Seminars in nephrology最新文献_第2页

Current Options for Kidney Protection: Are Renin-Angiotensin System Inhibitors Still Relevant? 肾保护的当前选择：肾素-血管紧张素系统抑制剂仍然相关吗？

IF 3.2 3区医学

Seminars in nephrology Pub Date : 2026-06-30 DOI: 10.1016/j.semnephrol.2026.151689

Waichi Wong

引用次数: 0

Proposed Role for Quantitative Podocyturia as a Clinical Marker of Systemic Endothelial Injury: Implications for Cardiovascular Disease and Longevity. 定量足尿作为全身性内皮损伤的临床标志：对心血管疾病和寿命的影响。

IF 3.5 3区医学

Seminars in nephrology Pub Date : 2026-03-11 DOI: 10.1016/j.semnephrol.2026.151685

Kamal F Badr

{"title":"Proposed Role for Quantitative Podocyturia as a Clinical Marker of Systemic Endothelial Injury: Implications for Cardiovascular Disease and Longevity.","authors":"Kamal F Badr","doi":"10.1016/j.semnephrol.2026.151685","DOIUrl":"https://doi.org/10.1016/j.semnephrol.2026.151685","url":null,"abstract":"Cardiovascular disease (CVD) remains the leading disability burden and cause of mortality worldwide. As emphasized by the cardiovascular-kidney-metabolic health construct, enhanced screening mechanisms are needed for the identification and prediction of subclinical endothelial injury and silent CVD. We hypothesized that urinary podocyte shedding (podocyturia), as a biomarker of ongoing glomerular endothelial injury, may be an earlier predictor of CVD than moderate albuminuria. Urinary podocin and nephrin messenger RNAs (podocyturia), as candidate biomarkers of endothelial/podocyte injury, were measured by quantitative polymerase chain reaction in type 2 diabetics with normal albumin excretion rates at baseline, at 3-4 years, and at 7 years. The development of CVD was collected as the outcome. On visit 1, podocyturia was significantly higher in individuals who subsequently developed CVD versus those who did not. We also found a significant association between podocyturia and obstructive coronary artery disease. Moreover, individuals with CVD risk factors that included male sex, metabolic syndrome, and type 2 diabetes were found to have significantly higher urinary podocin levels than individuals without these risk factors. Podocyturia may be an earlier predictor of cardiovascular events than moderate albuminuria. Semin Nephrol 36:x-xx © 20XX Elsevier Inc. All rights reserved.","PeriodicalId":21756,"journal":{"name":"Seminars in nephrology","volume":" ","pages":"151685"},"PeriodicalIF":3.5,"publicationDate":"2026-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147444902","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Kidney Protection Options in 2025: Are Renin-Angiotensin System Inhibitors Still Needed? 2025年的肾脏保护选择：还需要肾素-血管紧张素系统抑制剂吗？

IF 3.5 3区医学

Seminars in nephrology Pub Date : 2026-03-02 DOI: 10.1016/j.semnephrol.2026.151688

Matthew R Weir

{"title":"Kidney Protection Options in 2025: Are Renin-Angiotensin System Inhibitors Still Needed?","authors":"Matthew R Weir","doi":"10.1016/j.semnephrol.2026.151688","DOIUrl":"https://doi.org/10.1016/j.semnephrol.2026.151688","url":null,"abstract":"The therapeutic advantage of angiotensin-converting enzyme inhibitors was first described more than 40 years ago by Brenner and colleagues. Since then, a number of clinical trials have demonstrated the utility of drugs that modify the renin-angiotensin system (RAS) to slow the rate of progression of kidney disease in patients with and without diabetes. However, despite the well-known benefits of these drugs in reducing cardiorenal events, most clinicians are not using them consistently in their practice. The lack of use is related to concerns about increases in serum creatinine and the development of hyperkalemia. With the advent of many newer drugs to delay the progression of kidney disease and reduce the likelihood of cardiovascular events which have lesser effects on increasing serum creatinine or potassium, clinicians may prefer to use these therapies. Although trials of the newer cardiorenal protective therapies were conducted on the background of RAS inhibition, only the highest tolerated dose of RAS inhibition was used, a dose not shown to provide cardiorenal protection in a clinical trial. As multimodal therapy for slowing the progression of chronic kidney disease and reducing cardiovascular events moves into prime time, one has to wonder whether RAS inhibition will remain a foundation therapy.","PeriodicalId":21756,"journal":{"name":"Seminars in nephrology","volume":" ","pages":"151688"},"PeriodicalIF":3.5,"publicationDate":"2026-03-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147349036","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

From Nephron Number to Global Health. 从肾元数到全球健康。

IF 3.5 3区医学

Seminars in nephrology Pub Date : 2026-03-02 DOI: 10.1016/j.semnephrol.2026.151691

Valerie A Luyckx

{"title":"From Nephron Number to Global Health.","authors":"Valerie A Luyckx","doi":"10.1016/j.semnephrol.2026.151691","DOIUrl":"https://doi.org/10.1016/j.semnephrol.2026.151691","url":null,"abstract":"In 1988, in a seminal paper, Brenner and colleagues proposed that the numbers of nephrons acquired in utero may be a factor that determines an individual's lifelong risk of kidney disease. The hypothesis posited that a kidney with fewer nephrons would have a reduced filtration surface, a reduced capacity to excrete sodium, and a limited capacity to compensate for additional kidney injury and nephron loss. These factors increase the risk of high blood pressure and kidney dysfunction. Potential clinical markers for such risk include preterm birth, small-for-gestational-age birth and low birth weight, which have been associated with reduced nephron numbers and with population-level risk of kidney disease and kidney failure. As such, these birth circumstances are now recognized in mainstream guidelines on the identification of individuals at risk of kidney disease. Importantly, these circumstances depend to a large degree on maternal health in pregnancy, which, in turn, depends on many social and structural determinants of health. Optimization of maternal, fetal, and child health through achievement of the sustainable development goals therefore offers an opportunity to mitigate the growing global burden of kidney disease through supporting healthy fetal kidney development and minimizing the accumulation of additional kidney stressors throughout life. Awareness of the importance of nephron number for individual kidney health could translate into strategies to promote global kidney health.","PeriodicalId":21756,"journal":{"name":"Seminars in nephrology","volume":" ","pages":"151691"},"PeriodicalIF":3.5,"publicationDate":"2026-03-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147348999","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Chronic Kidney Disease Progression Mechanisms: Why They Matter in an Era of Novel Kidney Protective Therapies. 慢性肾脏疾病进展机制：为什么它们在新的肾脏保护疗法时代很重要。

IF 3.5 3区医学

Seminars in nephrology Pub Date : 2026-02-26 DOI: 10.1016/j.semnephrol.2026.151692

Maarten W Taal

{"title":"Chronic Kidney Disease Progression Mechanisms: Why They Matter in an Era of Novel Kidney Protective Therapies.","authors":"Maarten W Taal","doi":"10.1016/j.semnephrol.2026.151692","DOIUrl":"https://doi.org/10.1016/j.semnephrol.2026.151692","url":null,"abstract":"Research over several decades has identified multiple factors that contribute to a complex pathway of mechanisms that drive the progression of chronic kidney disease (CKD) across all etiologies. These include glomerular hypertension and hyperfiltration, proteinuria, and tubulointerstitial fibrosis. These endeavors identified multiple therapeutic targets for achieving kidney protection, starting with angiotensin II, which led to the development of renin-angiotensin-aldosterone system inhibitors as the first effective kidney protective therapies. Following a long period of stagnation, several additional kidney protective drug classes have been developed, including sodium glucose cotransporter 2 inhibitors, nonsteroidal mineralocorticoid antagonists, and glucagon-like peptide-1 receptor agonists. The effects of all of these drugs can readily be understood within the framework of previously described CKD progression mechanisms. The development of additional novel kidney protective drug classes has been informed by our understanding of progression mechanisms and include endothelin receptor antagonists, soluble guanylate cyclase stimulators or activators, and aldosterone synthase inhibitors. This review of novel therapies in the light of CKD progression mechanisms highlights the importance of ongoing research to identify new therapeutic targets as we seek to achieve complete arrest and even reversal of CKD progression.","PeriodicalId":21756,"journal":{"name":"Seminars in nephrology","volume":" ","pages":"151692"},"PeriodicalIF":3.5,"publicationDate":"2026-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147318213","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The Role of the Epidermal Growth Factor Receptor in Kidney Tubulointerstitial Fibrosis. 表皮生长因子受体在肾小管间质纤维化中的作用。

IF 3.5 3区医学

Seminars in nephrology Pub Date : 2026-02-24 DOI: 10.1016/j.semnephrol.2026.151690

Raymond C Harris, Ming-Zhi Zhang

{"title":"The Role of the Epidermal Growth Factor Receptor in Kidney Tubulointerstitial Fibrosis.","authors":"Raymond C Harris, Ming-Zhi Zhang","doi":"10.1016/j.semnephrol.2026.151690","DOIUrl":"https://doi.org/10.1016/j.semnephrol.2026.151690","url":null,"abstract":"Kidney fibrosis is a common cause of chronic kidney disease. Experimental studies have demonstrated a role for the epidermal growth factor receptor (EGFR) signaling pathway in mediating the development and progression of kidney fibrosis. Deletion of Rhbdf2 (iRhom2), a member of the rhomboid family that regulates A disintegrin and metalloproteinase domain 17-mediated release of membrane-anchored proteins, including EGFR ligands, inhibited kidney interstitial fibrosis, which was accompanied by decreased EGFR activation in interstitial fibroblasts/myofibroblasts. In addition, overexpression of another EGFR ligand, heparin-binding epidermal growth factor-like growth factor, induced interstitial fibrosis in kidneys. Although EGFR activation did not induce myofibroblast transformation, it was necessary for the initial pericyte/fibroblast migration and proliferation prior to subsequent myofibroblast transformation by transforming growth factor beta or other profibrotic factors. Therefore, EGFR activation in kidney fibroblasts and pericytes serves as a specific initiator of interstitial fibrosis in response to kidney injury by stimulating pericyte/fibroblast migration and proliferation. These findings may also provide insight into the development of fibrosis in other organs and in other conditions.","PeriodicalId":21756,"journal":{"name":"Seminars in nephrology","volume":" ","pages":"151690"},"PeriodicalIF":3.5,"publicationDate":"2026-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147310066","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Kidney Transplants From Marginal Donors: From Brenner's Abstract to Double Kidney Transplantation in Humans. 边缘供体肾移植：从Brenner的摘要到人类双肾移植。

IF 3.5 3区医学

Seminars in nephrology Pub Date : 2026-02-24 DOI: 10.1016/j.semnephrol.2026.151687

Monica Cortinovis, Norberto Perico, Giuseppe Remuzzi

引用次数: 0

Of Diuretics, Transporters, and Mechanisms of Hypertension. 利尿剂、转运蛋白和高血压的机制。

IF 3.5 3区医学

Seminars in nephrology Pub Date : 2026-02-24 DOI: 10.1016/j.semnephrol.2026.151686

Maria Castañeda-Bueno, Gerardo Gamba

引用次数: 0

Tension at the Barrier: Intraglomerular Pressure and the Podocyte Response. 屏障处的张力：肾小球内压力和足细胞反应。

IF 3.5 3区医学

Seminars in nephrology Pub Date : 2026-02-21 DOI: 10.1016/j.semnephrol.2026.151684

Martin R Pollak

{"title":"Tension at the Barrier: Intraglomerular Pressure and the Podocyte Response.","authors":"Martin R Pollak","doi":"10.1016/j.semnephrol.2026.151684","DOIUrl":"https://doi.org/10.1016/j.semnephrol.2026.151684","url":null,"abstract":"I synthesize how systemic drivers (hypertension, diabetes, renin-angiotensin-aldosterone system activation) elevate glomerular capillary hydrostatic pressure and cyclic strain and how podocytes sense and respond to these loads via integrins, the slit diaphragm, and stretch-activated ion channels. When podocytes' normal adaptation mechanisms are overwhelmed by higher loads, inflammatory priming, genetic risk, or loss of cytoskeletal resilience, podocytes retract, detach, and are not meaningfully replaced, driving progressive glomerulosclerosis. Therapeutically, benefit follows two complementary strategies: lowering glomerular capillary hydrostatic pressure (angiotensin-converting enzyme inhibitor/angiotensin receptor blocker, sodium-glucose cotransporter 2 inhibitors, endothelin antagonism) and reinforcing podocyte mechanoadaptation (stabilizing actin/adhesion, modulating Ca²⁺ signaling, targeting load-sensing nodes). Taken together, progressive glomerulosclerosis is best explained by a model in which elevated single-nephron pressure loads exceed podocyte mechanoadaptive capacity. Durable protection will therefore require concurrent control of intraglomerular pressure and podocyte mechanotransduction. Semin Nephrol 36:x-xx © 20XX Elsevier Inc. All rights reserved.","PeriodicalId":21756,"journal":{"name":"Seminars in nephrology","volume":" ","pages":"151684"},"PeriodicalIF":3.5,"publicationDate":"2026-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147271892","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Neuroimmune Regulation for Acute Kidney Injury Therapy: Insights Along the Path From Bench to Bedside 急性肾损伤治疗的神经免疫调节：从实验到临床的见解。

IF 3.5 3区医学

Seminars in nephrology Pub Date : 2026-01-01 Epub Date: 2025-10-08 DOI: 10.1016/j.semnephrol.2025.151674

William T. Nash PhD , Mark D. Okusa MD

引用次数: 0