidence","value":"2","value_numeric":null},{"paper_doi":"10.1001/jama.2026.9923","tag_type":"modality","value":"Mineralocorticoid Receptor Antagonist","value_numeric":null},{"paper_doi":"10.1001/jama.2026.9923","tag_type":"sample_size","value":"n=903","value_numeric":903},{"paper_doi":"10.1001/jama.2026.9923","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1001/jama.2026.9923","tag_type":"study_design","value":"Randomized Controlled Trial","value_numeric":null},{"paper_doi":"10.1001/jama.2026.9923","tag_type":"warning","value":"Brand name 'Kerendia' assigned based on known finerenone branding; the paper itself does not mention a brand name.","value_numeric":null},{"paper_doi":"10.1001/jama.2026.9923","tag_type":"warning","value":"Level of evidence tagged as '2' reflects the RCT design, but the subgroup/exploratory nature slightly reduces certainty compared to a primary powered trial.","value_numeric":null},{"paper_doi":"10.1001/jama.2026.9923","tag_type":"warning","value":"The main FIND-CKD trial results (Heerspink et al., NEJM, June 5, 2026) are referenced but not fully reproduced here; findings in the broader nondiabetic CKD population may differ.","value_numeric":null},{"paper_doi":"10.1001/jama.2026.9923","tag_type":"warning","value":"This is a prespecified exploratory subgroup analysis, not the primary trial report; causal conclusions should be interpreted cautiously despite the consistency of findings.","value_numeric":null}],"summaries":{"what_studied":"Prespecified exploratory subgroup analysis of the FIND-CKD phase 3 RCT evaluating finerenone (10–20 mg/day orally) vs placebo in 903 adults with nondiabetic CKD due to glomerular diseases (46% IgA nephropathy, 24% FSGS, 10% membranous nephropathy), all on maximum-tolerated RAS inhibitor, followed up to 32 months across 24 countries.","key_result":"Finerenone slowed eGFR decline by 0.73 mL/min/1.73 m² per year vs placebo (−3.50 vs −4.23; 95% CI 0.22–1.24), reduced albuminuria by 42% at 12 months (95% CI 35%–48%), and cut the risk of kidney failure or ≥40% eGFR decline by 26% (HR 0.74; 95% CI 0.57–0.97; 7.42 vs 9.60 events/100 patient-years). Effects were consistent across all glomerular disease subtypes and regardless of baseline SGLT2 inhibitor use.","limitations":"- Exploratory subgroup analysis; trial not powered for clinical outcomes in the glomerular disease subgroup or by subtype.\n- ~20% of glomerular disease cases lacked kidney biopsy confirmation (though results held in biopsy-confirmed analyses).\n- Patients on immunosuppression and those with lupus nephritis or ANCA vasculitis were excluded, limiting generalizability to these groups.","practice_takeaway":"Consider adding finerenone to RAS inhibitor therapy for patients with CKD due to glomerular diseases (IgA nephropathy, FSGS, membranous nephropathy) to slow kidney function loss and reduce albuminuria, even in those already on SGLT2 inhibitors. Monitor potassium; serious hyperkalemia rates were low and similar between arms (0.9% each)."}},{"doi":"10.1056/nejmoa2604625","pmid":"42246672","title":"Finerenone in Persons with Chronic Kidney Disease without Diabetes","journal_title":"New England Journal of Medicine","journal_issn":"0028-4793","published_at":"2026-06-04T00:00:00.000Z","url":"https://doi.org/10.1056/nejmoa2604625","source_score":316,"is_retracted":false,"is_open_access":false,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-06-11T13:42:56.228Z","updated_at":"2026-06-11T13:42:56.228Z","tags":[{"paper_doi":"10.1056/nejmoa2604625","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1056/nejmoa2604625","tag_type":"brand","value":"Kerendia","value_numeric":null},{"paper_doi":"10.1056/nejmoa2604625","tag_type":"category","value":"Medicine, General & Internal","value_numeric":null},{"paper_doi":"10.1056/nejmoa2604625","tag_type":"condition","value":"Chronic Kidney Disease","value_numeric":null},{"paper_doi":"10.1056/nejmoa2604625","tag_type":"generic","value":"finerenone","value_numeric":null},{"paper_doi":"10.1056/nejmoa2604625","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1056/nejmoa2604625","tag_type":"level_of_evidence","value":"1","value_numeric":null},{"paper_doi":"10.1056/nejmoa2604625","tag_type":"modality","value":"Mineralocorticoid Receptor Antagonist","value_numeric":null},{"paper_doi":"10.1056/nejmoa2604625","tag_type":"sample_size","value":"n=1584","value_numeric":1584},{"paper_doi":"10.1056/nejmoa2604625","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1056/nejmoa2604625","tag_type":"study_design","value":"Randomized Controlled Trial","value_numeric":null},{"paper_doi":"10.1056/nejmoa2604625","tag_type":"warning","value":"Exact etiologies of CKD in the trial population are not described in the abstract; applicability to specific CKD subtypes (e.g., IgA nephropathy, FSGS) is uncertain.","value_numeric":null},{"paper_doi":"10.1056/nejmoa2604625","tag_type":"warning","value":"Participants were required to already be on a RAS inhibitor — results may not generalize to patients who are RAS-inhibitor naive or intolerant.","value_numeric":null},{"paper_doi":"10.1056/nejmoa2604625","tag_type":"warning","value":"The cardiovascular composite secondary outcome was not statistically significant and the confidence interval was wide; CV benefit should not be assumed in non-diabetic CKD based on this trial alone.","value_numeric":null}],"summaries":{"what_studied":"This RCT (FIND-CKD) evaluated finerenone (10 or 20 mg daily) vs. placebo in 1,584 adults with CKD (eGFR 25–<90 ml/min/1.73 m²) and albuminuria (UACR 200–3500 mg/g) who did **not** have diabetes, all on background RAS inhibitor therapy, over 32 months.","key_result":"Finerenone slowed eGFR decline vs. placebo (−3.3 vs. −4.0 ml/min/1.73 m²/year; difference +0.7, 95% CI 0.3–1.1; P<0.001) and reduced the composite kidney/CV outcome (HR 0.77, 95% CI 0.60–0.99; P=0.04). Hyperkalemia occurred in 17.0% vs. 13.3%; discontinuations due to hyperkalemia were 1.5% vs. 0.1%.","limitations":"- The cardiovascular composite alone was underpowered (HR 0.60, 95% CI 0.27–1.33), limiting CV conclusions.\n- Trial duration was 32 months; longer-term kidney protection and safety data are lacking.\n- Industry-funded (Bayer), which may introduce sponsor bias.","practice_takeaway":"Consider adding finerenone to RAS inhibitor therapy for non-diabetic CKD patients with significant albuminuria (UACR 200–3500 mg/g) to slow eGFR decline and reduce kidney/CV events. Monitor potassium closely — hyperkalemia requiring drug discontinuation was 15× more common with finerenone (1.5% vs. 0.1%)."}},{"doi":"10.1111/dom.70934","pmid":"42219273","title":"Adding Finerenone to\n SGLT2\n Inhibitors and Long‐Term Kidney Outcomes in Diabetic Kidney Disease","journal_title":"Diabetes, Obesity and Metabolism","journal_issn":"1462-8902","published_at":"2026-05-31T00:00:00.000Z","url":"https://doi.org/10.1111/dom.70934","source_score":2,"is_retracted":false,"is_open_access":false,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-06-07T13:26:42.698Z","updated_at":"2026-06-07T13:26:42.698Z","tags":[{"paper_doi":"10.1111/dom.70934","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1111/dom.70934","tag_type":"brand","value":"Kerendia","value_numeric":null},{"paper_doi":"10.1111/dom.70934","tag_type":"category","value":"Endocrinology & Metabolism","value_numeric":null},{"paper_doi":"10.1111/dom.70934","tag_type":"condition","value":"Diabetic Kidney Disease","value_numeric":null},{"paper_doi":"10.1111/dom.70934","tag_type":"generic","value":"finerenone","value_numeric":null},{"paper_doi":"10.1111/dom.70934","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1111/dom.70934","tag_type":"level_of_evidence","value":"3","value_numeric":null},{"paper_doi":"10.1111/dom.70934","tag_type":"modality","value":"Mineralocorticoid Receptor Antagonist","value_numeric":null},{"paper_doi":"10.1111/dom.70934","tag_type":"modality","value":"Renin-Angiotensin System Inhibitor","value_numeric":null},{"paper_doi":"10.1111/dom.70934","tag_type":"modality","value":"SGLT2 Inhibitor","value_numeric":null},{"paper_doi":"10.1111/dom.70934","tag_type":"sample_size","value":"n=255","value_numeric":255},{"paper_doi":"10.1111/dom.70934","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1111/dom.70934","tag_type":"study_design","value":"Observational Cohort Study with Propensity Score Matching","value_numeric":null},{"paper_doi":"10.1111/dom.70934","tag_type":"warning","value":"Sex distribution of the study population is not explicitly reported in the abstract; 'mixed' is inferred from typical DKD trial populations.","value_numeric":null},{"paper_doi":"10.1111/dom.70934","tag_type":"warning","value":"The brand name 'Kerendia' is assumed for finerenone; the paper does not explicitly state the brand.","value_numeric":null},{"paper_doi":"10.1111/dom.70934","tag_type":"warning","value":"The 'impact_flag' of practice_changing is applied cautiously — this is an observational study and not an RCT; findings are hypothesis-generating and supportive, not definitive.","value_numeric":null},{"paper_doi":"10.1111/dom.70934","tag_type":"warning","value":"The study does not report hard clinical endpoints (e.g., ESKD, cardiovascular mortality), limiting direct clinical impact assessment.","value_numeric":null}],"summaries":{"what_studied":"In 255 patients with diabetic kidney disease (DKD) already on combined RASi + SGLT2i therapy, this study evaluated whether adding finerenone (triple combination therapy, TCT) improved proteinuria, eGFR slope, and serum potassium over 24 months compared to dual therapy (DCT) alone, using intention-to-treat analysis with propensity score matching.","key_result":"TCT reduced proteinuria by 47% at 24 months (p=0.028). The post-initial dip eGFR slope was significantly better with TCT vs. DCT: ~1.31 mL/min/1.73 m²/year less annual decline (95% CI: 0.25–2.36; p=0.015), persisting after PS matching (difference 1.45 mL/min/1.73 m²/year; 95% CI: 0.32–2.58; p=0.012). Total eGFR slope did not differ significantly. Serum potassium rose modestly early but equalized by 24 months.","limitations":"- Observational, single-arm propensity score–matched design limits causal inference and may not fully control for confounding.\n- Relatively small sample (n=255) with only 24-month follow-up; longer-term hard outcomes (ESKD, doubling of creatinine, cardiovascular events) not reported.\n- Real-world adherence and dose titration of finerenone not described, which could affect generalizability.","practice_takeaway":"For patients with DKD already on RASi + SGLT2i, adding finerenone may further slow kidney function decline and meaningfully reduce proteinuria — consider triple therapy as part of a comprehensive kidney-protective strategy. Monitor potassium closely in the early weeks after starting finerenone, though levels appear to stabilize by 24 months."}},{"doi":"10.1161/circheartfailure.125.013877","pmid":"42206402","title":"Changes in Pulmonary Artery Pressure Following Initiation of Guideline-Directed Medical Therapies in Patients With Heart Failure: Insights From GUIDE-HF","journal_title":"Circulation: Heart Failure","journal_issn":"1941-3289","published_at":"2026-05-28T00:00:00.000Z","url":"https://doi.org/10.1161/circheartfailure.125.013877","source_score":9,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-06-07T13:26:45.417Z","updated_at":"2026-06-07T13:26:45.417Z","tags":[{"paper_doi":"10.1161/circheartfailure.125.013877","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1161/circheartfailure.125.013877","tag_type":"brand","value":"CardioMEMS","value_numeric":null},{"paper_doi":"10.1161/circheartfailure.125.013877","tag_type":"category","value":"Cardiac & Cardiovascular Systems","value_numeric":null},{"paper_doi":"10.1161/circheartfailure.125.013877","tag_type":"condition","value":"Heart Failure","value_numeric":null},{"paper_doi":"10.1161/circheartfailure.125.013877","tag_type":"impact_flag","value":"confirms_prior","value_numeric":null},{"paper_doi":"10.1161/circheartfailure.125.013877","tag_type":"level_of_evidence","value":"3","value_numeric":null},{"paper_doi":"10.1161/circheartfailure.125.013877","tag_type":"modality","value":"Angiotensin Receptor-Neprilysin Inhibitor","value_numeric":null},{"paper_doi":"10.1161/circheartfailure.125.013877","tag_type":"modality","value":"Beta-Blocker","value_numeric":null},{"paper_doi":"10.1161/circheartfailure.125.013877","tag_type":"modality","value":"Hemodynamic Monitoring","value_numeric":null},{"paper_doi":"10.1161/circheartfailure.125.013877","tag_type":"modality","value":"Mineralocorticoid Receptor Antagonist","value_numeric":null},{"paper_doi":"10.1161/circheartfailure.125.013877","tag_type":"modality","value":"SGLT2 Inhibitor","value_numeric":null},{"paper_doi":"10.1161/circheartfailure.125.013877","tag_type":"sample_size","value":"n=2358","value_numeric":2358},{"paper_doi":"10.1161/circheartfailure.125.013877","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1161/circheartfailure.125.013877","tag_type":"study_design","value":"Prospective Cohort Study (Sub-analysis of RCT)","value_numeric":null},{"paper_doi":"10.1161/circheartfailure.125.013877","tag_type":"warning","value":"Sex and specific age distribution of included subgroups are not reported in the abstract; the 'mixed' sex and 'adult' age-group tags are inferred from the broader GUIDE-HF trial population.","value_numeric":null},{"paper_doi":"10.1161/circheartfailure.125.013877","tag_type":"warning","value":"The level of evidence is rated 3 (cohort sub-analysis) rather than 1, despite originating from an RCT, because medication initiation was not randomized in this analysis.","value_numeric":null},{"paper_doi":"10.1161/circheartfailure.125.013877","tag_type":"warning","value":"The study design is a post-hoc sub-analysis of the GUIDE-HF RCT; subgroup Ns are small (33–112 per therapy), so estimates carry wide confidence intervals and the β-blocker trend toward higher PAP is not statistically significant — interpret with caution.","value_numeric":null}],"summaries":{"what_studied":"This sub-analysis of the GUIDE-HF trial examined acute changes in wireless pulmonary artery pressure (PAP) before (7 days pre-initiation) and after (day 30–37 post-initiation) newly starting one of four guideline-directed medical therapies — ARNI, SGLT2i, MRA, or β-blocker — in HF patients with an implanted CardioMEMS sensor, excluding those with concurrent loop diuretic or other core HF therapy changes.","key_result":"ARNI initiation reduced diastolic PAP by −1.56 mmHg (95% CI, −3.54 to −0.40) and MRA initiation reduced it by −1.15 mmHg (95% CI, −1.82 to −0.47); SGLT2i showed no detectable PAP change; β-blocker initiation showed a non-significant trend toward higher PAP.","limitations":"- Very small subgroup sizes (n=33–112 per therapy arm) limit statistical power and generalizability.\n- Observational design with potential for residual confounding despite exclusion of concurrent therapy changes.\n- Findings reflect only short-term hemodynamic changes (around day 30–37) and may not reflect longer-term effects.","practice_takeaway":"When using hemodynamic-guided HF management, ARNIs and MRAs appear to actively lower filling pressures and may be preferred add-on agents for patients with elevated PAP. SGLT2i and β-blockers did not show early PAP reduction in this analysis, though their established clinical benefits remain unaffected."}},{"doi":"10.1038/s41574-026-01259-4","pmid":"42174224","title":"Aldosterone synthase inhibitors for the treatment of cardiovascular disease","journal_title":"Nature Reviews Endocrinology","journal_issn":"1759-5029","published_at":"2026-05-22T00:00:00.000Z","url":"https://doi.org/10.1038/s41574-026-01259-4","source_score":15,"is_retracted":false,"is_open_access":false,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-05-29T13:23:15.934Z","updated_at":"2026-05-29T13:23:15.934Z","tags":[{"paper_doi":"10.1038/s41574-026-01259-4","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1038/s41574-026-01259-4","tag_type":"category","value":"Endocrinology & Metabolism","value_numeric":null},{"paper_doi":"10.1038/s41574-026-01259-4","tag_type":"condition","value":"Cardiovascular Disease","value_numeric":null},{"paper_doi":"10.1038/s41574-026-01259-4","tag_type":"condition","value":"Chronic Kidney Disease","value_numeric":null},{"paper_doi":"10.1038/s41574-026-01259-4","tag_type":"condition","value":"Heart Failure","value_numeric":null},{"paper_doi":"10.1038/s41574-026-01259-4","tag_type":"condition","value":"Primary Aldosteronism","value_numeric":null},{"paper_doi":"10.1038/s41574-026-01259-4","tag_type":"condition","value":"Resistant Hypertension","value_numeric":null},{"paper_doi":"10.1038/s41574-026-01259-4","tag_type":"impact_flag","value":"limited_evidence","value_numeric":null},{"paper_doi":"10.1038/s41574-026-01259-4","tag_type":"level_of_evidence","value":"5","value_numeric":null},{"paper_doi":"10.1038/s41574-026-01259-4","tag_type":"modality","value":"Aldosterone Synthase Inhibitor","value_numeric":null},{"paper_doi":"10.1038/s41574-026-01259-4","tag_type":"modality","value":"Mineralocorticoid Receptor Antagonist","value_numeric":null},{"paper_doi":"10.1038/s41574-026-01259-4","tag_type":"study_design","value":"Narrative Review","value_numeric":null},{"paper_doi":"10.1038/s41574-026-01259-4","tag_type":"warning","value":"Full text body appears largely unpopulated in the provided source (only metadata and abstract were extractable); summary is based solely on the abstract.","value_numeric":null},{"paper_doi":"10.1038/s41574-026-01259-4","tag_type":"warning","value":"No specific drug names (brand or generic) for aldosterone synthase inhibitors were mentioned in the available text; tags for specific agents could not be added.","value_numeric":null},{"paper_doi":"10.1038/s41574-026-01259-4","tag_type":"warning","value":"Sample size tag omitted as no aggregate trial N was reported in the abstract.","value_numeric":null}],"summaries":{"what_studied":"This review evaluates aldosterone synthase inhibitors (ASIs) as a novel therapeutic strategy for cardiovascular disease, focusing on their mechanism of action, efficacy in lowering aldosterone and blood pressure, and current evidence from randomized clinical trials in patients with resistant/uncontrolled hypertension and chronic kidney disease.","key_result":"ASIs effectively lowered aldosterone concentrations and reduced blood pressure in RCTs across patients with resistant or uncontrolled hypertension and chronic kidney disease; however, long-term safety data, head-to-head comparisons with mineralocorticoid receptor antagonists (MRAs), and cardiovascular outcome data are still lacking.","limitations":"- No long-term safety data available for ASIs\n- No direct comparative trials against mineralocorticoid receptor antagonists\n- No cardiovascular outcomes data yet from clinical trials","practice_takeaway":"ASIs represent a promising add-on strategy for patients with resistant hypertension or primary aldosteronism where MRAs leave residual cardiovascular risk, but clinicians should await outcome trial data before broad adoption. MRA therapy remains the current standard, as ASI evidence is limited to blood pressure and surrogate endpoints."}},{"doi":"10.1161/jaha.125.046643","pmid":"42047207","title":"Patterns of Adherence and Persistence to Triple and Quadruple Guideline‐Directed Medical Therapy Among US Patients With Heart Failure With Reduced Ejection Fraction","journal_title":"Journal of the American Heart Association","journal_issn":"2047-9980","published_at":"2026-04-28T00:00:00.000Z","url":"https://doi.org/10.1161/jaha.125.046643","source_score":4,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-06-09T13:50:38.440Z","updated_at":"2026-06-09T13:50:38.440Z","tags":[{"paper_doi":"10.1161/jaha.125.046643","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1161/jaha.125.046643","tag_type":"category","value":"Cardiac & Cardiovascular Systems","value_numeric":null},{"paper_doi":"10.1161/jaha.125.046643","tag_type":"condition","value":"Heart Failure With Reduced Ejection Fraction","value_numeric":null},{"paper_doi":"10.1161/jaha.125.046643","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1161/jaha.125.046643","tag_type":"level_of_evidence","value":"3","value_numeric":null},{"paper_doi":"10.1161/jaha.125.046643","tag_type":"modality","value":"ACE Inhibitor / ARB / ARNI","value_numeric":null},{"paper_doi":"10.1161/jaha.125.046643","tag_type":"modality","value":"Beta Blocker","value_numeric":null},{"paper_doi":"10.1161/jaha.125.046643","tag_type":"modality","value":"Guideline-Directed Medical Therapy","value_numeric":null},{"paper_doi":"10.1161/jaha.125.046643","tag_type":"modality","value":"Mineralocorticoid Receptor Antagonist","value_numeric":null},{"paper_doi":"10.1161/jaha.125.046643","tag_type":"modality","value":"SGLT2 Inhibitor","value_numeric":null},{"paper_doi":"10.1161/jaha.125.046643","tag_type":"sample_size","value":"n=107849","value_numeric":107849},{"paper_doi":"10.1161/jaha.125.046643","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1161/jaha.125.046643","tag_type":"study_design","value":"Retrospective Cohort Study","value_numeric":null},{"paper_doi":"10.1161/jaha.125.046643","tag_type":"warning","value":"Claims data may underestimate true GDMT use if out-of-pocket or non-claims-captured prescriptions are excluded.","value_numeric":null},{"paper_doi":"10.1161/jaha.125.046643","tag_type":"warning","value":"The impact_flag 'practice_changing' reflects the striking underuse findings (2.3% on quadruple GDMT) rather than a new intervention; clinicians should interpret accordingly.","value_numeric":null},{"paper_doi":"10.1161/jaha.125.046643","tag_type":"warning","value":"The study identifies 'distinct profiles' of early discontinuers but specific sociodemographic/clinical factors are described in the full paper — not fully detailed in the abstract; summary reflects available abstract data only.","value_numeric":null}],"summaries":{"what_studied":"This retrospective cohort study examined adherence and persistence to triple and quadruple guideline-directed medical therapy (GDMT) in US patients with HFrEF, using Optum Clinformatics claims data from January 2021 to December 2022. It also identified patient profiles associated with early GDMT discontinuation via latent trajectory analysis.","key_result":"Of 107,849 HFrEF patients, only 12.3% received triple GDMT and 2.3% received quadruple GDMT. Adherence was suboptimal: 45.0% (triple) and 40.8% (quadruple). Early discontinuation occurred in 10.5% of triple GDMT patients and 11.9% of quadruple GDMT patients, with distinct sociodemographic and clinical profiles driving discontinuation.","limitations":"- Claims-based design may miss prescriptions filled outside the database or samples from clinical trials.\n- No clinical outcomes (hospitalizations, mortality) were assessed, limiting insight into the consequences of non-adherence.\n- Study period (2021–2022) may not reflect current prescribing patterns, particularly as SGLT2 inhibitors became more established.","practice_takeaway":"Fewer than 1 in 8 HFrEF patients received triple GDMT, and fewer than 1 in 25 received quadruple GDMT — well below guideline targets. Clinicians should actively screen for early discontinuation risk, especially in patients with distinct sociodemographic or clinical profiles, and deploy targeted support strategies to sustain GDMT."}},{"doi":"10.1093/ndt/gfag090","pmid":"42008148","title":"RAAS blockade in the kidney life-cycle–treatment standard","journal_title":"Nephrology Dialysis Transplantation","journal_issn":"0931-0509","published_at":"2026-04-21T00:00:00.000Z","url":"https://doi.org/10.1093/ndt/gfag090","source_score":43,"is_retracted":false,"is_open_access":false,"raw_metadata":{"ooir":{"day":"2026-04-22","doi":"10.1093/ndt/gfag090","days":"30","issn":"0931-0509","rank":"3","field":"Clinical Medicine","score":"43","category":"Urology & Nephrology","categories":["Urology & Nephrology"],"_categories":["Urology & Nephrology"]},"pubmed":{"doi":"10.1093/ndt/gfag090","title":"RAAS blockade in the kidney Life-Cycle - Treatment Standard.","journal":"Nephrology, dialysis, transplantation : official publication of the 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the sample_size tag has been omitted.","value_numeric":null},{"paper_doi":"10.1093/ndt/gfag090","tag_type":"warning","value":"The benefit of steroidal MRAs in dialysis patients is explicitly noted as uncertain; clinicians should interpret those recommendations cautiously.","value_numeric":null},{"paper_doi":"10.1093/ndt/gfag090","tag_type":"warning","value":"This is a narrative review ('Treatment Standard' article); no pooled statistics or original data are reported — all numerical conclusions reflect cited trial-level evidence.","value_numeric":null}],"summaries":{"what_studied":"This review evaluates RAAS blockade (RAASb) — including ACE inhibitors, ARBs, direct renin inhibitors, and mineralocorticoid receptor antagonists — across the full kidney care continuum: primary prevention, proteinuric and non-proteinuric CKD, dialysis, and kidney transplantation, including interactions with SGLT2 inhibitors and GLP-1 receptor agonists.","key_result":"RAASb reduces proteinuria, slows CKD progression, and lowers cardiovascular risk, with strongest evidence in proteinuric CKD; novel non-steroidal MRAs (e.g., finerenone) add renal and cardiovascular protection in diabetic CKD; benefit in non-proteinuric disease is limited; in dialysis, RAASb may preserve residual kidney function and improve cardiac structure; in transplantation, early RAASb appears safe and may improve graft and patient survival.","limitations":"- Review article (not a meta-analysis or RCT); conclusions are synthesis-level and inherit the limitations of underlying studies.\n- Efficacy and safety data in dialysis populations and transplant recipients remain uncertain, particularly for steroidal MRAs in dialysis.\n- Evidence on optimal timing, agent selection, and combination with newer agents (SGLT2i, GLP-1 RA) across all lifecycle stages is still evolving.","practice_takeaway":"Use RAASb as first-line therapy in proteinuric CKD and consider adding finerenone in patients with diabetes and CKD for added renal and cardiovascular protection. In transplant recipients, early initiation of RAASb appears safe and may improve long-term outcomes; SGLT2 inhibitors and GLP-1 receptor agonists play a complementary — not competing — role alongside RAASb."}}],"initialOffset":16,"fetchConfig":{"kind":"tags","tags":[{"tag_type":"modality","value":"Mineralocorticoid Receptor Antagonist"}]},"breadcrumbItems":[{"name":"Home","href":"/"},{"name":"Research Hub","href":"/hub"},{"name":"Modalities","href":"/hub/tag/modality"},{"name":"Mineralocorticoid Receptor Antagonist"}],"hrefConfig":{"basePath":"/hub/papers","webViewQueryParams":{"hub_ctx":"tag","hub_tag_type":"modality","hub_tag_value":"Mineralocorticoid Receptor Antagonist"}}}]]

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