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.32:T76a,Focal segmental glomerulosclerosis (FSGS) is a podocytopathy that is diagnosed based on characteristic histopathological lesions. Certain forms of FSGS with underlying genetic variants associated with the disease, including variants in podocyte proteins, as well as apolipoprotein L1 (APOL1) risk alleles, and variants in collagen type IV (COL4) α3, α4, and α5 (COL4A3-5) proteins, are typically resistant to current treatments. The DUPLEX clinical trial assessed the efficacy and safety of sparsentan, a dual endothelin angiotensin receptor antagonist (DEARA), in patients with biopsy-proven or genetic FSGS and demonstrated a greater antiproteinuric effect over 108 weeks compared to the active control irbesartan. This post hoc, exploratory analysis assessed the efficacy of sparsentan in the subset of patients enrolled in DUPLEX who had pathogenic variants in genes coding for podocyte proteins, COL4A3-5 variants, and APOL1 high-risk genotypes, altogether referred to as genetic FSGS (gFSGS). Next-generation sequencing identified 31 patients with podocyte gene variants, 25 with COL4A3-5 gene variants, and 14 with APOL1 high-risk genotypes. Baseline characteristics varied between genetic subgroups, with slightly younger patients, on average, in the podocyte gene variant group, and more African American patients in the APOL1 high-risk genotype group. In this exploratory analysis, sparsentan treatment resulted in substantial and sustained proteinuria reductions and numerically more frequent complete remission of proteinuria compared with irbesartan, consistent with observations in the full DUPLEX study population. Moreover, a lower proportion of sparsentan- vs irbesartan-treated patients reached composite kidney endpoints. These findings support sparsentan's antiproteinuric benefit in patients with gFSGS, a subgroup that is often resistant to other therapeutic interventions.33:Tc8d, Background: Focal segmental glomerulosclerosis (FSGS) is a podocytopathy that is diagnosed based on characteristic histopathological lesions. Certain forms of FSGS with underlying genetic variants associated with the disease, including variants in podocyte proteins, as well as apolipoprotein L1 ( APOL1 ) risk alleles, and variants in collagen type IV (COL4) α3, α4, and α5 ( COL4A3-5 ) proteins, are typically resistant to current treatments. Methods: The DUPLEX clinical trial assessed the efficacy and safety of sparsentan, a dual endothelin angiotensin receptor antagonist (DEARA), in patients with biopsy-proven or genetic FSGS and demonstrated a greater antiproteinuric effect over 108 weeks compared to the active control irbesartan. This post hoc, exploratory analysis assessed the efficacy of sparsentan in the subset of patients enrolled in DUPLEX who had pathogenic variants in genes coding for podocyte proteins, COL4A3-5 variants, and APOL1 high-risk genotypes, altogether referred to as genetic FSGS (gFSGS). Results: Next-generation sequencing identified 31 patients with podocyte gene variants, 25 with COL4A3-5 gene variants, and 14 with APOL1 high-risk genotypes. Baseline characteristics varied between genetic subgroups, with slightly younger patients, on average, in the podocyte gene variant group, and more African American patients in the APOL1 high-risk genotype group. In this exploratory analysis, sparsentan treatment resulted in substantial and sustained proteinuria reductions and numerically more frequent complete remission of proteinuria compared with irbesartan, consistent with observations in the full DUPLEX study population. Moreover, a lower proportion of sparsentan- vs irbesartan-treated patients reached composite kidney endpoints. Conclusions: These findings support sparsentan’s antiproteinuric benefit in patients with gFSGS, a subgroup that is often resistant to other therapeutic interventions. 25:[[["$","script","0",{"type":"application/ld+json","dangerouslySetInnerHTML":{"__html":"{\"@context\":\"https://schema.org\",\"@type\":\"CollectionPage\",\"name\":\"Angiotensin Receptor Blocker: modality Research & Clinical Takeaways\",\"description\":\"Explore peer-reviewed papers on Angiotensin Receptor Blocker (modality). Clinician-written summaries and actionable practice insights. 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The effect was strongest for vascular dementia (HR 0.617, 95% CI 0.409–0.930) but not statistically significant for Alzheimer's disease (HR 0.930, 95% CI 0.849–1.018). Achieved blood pressure was nearly identical between groups (<1 mmHg difference at each follow-up year).","limitations":"- Residual confounding from unmeasured factors (education, socioeconomic status, baseline cognition, BP variability) cannot be excluded.\n- Dementia diagnosis and subtype classification relied on ICD-10 administrative codes, risking nondifferential misclassification that could attenuate associations.\n- Findings are from a Japanese cohort; generalizability to other healthcare systems with different prescribing patterns is uncertain.","practice_takeaway":"When selecting a first-line antihypertensive in older adults where ARBs and CCBs are otherwise equivalent, ARB-based therapy may offer a modest cognitive benefit—particularly for vascular dementia—beyond blood pressure control alone. The absolute risk difference is small (~0.8 pp over 5 years), so individual comorbidities, tolerability, and patient preference should still guide choice."}},{"doi":"10.1093/ndt/gfag184","pmid":"42584660","title":"Renin-Angiotensin System Inhibition in Dialysis-Dependent Patients with Chronic Heart Failure due to Reduced Ejection Fraction: A Systematic Review and Meta-Analysis","journal_title":"Nephrology Dialysis Transplantation","journal_issn":"0931-0509","published_at":"2026-08-12T00:00:00.000Z","url":"https://doi.org/10.1093/ndt/gfag184","source_score":24,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-08-19T06:28:54.888Z","updated_at":"2026-08-19T06:28:54.888Z","tags":[{"paper_doi":"10.1093/ndt/gfag184","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1093/ndt/gfag184","tag_type":"category","value":"Urology & Nephrology","value_numeric":null},{"paper_doi":"10.1093/ndt/gfag184","tag_type":"condition","value":"End-Stage Kidney Disease","value_numeric":null},{"paper_doi":"10.1093/ndt/gfag184","tag_type":"condition","value":"Heart Failure with Reduced Ejection Fraction","value_numeric":null},{"paper_doi":"10.1093/ndt/gfag184","tag_type":"generic","value":"sacubitril-valsartan","value_numeric":null},{"paper_doi":"10.1093/ndt/gfag184","tag_type":"impact_flag","value":"limited_evidence","value_numeric":null},{"paper_doi":"10.1093/ndt/gfag184","tag_type":"level_of_evidence","value":"2","value_numeric":null},{"paper_doi":"10.1093/ndt/gfag184","tag_type":"modality","value":"ACE Inhibitor","value_numeric":null},{"paper_doi":"10.1093/ndt/gfag184","tag_type":"modality","value":"Angiotensin Receptor Blocker","value_numeric":null},{"paper_doi":"10.1093/ndt/gfag184","tag_type":"modality","value":"Angiotensin Receptor-Neprilysin Inhibitor","value_numeric":null},{"paper_doi":"10.1093/ndt/gfag184","tag_type":"modality","value":"Renin-Angiotensin System Inhibitor","value_numeric":null},{"paper_doi":"10.1093/ndt/gfag184","tag_type":"sample_size","value":"n=13437","value_numeric":13437},{"paper_doi":"10.1093/ndt/gfag184","tag_type":"study_design","value":"Systematic Review and Meta-Analysis","value_numeric":null},{"paper_doi":"10.1093/ndt/gfag184","tag_type":"warning","value":"Level of evidence rated '2' reflects the systematic review design, but the underlying studies are predominantly observational — causal inference is explicitly cautioned against by the authors.","value_numeric":null},{"paper_doi":"10.1093/ndt/gfag184","tag_type":"warning","value":"No specific ARNI brand or generic name is stated in the abstract; sacubitril-valsartan is inferred as the representative ARNI class agent.","value_numeric":null},{"paper_doi":"10.1093/ndt/gfag184","tag_type":"warning","value":"Sex distribution of the study population is not reported in the abstract.","value_numeric":null},{"paper_doi":"10.1093/ndt/gfag184","tag_type":"warning","value":"The total sample size (n=13,437) is approximated by summing treated and control groups across both ARNI and ACEi/ARB study pools; individual patient overlap between studies cannot be ruled out.","value_numeric":null}],"summaries":{"what_studied":"This systematic review and meta-analysis evaluated the efficacy and safety of ARNIs and ACEi/ARBs versus control regimens in adult dialysis-dependent patients (hemodialysis or peritoneal dialysis) with chronic HFrEF, with outcomes of all-cause and cardiovascular mortality (literature searched through December 2025).","key_result":"ARNI vs. non-ARNI was associated with lower all-cause mortality (pooled HR 0.78, 95% CI 0.71–0.87); ACEi/ARB vs. placebo/no RAS blockade also reduced all-cause mortality (HR 0.76, 95% CI 0.68–0.84) and cardiovascular mortality (HR 0.62, 95% CI 0.54–0.71). ARNIs showed no significant benefit for cardiovascular mortality (HR 0.91, 95% CI 0.79–1.04). Safety data (ARNI studies only) showed no excess hypotension and a lower hyperkalemia risk vs. ACEi/ARBs.","limitations":"- Findings are derived predominantly from observational studies with high susceptibility to residual confounding, limiting causal inference.\n- Safety data were available only for ARNI studies, leaving ACEi/ARB safety largely uncharacterized in this population.\n- The meta-analysis pooled only 9 studies total, with relatively modest sample sizes for such a high-risk subgroup.","practice_takeaway":"RAS blockade with either ARNIs or ACEi/ARBs appears associated with lower mortality in dialysis-dependent HFrEF patients, but these are observational data — clinicians should weigh potential benefit against individual risk and avoid assuming causality. Hyperkalemia risk may favor ARNIs over ACEi/ARBs when RAS inhibition is pursued in this population."}},{"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":"10.1093/ndt/gfag140","pmid":"42294943","title":"FINE-ONE, more to come: moving beyond ACEis and ARBs in type 1 diabetes with kidney disease?","journal_title":"Nephrology Dialysis Transplantation","journal_issn":"0931-0509","published_at":"2026-06-15T00:00:00.000Z","url":"https://doi.org/10.1093/ndt/gfag140","source_score":9,"is_retracted":false,"is_open_access":false,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-06-20T13:24:56.864Z","updated_at":"2026-06-20T13:24:56.864Z","tags":[{"paper_doi":"10.1093/ndt/gfag140","tag_type":"category","value":"Urology & Nephrology","value_numeric":null},{"paper_doi":"10.1093/ndt/gfag140","tag_type":"condition","value":"Diabetic Kidney Disease","value_numeric":null},{"paper_doi":"10.1093/ndt/gfag140","tag_type":"condition","value":"Type 1 Diabetes","value_numeric":null},{"paper_doi":"10.1093/ndt/gfag140","tag_type":"level_of_evidence","value":"7","value_numeric":null},{"paper_doi":"10.1093/ndt/gfag140","tag_type":"modality","value":"ACE Inhibitor","value_numeric":null},{"paper_doi":"10.1093/ndt/gfag140","tag_type":"modality","value":"Angiotensin Receptor Blocker","value_numeric":null},{"paper_doi":"10.1093/ndt/gfag140","tag_type":"study_design","value":"Editorial","value_numeric":null},{"paper_doi":"10.1093/ndt/gfag140","tag_type":"warning","value":"No sample size, outcomes, or drug-specific data could be extracted.","value_numeric":null},{"paper_doi":"10.1093/ndt/gfag140","tag_type":"warning","value":"Only bibliographic metadata was provided — no abstract, results, or methods text. All structured content is inferred from the title alone and may be incomplete or inaccurate.","value_numeric":null},{"paper_doi":"10.1093/ndt/gfag140","tag_type":"warning","value":"Study design classified as 'Editorial' based on the commentary-style title, but this cannot be confirmed without full text.","value_numeric":null}],"summaries":{"what_studied":"This appears to be an editorial or commentary evaluating the FINE-ONE trial and the potential role of therapies beyond ACE inhibitors (ACEis) and angiotensin receptor blockers (ARBs) for kidney protection in type 1 diabetes with kidney disease.","limitations":"The source text provides only the title, DOI, journal, and publication date — no abstract, methods, results, or conclusions are available for extraction."}},{"doi":"10.1186/s12876-026-04935-x","pmid":"42204478","title":"ACE inhibitor–induced isolated intestinal angioedema mimicking functional bowel disorder: a case report","journal_title":"BMC Gastroenterology","journal_issn":"1471-230X","published_at":"2026-05-27T00:00:00.000Z","url":"https://doi.org/10.1186/s12876-026-04935-x","source_score":2,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-06-06T13:22:59.289Z","updated_at":"2026-06-06T13:22:59.289Z","tags":[{"paper_doi":"10.1186/s12876-026-04935-x","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1186/s12876-026-04935-x","tag_type":"category","value":"Gastroenterology & Hepatology","value_numeric":null},{"paper_doi":"10.1186/s12876-026-04935-x","tag_type":"condition","value":"Angioedema","value_numeric":null},{"paper_doi":"10.1186/s12876-026-04935-x","tag_type":"condition","value":"Essential Hypertension","value_numeric":null},{"paper_doi":"10.1186/s12876-026-04935-x","tag_type":"condition","value":"Intestinal Angioedema","value_numeric":null},{"paper_doi":"10.1186/s12876-026-04935-x","tag_type":"generic","value":"enalapril","value_numeric":null},{"paper_doi":"10.1186/s12876-026-04935-x","tag_type":"generic","value":"losartan","value_numeric":null},{"paper_doi":"10.1186/s12876-026-04935-x","tag_type":"impact_flag","value":"safety_signal","value_numeric":null},{"paper_doi":"10.1186/s12876-026-04935-x","tag_type":"level_of_evidence","value":"5","value_numeric":null},{"paper_doi":"10.1186/s12876-026-04935-x","tag_type":"modality","value":"ACE Inhibitor","value_numeric":null},{"paper_doi":"10.1186/s12876-026-04935-x","tag_type":"modality","value":"Angiotensin Receptor Blocker","value_numeric":null},{"paper_doi":"10.1186/s12876-026-04935-x","tag_type":"sample_size","value":"n=1","value_numeric":1},{"paper_doi":"10.1186/s12876-026-04935-x","tag_type":"sex","value":"female","value_numeric":null},{"paper_doi":"10.1186/s12876-026-04935-x","tag_type":"study_design","value":"Case Report","value_numeric":null},{"paper_doi":"10.1186/s12876-026-04935-x","tag_type":"warning","value":"Diagnosis of intestinal angioedema was clinical; no imaging (e.g., CT showing bowel wall thickening) is mentioned in the abstract, limiting diagnostic certainty.","value_numeric":null},{"paper_doi":"10.1186/s12876-026-04935-x","tag_type":"warning","value":"Single case report — findings should not be generalised without further evidence.","value_numeric":null},{"paper_doi":"10.1186/s12876-026-04935-x","tag_type":"warning","value":"The DOI year (2026) is consistent with the publication date provided; no discrepancy detected.","value_numeric":null}],"summaries":{"what_studied":"A case of ACE inhibitor–induced isolated intestinal angioedema in a 54-year-old Indian woman on enalapril 10 mg daily, presenting with recurrent abdominal pain, loose stools, and nausea over six weeks — without any cutaneous or oropharyngeal features — and initially misdiagnosed as acute gastroenteritis and then irritable bowel syndrome.","key_result":"Complete symptom resolution occurred after enalapril was withdrawn; causality was rated 'probable' by the Naranjo scale (score 7) and WHO-UMC criteria. Transition to losartan achieved sustained blood pressure control with no recurrence at 3 months.","limitations":"Single case report limits generalisability. Diagnosis was clinical (no imaging confirmation of bowel wall edema reported). Follow-up was only 3 months.","practice_takeaway":"In any patient taking an ACE inhibitor who has unexplained, treatment-refractory GI symptoms — even without skin or throat swelling — consider an empirical drug-withdrawal trial. 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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."}},{"doi":"10.1016/j.jacc.2026.03.025","pmid":"41941267","title":"Masters Athletes With Abnormal Cardiovascular Findings","journal_title":"JACC","journal_issn":"0735-1097","published_at":"2026-04-06T00:00:00.000Z","url":"https://pmc.ncbi.nlm.nih.gov/articles/PMC13185526/","source_score":31,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-07-27T14:09:18.608Z","updated_at":"2026-07-27T14:09:18.608Z","tags":[{"paper_doi":"10.1016/j.jacc.2026.03.025","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1016/j.jacc.2026.03.025","tag_type":"age_group","value":"older_adult","value_numeric":null},{"paper_doi":"10.1016/j.jacc.2026.03.025","tag_type":"category","value":"Cardiac & Cardiovascular Systems","value_numeric":null},{"paper_doi":"10.1016/j.jacc.2026.03.025","tag_type":"condition","value":"Aortic Dilatation","value_numeric":null},{"paper_doi":"10.1016/j.jacc.2026.03.025","tag_type":"condition","value":"Arrhythmogenic Cardiomyopathy","value_numeric":null},{"paper_doi":"10.1016/j.jacc.2026.03.025","tag_type":"condition","value":"Atrial Fibrillation","value_numeric":null},{"paper_doi":"10.1016/j.jacc.2026.03.025","tag_type":"condition","value":"Bradyarrhythmia","value_numeric":null},{"paper_doi":"10.1016/j.jacc.2026.03.025","tag_type":"condition","value":"Coronary Atherosclerosis","value_numeric":null},{"paper_doi":"10.1016/j.jacc.2026.03.025","tag_type":"condition","value":"Myocardial Fibrosis","value_numeric":null},{"paper_doi":"10.1016/j.jacc.2026.03.025","tag_type":"condition","value":"Ventricular Arrhythmia","value_numeric":null},{"paper_doi":"10.1016/j.jacc.2026.03.025","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1016/j.jacc.2026.03.025","tag_type":"level_of_evidence","value":"5","value_numeric":null},{"paper_doi":"10.1016/j.jacc.2026.03.025","tag_type":"modality","value":"Angiotensin Receptor Blocker","value_numeric":null},{"paper_doi":"10.1016/j.jacc.2026.03.025","tag_type":"modality","value":"Antiarrhythmic Drug","value_numeric":null},{"paper_doi":"10.1016/j.jacc.2026.03.025","tag_type":"modality","value":"Cardiac Magnetic Resonance Imaging","value_numeric":null},{"paper_doi":"10.1016/j.jacc.2026.03.025","tag_type":"modality","value":"Catheter Ablation","value_numeric":null},{"paper_doi":"10.1016/j.jacc.2026.03.025","tag_type":"modality","value":"Implantable Cardioverter-Defibrillator","value_numeric":null},{"paper_doi":"10.1016/j.jacc.2026.03.025","tag_type":"modality","value":"Statin","value_numeric":null},{"paper_doi":"10.1016/j.jacc.2026.03.025","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1016/j.jacc.2026.03.025","tag_type":"study_design","value":"Clinical Consensus Statement","value_numeric":null},{"paper_doi":"10.1016/j.jacc.2026.03.025","tag_type":"warning","value":"Female Masters athletes are substantially underrepresented in the cited literature; sex-specific findings (e.g., coronary atherosclerosis not elevated in females) may not be fully generalizable.","value_numeric":null},{"paper_doi":"10.1016/j.jacc.2026.03.025","tag_type":"warning","value":"Myocardial fibrosis prevalence figures (3–50%) vary widely due to heterogeneous study designs, small samples, and male-dominant cohorts; the true population prevalence is uncertain.","value_numeric":null},{"paper_doi":"10.1016/j.jacc.2026.03.025","tag_type":"warning","value":"No randomized controlled trials in Masters athletes underpin these recommendations; all advice is expert consensus or extrapolated from non-athlete populations. Treat strength of advice categories accordingly.","value_numeric":null},{"paper_doi":"10.1016/j.jacc.2026.03.025","tag_type":"warning","value":"The 'impact_flag: practice_changing' tag reflects the novelty of joint EAPC/ESC-ACC consensus guidance for this population, not RCT-level evidence.","value_numeric":null}],"summaries":{"what_studied":"This EAPC/ESC and ACC joint Clinical Consensus Statement evaluates the diagnostic assessment, management, and prognosis of seven cardiovascular abnormalities in Masters athletes (≥35 years old with high habitual exercise): atrial fibrillation, bradyarrhythmias, ventricular arrhythmias, coronary atherosclerosis, aortic dilatation, myocardial fibrosis, and exercise-induced arrhythmogenic cardiomyopathy (ExI-ACM).","key_result":"Masters athletes carry a 2.5–4× higher adjusted hazard for AF vs. peers; coronary artery calcification (CACS ≥100 AU) blunts the mortality benefit of high exercise volume in men; myocardial fibrosis (LGE) prevalence ranges 3–50% across studies; mild aortic dilatation (40–45 mm) affects ~20% of Masters endurance athletes vs. up to 41% of former elite strength athletes; and pacemaker implantation rates are 17% higher in elite male skiers vs. the general population.","limitations":"All recommendations rest on expert consensus and data extrapolated from sedentary or general-population cohorts—no randomized controlled trials in Masters athletes exist. Most myocardial fibrosis and aortic dilatation studies are small, male-dominated, and rely on self-reported training histories. Prospective outcome data for coronary atherosclerosis and ExI-ACM in this population are largely unavailable.","practice_takeaway":"Treat Masters athletes with high CACS (≥100 AU) aggressively with guideline-directed pharmacotherapy (statins, BP control), as exercise volume does not offset event risk at this threshold. Use shared decision-making for sport participation, rhythm control (preferring pulmonary vein isolation over rate control for AF), and exercise restriction decisions, given the absence of athlete-specific trial data."}},{"doi":"10.2215/cjn.0000000948","pmid":"41433094","title":"Antiproteinuric Effect of Sparsentan in Patients with Genetic-Associated Focal Segmental Glomerulosclerosis Enrolled in the DUPLEX Trial","journal_title":"Clinical Journal of the American Society of Nephrology","journal_issn":"1555-9041","published_at":"2025-12-23T00:00:00.000Z","url":"https://doi.org/10.2215/cjn.0000000948","source_score":31,"is_retracted":false,"is_open_access":true,"raw_metadata":{"ooir":{"day":"2025-12-24","doi":"10.2215/cjn.0000000948","days":"30","issn":"1555-9041","rank":"5","field":"Clinical Medicine","score":"31","category":"Urology & Nephrology","categories":["Urology & Nephrology"],"_categories":["Urology & Nephrology"]},"pubmed":{"doi":"10.2215/CJN.0000000948","title":"Antiproteinuric Effect of Sparsentan in Patients with Genetic-Associated Focal Segmental Glomerulosclerosis Enrolled in the DUPLEX Trial.","journal":"Clinical journal of the American Society of Nephrology : CJASN","methods":"","results":"Next-generation sequencing identified 31 patients with podocyte gene variants, 25 with COL4A3-5 gene variants, and 14 with APOL1 high-risk genotypes. Baseline characteristics varied between genetic subgroups, with slightly younger patients, on average, in the podocyte gene variant group, and more African American patients in the APOL1 high-risk genotype group. In this exploratory analysis, sparsentan treatment resulted in substantial and sustained proteinuria reductions and numerically more frequent complete remission of proteinuria compared with irbesartan, consistent with observations in the full DUPLEX study population. Moreover, a lower proportion of sparsentan- vs irbesartan-treated patients reached composite kidney endpoints.","abstract":"$32","keywords":[],"pubmed_id":"41433094","conclusions":"","publication_date":"2025-12-23T00:00:00"},"crossref":{"DOI":"10.2215/cjn.0000000948","URL":"https://doi.org/10.2215/cjn.0000000948","ISSN":["1555-9041","1555-905X"],"link":[{"URL":"https://journals.lww.com/10.2215/CJN.0000000948","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"page":null,"type":"journal-article","issue":null,"score":1,"title":["Antiproteinuric Effect of Sparsentan in Patients with Genetic-Associated Focal Segmental Glomerulosclerosis Enrolled in the DUPLEX Trial"],"author":[{"given":"Jennifer","family":"Yee","sequence":"first","affiliation":[{"name":"Division of Nephrology, Department of Pediatrics, University of Michigan, Ann Arbor, MI, USA"}]},{"given":"Wu","family":"Gong","sequence":"additional","affiliation":[{"name":"Travere Therapeutics, Inc., San Diego, CA, USA"}]},{"given":"Jula","family":"Inrig","sequence":"additional","affiliation":[{"name":"Travere Therapeutics, Inc., San Diego, CA, USA"}]},{"given":"Michelle N","family":"Rheault","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, University of Minnesota Medical School, Minneapolis, MN, USA"}]},{"given":"Angela J","family":"Gruber","sequence":"additional","affiliation":[{"name":"PreventionGenetics, Marshfield, WI, USA"}]},{"given":"Patricia W","family":"Bedard","sequence":"additional","affiliation":[{"name":"Travere Therapeutics, Inc., San Diego, CA, USA"}]},{"given":"Radko","family":"Komers","sequence":"additional","affiliation":[{"name":"Travere Therapeutics, Inc., San Diego, CA, USA"}]},{"given":"Howard","family":"Trachtman","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Pediatrics, University of Michigan, Ann Arbor, MI, USA"}]}],"issued":{"date-parts":[[2025,12,23]]},"member":"276","prefix":"10.2215","source":"Crossref","volume":null,"created":{"date-time":"2025-12-23T17:00:44Z","timestamp":1766509244000,"date-parts":[[2025,12,23]]},"indexed":{"date-time":"2025-12-23T17:18:17Z","timestamp":1766510297847,"date-parts":[[2025,12,23]]},"license":[{"URL":"http://creativecommons.org/licenses/by/4.0/","start":{"date-time":"2025-12-23T00:00:00Z","timestamp":1766448000000,"date-parts":[[2025,12,23]]},"delay-in-days":0,"content-version":"unspecified"}],"subject":[],"abstract":"$33","language":"en","relation":{},"resource":{"primary":{"URL":"https://journals.lww.com/10.2215/CJN.0000000948"}},"subtitle":[],"assertion":[{"name":"received","group":{"name":"publication_history","label":"Publication History"},"label":"Received","value":"2025-06-26"},{"name":"accepted","group":{"name":"publication_history","label":"Publication History"},"label":"Accepted","value":"2025-12-18"}],"deposited":{"date-time":"2025-12-23T17:00:44Z","timestamp":1766509244000,"date-parts":[[2025,12,23]]},"issn-type":[{"type":"print","value":"1555-9041"},{"type":"electronic","value":"1555-905X"}],"published":{"date-parts":[[2025,12,23]]},"publisher":"Ovid Technologies (Wolters Kluwer Health)","reference":null,"short-title":[],"update-policy":"https://doi.org/10.1097/lww.0000000000001000","content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"original-title":[],"container-title":["Clinical Journal of the American Society of Nephrology"],"reference-count":0,"published-online":{"date-time":null,"timestamp":null,"date-parts":[[2025,12,23]]},"references-count":0,"short-container-title":["CJASN"],"is-referenced-by-count":0},"unpaywall":{"doi":"10.2215/cjn.0000000948","is_oa":true,"title":"Antiproteinuric Effect of Sparsentan in Patients with Genetic-Associated Focal Segmental Glomerulosclerosis Enrolled in the DUPLEX Trial","updated":"2025-12-24T00:55:44+00:00","published_date":"2025-12-23","best_oa_location":{"url":"https://doi.org/10.2215/cjn.0000000948","pmh_id":null,"url_for_pdf":null,"url_for_landing_page":"https://doi.org/10.2215/cjn.0000000948"}}},"created_at":"2026-01-11T11:19:33.869Z","updated_at":"2026-01-21T12:05:26.220Z","tags":[{"paper_doi":"10.2215/cjn.0000000948","tag_type":"category","value":"Urology & Nephrology","value_numeric":null},{"paper_doi":"10.2215/cjn.0000000948","tag_type":"condition","value":"Focal Segmental Glomerulosclerosis","value_numeric":null},{"paper_doi":"10.2215/cjn.0000000948","tag_type":"generic","value":"irbesartan","value_numeric":null},{"paper_doi":"10.2215/cjn.0000000948","tag_type":"generic","value":"sparsentan","value_numeric":null},{"paper_doi":"10.2215/cjn.0000000948","tag_type":"impact_flag","value":"limited_evidence","value_numeric":null},{"paper_doi":"10.2215/cjn.0000000948","tag_type":"modality","value":"Angiotensin Receptor Blocker","value_numeric":null},{"paper_doi":"10.2215/cjn.0000000948","tag_type":"modality","value":"Dual Endothelin Angiotensin Receptor Antagonist","value_numeric":null},{"paper_doi":"10.2215/cjn.0000000948","tag_type":"study_design","value":"Post Hoc Analysis","value_numeric":null},{"paper_doi":"10.2215/cjn.0000000948","tag_type":"warning","value":"No numeric effect sizes or event counts were provided in the abstract.","value_numeric":null},{"paper_doi":"10.2215/cjn.0000000948","tag_type":"warning","value":"Results are from an exploratory post hoc subgroup analysis of an RCT.","value_numeric":null},{"paper_doi":"10.2215/cjn.0000000948","tag_type":"warning","value":"Subgroup counts may overlap; total N for genetic FSGS was not specified.","value_numeric":null},{"paper_doi":"10.2215/cjn.0000000948","tag_type":"warning","value":"Timeframe for subgroup outcomes was not explicitly stated.","value_numeric":null}],"summaries":{"what_studied":"Post hoc, exploratory analysis of DUPLEX evaluated sparsentan versus irbesartan in participants with genetic-associated FSGS, including podocyte gene variants (n=31), COL4A3-5 variants (n=25), and APOL1 high-risk genotypes (n=14).","key_result":"Sparsentan produced substantial, sustained reductions in proteinuria, with numerically more complete remissions versus irbesartan, and a lower proportion reached composite kidney endpoints; no effect sizes were reported.","limitations":"Post hoc exploratory design with small genetic subgroups; baseline differences between groups (younger in the podocyte-variant group; more African American participants in the APOL1 group) may confound results.","practice_takeaway":"Findings support an antiproteinuric benefit of sparsentan in genetic FSGS, consistent with DUPLEX overall, but conclusions should be cautious due to exploratory subgroup analysis and small numbers."}}],"initialOffset":9,"fetchConfig":{"kind":"tags","tags":[{"tag_type":"modality","value":"Angiotensin Receptor 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