Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association最新文献

筛选
英文 中文
Correction to: Upcoming drug targets for kidney protective effects in chronic kidney disease. 更正:即将推出的用于慢性肾脏疾病肾脏保护作用的药物靶点。
IF 5.6
{"title":"Correction to: Upcoming drug targets for kidney protective effects in chronic kidney disease.","authors":"","doi":"10.1093/ndt/gfaf099","DOIUrl":"10.1093/ndt/gfaf099","url":null,"abstract":"","PeriodicalId":520717,"journal":{"name":"Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association","volume":" ","pages":"1636"},"PeriodicalIF":5.6,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144228413","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Correction to: Clinical and patient-reported trajectories at end-of-life in older patients with advanced CKD. 更正:老年晚期CKD患者的临床和患者报告的生命末期轨迹。
IF 5.6
{"title":"Correction to: Clinical and patient-reported trajectories at end-of-life in older patients with advanced CKD.","authors":"","doi":"10.1093/ndt/gfaf096","DOIUrl":"10.1093/ndt/gfaf096","url":null,"abstract":"","PeriodicalId":520717,"journal":{"name":"Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association","volume":" ","pages":"1635"},"PeriodicalIF":5.6,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144510466","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Antibody-mediated rejection-treatment standard. 抗体介导的排斥反应-治疗标准。
IF 5.6
Georg A Böhmig, Maarten Naesens, Ondrej Viklicky, Olivier Thaunat, Matthias Diebold, Lionel Rostaing, Klemens Budde
{"title":"Antibody-mediated rejection-treatment standard.","authors":"Georg A Böhmig, Maarten Naesens, Ondrej Viklicky, Olivier Thaunat, Matthias Diebold, Lionel Rostaing, Klemens Budde","doi":"10.1093/ndt/gfaf097","DOIUrl":"10.1093/ndt/gfaf097","url":null,"abstract":"<p><p>Antibody-mediated rejection (AMR) remains a major cause of graft failure, with significant health and economic burden. Despite being recognized >25 years ago, AMR treatment remains unstandardized, and no therapy has gained robust regulatory approval. While uncontrolled series have shown promise, few well-designed trials exist, with most yielding negative results. In the absence of strong trial data, a Transplantation Society expert consensus recommended potential treatment options with low levels of evidence, tailored to clinical phenotypes. Here, we re-evaluate the current evidence for AMR treatment decisions. We conclude that steroids, rituximab, bortezomib, and interleukin-6 (IL-6) antagonists lack sufficiently robust evidence to support their use in AMR. For early AMR, antibody depletion using immunoadsorption could be considered as an alternative to plasmapheresis. High-dose intravenous immunoglobulin (IVIG) may be added, though the supporting evidence remains limited. While previous trials primarily targeted the cause of AMR, recent data on the successful reversal of AMR activity by CD38 antibodies-particularly recent phase 2 trial results-suggest that targeting the cellular inflammation resulting from antibody binding to the endothelium could be a rational approach. Along these lines, in severe early AMR, complement inhibition may also be an option. Ongoing phase 2 trials evaluating prolonged courses of high-dose IVIG, the neonatal Fc receptor blocker efgartigimod, the tyrosine kinase inhibitor fostamatinib, and the complement inhibitor BIVV020, along with phase 3 trials of the anti-IL-6 receptor antibody tocilizumab and the CD38 antibody felzartamab, offer hope for effective, approved therapies targeting different aspects of AMR pathobiology.</p>","PeriodicalId":520717,"journal":{"name":"Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association","volume":" ","pages":"1615-1627"},"PeriodicalIF":5.6,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144182957","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Correction to: Hypocalcemia and cardiovascular mortality in cinacalcet users. 修正:cinacalcet使用者的低钙血症和心血管死亡率。
IF 5.6
{"title":"Correction to: Hypocalcemia and cardiovascular mortality in cinacalcet users.","authors":"","doi":"10.1093/ndt/gfaf100","DOIUrl":"10.1093/ndt/gfaf100","url":null,"abstract":"","PeriodicalId":520717,"journal":{"name":"Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association","volume":" ","pages":"1637"},"PeriodicalIF":5.6,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144251958","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Hemodialysis removes protective metabolites and disrupts mitochondrial function. 血液透析去除保护性代谢物,破坏线粒体功能。
IF 5.6
María Peris-Fernández, Marta Isabel Roca-Marugán, Iris Viejo-Boyano, Amparo Soldevila-Orient, Ramon Devesa-Such, Pilar Sánchez-Pérez, Julio Hernández-Jaras
{"title":"Hemodialysis removes protective metabolites and disrupts mitochondrial function.","authors":"María Peris-Fernández, Marta Isabel Roca-Marugán, Iris Viejo-Boyano, Amparo Soldevila-Orient, Ramon Devesa-Such, Pilar Sánchez-Pérez, Julio Hernández-Jaras","doi":"10.1093/ndt/gfaf145","DOIUrl":"https://doi.org/10.1093/ndt/gfaf145","url":null,"abstract":"<p><strong>Background: </strong>Metabolic analyses offer valuable insights into the biochemical changes induced by hemodialysis, yet prior studies have focused on targeted approaches or lacked comprehensive pathway analysis. This study employs semi-targeted metabolomics to explore metabolic shifts in hemodialysis patients.</p><p><strong>Methods: </strong>Pre- and post- dialysis plasma samples were collected from 43 hemodialysis patients and analyzed using ultra-performance liquid chromatography coupled with quadrupole time-of-flight mass spectrometry (UPLC-QToF-MS). Principal component analysis (PCA) and orthogonal partial least squares discriminant analysis (OPLS-DA) were used to assess metabolic separation, and variable importance in projection (VIP) scores ranked the most significant metabolites.</p><p><strong>Results: </strong>Hemodialysis significantly altered the plasma metabolome, with 79 metabolites showing relevant changes. Most were reduced, including harmful solutes like 3-indoxyl sulfate (FC: 0.29-fold) and D-galactonic acid (0.14-fold), but also protective compounds such as L-carnitine (0.38-fold), quinic acid (0.16-fold) and homocarnosine (0.15-fold). Meanwhile, lipotoxic intermediates like myristic acid (2.51-fold) and linoleic acid (2.28-fold) increased. Enrichment analysis revealed disruptions in amino acid, lipid, and energy metabolism, underscoring the dual impact of dialysis on both toxic and beneficial metabolites.</p><p><strong>Conclusions: </strong>Hemodialysis alters the plasma metabolome by removing toxins but also depleting protective metabolites and promoting lipotoxic intermediates. These shifts may undermine therapy benefits, highlighting the need for strategies that preserve metabolic homeostasis in dialysis patients.</p>","PeriodicalId":520717,"journal":{"name":"Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association","volume":" ","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144755606","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Myocardial Ischaemic Syndromes in Chronic Kidney Disease: Risky Pathways from Non-Acute to Acute Events. 慢性肾脏疾病的心肌缺血综合征:从非急性到急性事件的危险途径
IF 5.6
Carmine Zoccali, Shanmugakumar Chinnappa, Beatriz Fernández-Fernández, Fotini Iatridi, Francesca Mallamaci, Patrick B Mark, Evangelia Ntounousi, Nejc Piko, Joannes Stegbauer, Claudia Torino, José Manuel Valdivielso, Amaryllis Van Craenenbroeck, Liffert Vogt, Raffaele De Caterina
{"title":"Myocardial Ischaemic Syndromes in Chronic Kidney Disease: Risky Pathways from Non-Acute to Acute Events.","authors":"Carmine Zoccali, Shanmugakumar Chinnappa, Beatriz Fernández-Fernández, Fotini Iatridi, Francesca Mallamaci, Patrick B Mark, Evangelia Ntounousi, Nejc Piko, Joannes Stegbauer, Claudia Torino, José Manuel Valdivielso, Amaryllis Van Craenenbroeck, Liffert Vogt, Raffaele De Caterina","doi":"10.1093/ndt/gfaf142","DOIUrl":"https://doi.org/10.1093/ndt/gfaf142","url":null,"abstract":"<p><p>Chronic kidney disease (CKD) has emerged as a critical global public health concern. This condition is strongly associated with an increased risk of atherosclerotic cardiovascular disease and acute coronary syndromes (ACS) which have been recently renamed as acute myocardial ischemic syndromes (AMIS). In CKD patients, the atypical presentation of symptoms complicates the diagnosis and management of angina, a condition that can, if not promptly addressed, rapidly progress to myocardial infarction. Traditional diagnostic tools, such as the electrocardiogram and cardiac biomarkers, are less reliable in this population due to CKD-related baseline alterations, necessitating advanced imaging techniques for accurate assessment. Management strategies for transient myocardial ischaemia in CKD must also carefully balance the risk related to myocardial ischemia against potential complications from invasive procedures, such as further renal impairment and bleeding. Tailored therapeutic approaches, including adjusted medication regimens and innovative revascularization techniques, are crucial to improve outcomes in this high-risk population. Additionally, asymptomatic myocardial infarction is notably prevalent in CKD, often remaining undetected and posing significant prognostic implications. The interplay of traditional and non-traditional risk factors, such as uremia-induced toxicity and chronic inflammation, further exacerbates the risk for plaque instability in CKD patients. This review highlights the necessity of a multidisciplinary approach to managing myocardial ischemia in chronic kidney disease (CKD), incorporating meticulous risk stratification and personalized treatment plans.</p>","PeriodicalId":520717,"journal":{"name":"Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association","volume":" ","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144746988","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
SGLT2 inhibitors and acute kidney injury. SGLT2抑制剂与急性肾损伤。
IF 5.6
Yuki Nakao, Makiko Mori, Yutaro Mori, Joseph V Bonventre
{"title":"SGLT2 inhibitors and acute kidney injury.","authors":"Yuki Nakao, Makiko Mori, Yutaro Mori, Joseph V Bonventre","doi":"10.1093/ndt/gfaf132","DOIUrl":"https://doi.org/10.1093/ndt/gfaf132","url":null,"abstract":"<p><p>Sodium-glucose co-transporter-2 inhibitors (SGLT2i) are glucose-lowering agents that inhibit glucose reabsorption by the proximal tubules of the kidney. Since the introduction of the first SGLT2 inhibitor in 2012, dapagliflozin, canagliflozin and empagliflozin have been developed and been rapidly integrated into clinical medicine, initially to manage type 2 diabetes. Over a short period of time, however, it has become apparent that SGLT2i not only reduces blood glucose but also provides long-term protective effects on the kidneys and heart. In this review, we present physiological data on what is known about SGLT2i effects on the kidney, present the ever-expanding clinical data relating to the effects of SGLT2i on the occurrence of acute kidney injury (AKI) and integrate what is known about molecular mechanisms with clinical experience. We conclude that SGLT2i may reduce the risks for AKI in humans. We speculate on mechanisms by which SGLT2 inhibitors may protect against AKI.</p>","PeriodicalId":520717,"journal":{"name":"Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association","volume":" ","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144746989","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Correction to: Biology of calcium homeostasis regulation in intestine and kidney. 更正:肠和肾钙稳态调节的生物学。
{"title":"Correction to: Biology of calcium homeostasis regulation in intestine and kidney.","authors":"","doi":"10.1093/ndt/gfaf131","DOIUrl":"https://doi.org/10.1093/ndt/gfaf131","url":null,"abstract":"","PeriodicalId":520717,"journal":{"name":"Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144700959","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Prevalence of reduced eGFR in European adults using KDIGO and age-adapted eGFR thresholds. 使用KDIGO和年龄适应eGFR阈值的欧洲成年人eGFR降低的患病率
Megan E Astley, Nicholas C Chesnaye, Giovanni Gambaro, Alberto Ortiz, Stein Hallan, Juan-Jesus Carrero, Natalie Ebert, Bjørn Odvar Eriksen, Anne-Laure Faucon, Pietro Manuel Ferraro, Till Ittermann, Arnar J Jonsson, Knut Asbjørn Rise Langlo, Toralf Melsom, Elke Schaeffner, Sylvia Stracke, Runolfur Palsson, Kitty J Jager, Vianda S Stel
{"title":"Prevalence of reduced eGFR in European adults using KDIGO and age-adapted eGFR thresholds.","authors":"Megan E Astley, Nicholas C Chesnaye, Giovanni Gambaro, Alberto Ortiz, Stein Hallan, Juan-Jesus Carrero, Natalie Ebert, Bjørn Odvar Eriksen, Anne-Laure Faucon, Pietro Manuel Ferraro, Till Ittermann, Arnar J Jonsson, Knut Asbjørn Rise Langlo, Toralf Melsom, Elke Schaeffner, Sylvia Stracke, Runolfur Palsson, Kitty J Jager, Vianda S Stel","doi":"10.1093/ndt/gfaf112","DOIUrl":"https://doi.org/10.1093/ndt/gfaf112","url":null,"abstract":"<p><strong>Background: </strong>The current definition for chronic kidney disease (CKD) does not account for age-related kidney function decline. Age-adapted CKD definitions have been suggested, but their impact on the estimates of reduced kidney function prevalence remains unclear. We aimed to compare the prevalence of reduced estimated glomerular filtration rate (eGFR) in European adults using the KDIGO eGFR threshold and three age-adapted eGFR thresholds.</p><p><strong>Methods: </strong>This cross-sectional study included data collected after 1999 from nine general population-based studies from seven European countries. eGFR was calculated using the European Kidney Function Consortium (EKFC) equation. Prevalence of reduced eGFR was estimated over age using four eGFR thresholds: the KDIGO eGFR threshold (eGFR < 60 mL/min per 1.73 m2), the categorical age-adapted eGFR threshold (eGFR < 75 mL/min per 1.73 m2 if aged < 40 years, eGFR < 60 mL/min per 1.73 m2 if aged 40-65 years, eGFR < 45 mL/min per 1.73 m2 if aged > 65 years), and two novel continuous age- and sex-adapted eGFR thresholds based on the 5th and 2.5th percentile of eGFR in healthy individuals.</p><p><strong>Results: </strong>We used data from over 2.5 million European adults (46% men). Among those under 40 years, the KDIGO threshold provided the lowest average prevalence estimate (<1%), followed by the categorical age-adapted threshold (3%) and the 2.5th and 5th continuous age- and sex-adapted thresholds (4% and 7%). In adults over 65 years, the 2.5th continuous age- and sex-adapted threshold (10%) estimated the lowest prevalence, then the 5th continuous age- and sex-adapted threshold (15%), categorical age-adapted threshold (19%) and KDIGO threshold (45%).</p><p><strong>Conclusion: </strong>Using age-adapted eGFR thresholds would likely cause a shift in the prevalence of reduced kidney function. However, the association between these novel age-adapted thresholds and clinical outcomes needs to be established before considering their incorporation into the definition of CKD.</p>","PeriodicalId":520717,"journal":{"name":"Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144652073","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Kidney disease after hematopoietic stem cell transplant - treatment standard. 造血干细胞移植后肾脏疾病的治疗标准。
Yu Zhang, Weiwei Fu, Xianghua Huang
{"title":"Kidney disease after hematopoietic stem cell transplant - treatment standard.","authors":"Yu Zhang, Weiwei Fu, Xianghua Huang","doi":"10.1093/ndt/gfaf139","DOIUrl":"https://doi.org/10.1093/ndt/gfaf139","url":null,"abstract":"<p><p>Hematopoietic stem cell transplant (HSCT) is a well-established procedure for malignant and nonmalignant conditions. Despite its therapeutic benefits, kidney disease remains a common complication that significantly impacts patient outcomes. Kidney injury post-HSCT manifests as acute kidney injury (AKI) and chronic kidney disease (CKD), with multifactorial causes such as conditioning regimens, nephrotoxic drugs, graft-versus-host disease (GVHD), and transplant-associated thrombotic microangiopathy (TA-TMA). Accurate diagnosis often requires a kidney biopsy due to overlapping risk factors and complex clinical presentations. This review summarizes current diagnostic and therapeutic standards, highlights advance in biomarkers and pathophysiology, and discusses targeted therapies such as rituximab for GVHD-related glomerulopathies and eculizumab for TA-TMA. Supportive care, immunomodulation, and early intervention remain critical. For patients progressing to end stage renal disease, renal replacement therapy and kidney transplantation post-HSCT offer viable long-term options. Despite these advances, challenges persist, including the need for noninvasive diagnostic tools and standardized management protocols. Future research into pathophysiology, biomarkers, and targeted therapies holds promise for improving outcomes in this field.</p>","PeriodicalId":520717,"journal":{"name":"Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144652072","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
相关产品
×
本文献相关产品
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术官方微信