Nature Reviews Nephrology最新文献_第5页

A difficult path to point-of-care measurement of glomerular filtration rate 对肾小球滤过率进行即时测量的困难途径

IF 41.5 1区医学

Nature Reviews Nephrology Pub Date : 2025-03-12 DOI: 10.1038/s41581-025-00947-0

Pierre Delanaye, Richard J. Glassock

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The role of implementation science in advancing equity in kidney health 实施科学在促进肾脏健康公平中的作用

IF 41.5 1区医学

Nature Reviews Nephrology Pub Date : 2025-03-11 DOI: 10.1038/s41581-025-00949-y

Lilia Cervantes, Sri Lekha Tummalapalli, Delphine Tuot, Russell E. Glasgow

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Systemic interventions towards kidney health equity in American Indian and Alaska Native communities 对美国印第安人和阿拉斯加土著社区肾脏健康公平的系统干预

IF 41.5 1区医学

Nature Reviews Nephrology Pub Date : 2025-03-06 DOI: 10.1038/s41581-025-00943-4

Reya H. Mokiao, Jason F. Deen, Amanda M. Fretts, Bessie A. Young

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Fiji’s rising tide: the growing burden of diabetic kidney disease on emerging nephrology services 斐济的上升趋势：糖尿病肾病对新兴肾脏病服务日益加重的负担

IF 41.5 1区医学

Nature Reviews Nephrology Pub Date : 2025-02-28 DOI: 10.1038/s41581-025-00942-5

Anis Ta’eed, Abhitesh Raj, Yogeshni Chandra, Shilpanjali Jesudason, Angus Ritchie

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Cross-species evolution of capsid libraries for gene delivery to the kidneys 基因传递到肾脏的衣壳文库的跨物种进化

IF 28.6 1区医学

Nature Reviews Nephrology Pub Date : 2025-02-26 DOI: 10.1038/s41581-025-00945-2

Monica Wang

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A personalized vaccine for kidney cancer 一种针对肾癌的个性化疫苗

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Nature Reviews Nephrology Pub Date : 2025-02-25 DOI: 10.1038/s41581-025-00941-6

Susan J. Allison

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Endoplasmic reticulum stress as a driver and therapeutic target for kidney disease 内质网应激是肾脏疾病的驱动因素和治疗靶点

IF 41.5 1区医学

Nature Reviews Nephrology Pub Date : 2025-02-24 DOI: 10.1038/s41581-025-00938-1

Jae Hyun Byun, Paul F. Lebeau, Jackie Trink, Nikhil Uppal, Matthew B. Lanktree, Joan C. Krepinsky, Richard C. Austin

{"title":"Endoplasmic reticulum stress as a driver and therapeutic target for kidney disease","authors":"Jae Hyun Byun, Paul F. Lebeau, Jackie Trink, Nikhil Uppal, Matthew B. Lanktree, Joan C. Krepinsky, Richard C. Austin","doi":"10.1038/s41581-025-00938-1","DOIUrl":"https://doi.org/10.1038/s41581-025-00938-1","url":null,"abstract":"<p>The endoplasmic reticulum (ER) has crucial roles in metabolically active cells, including protein translation, protein folding and quality control, lipid biosynthesis, and calcium homeostasis. Adverse metabolic conditions or pathogenic genetic variants that cause misfolding and accumulation of proteins within the ER of kidney cells initiate an injurious process known as ER stress that contributes to kidney disease and its cardiovascular complications. Initiation of ER stress activates the unfolded protein response (UPR), a cellular defence mechanism that functions to restore ER homeostasis. However, severe or chronic ER stress rewires the UPR to activate deleterious pathways that exacerbate inflammation, apoptosis and fibrosis, resulting in kidney injury. This insidious crosstalk between ER stress, UPR activation, oxidative stress and inflammation forms a vicious cycle that drives kidney disease and vascular damage. Furthermore, genetic variants that disrupt protein-folding mechanisms trigger ER stress, as evidenced in autosomal-dominant tubulointerstitial kidney disease and Fabry disease. Emerging therapeutic strategies that enhance protein-folding capacity and reduce the burden of ER stress have shown promising results in kidney diseases. Thus, integrating knowledge of how genetic variants cause protein misfolding and ER stress into clinical practice will enhance treatment strategies and potentially improve outcomes for various kidney diseases and their vascular complications.</p>","PeriodicalId":19059,"journal":{"name":"Nature Reviews Nephrology","volume":"25 1","pages":""},"PeriodicalIF":41.5,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143477475","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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Advances and challenges in kidney fibrosis therapeutics 肾纤维化治疗的进展和挑战

IF 41.5 1区医学

Nature Reviews Nephrology Pub Date : 2025-02-11 DOI: 10.1038/s41581-025-00934-5

Lilia Abbad, Emmanuel Esteve, Christos Chatziantoniou

{"title":"Advances and challenges in kidney fibrosis therapeutics","authors":"Lilia Abbad, Emmanuel Esteve, Christos Chatziantoniou","doi":"10.1038/s41581-025-00934-5","DOIUrl":"https://doi.org/10.1038/s41581-025-00934-5","url":null,"abstract":"<p>Chronic kidney disease (CKD) is a major global health burden that affects more than 10% of the adult population. Current treatments, including dialysis and transplantation, are costly and not curative. Kidney fibrosis, defined as an abnormal accumulation of extracellular matrix in the kidney parenchyma, is a common outcome in CKD, regardless of disease aetiology, and is a major cause of loss of kidney function and kidney failure. For this reason, research efforts have focused on identifying mediators of kidney fibrosis to inform the development of effective anti-fibrotic treatments. Given the prominent role of the transforming growth factor-β (TGFβ) family in fibrosis, efforts have focused on inhibiting TGFβ signalling. Despite hopes raised by the efficacy of this approach in preclinical models, translation into clinical practice has not met expectations. Antihypertensive and antidiabetic drugs slow the decline in kidney function and could slow fibrosis but, owing to the lack of technologies for in vivo renal imaging, their anti-fibrotic effect cannot be truly assessed at present. The emergence of new drugs targeting pro-fibrotic signalling, or enabling cell repair and cell metabolic reprogramming, combined with better stratification of people with CKD and the arrival of nanotechnologies for kidney-specific drug delivery, open up new perspectives for the treatment of this major public health challenge.</p>","PeriodicalId":19059,"journal":{"name":"Nature Reviews Nephrology","volume":"50 1","pages":""},"PeriodicalIF":41.5,"publicationDate":"2025-02-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143393137","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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Publisher Correction: Clinical practice recommendations for the diagnosis and management of X-linked hypophosphataemia 出版者更正：诊断和管理x连锁低磷血症的临床实践建议

IF 41.5 1区医学

Nature Reviews Nephrology Pub Date : 2025-02-04 DOI: 10.1038/s41581-025-00939-0

Dieter Haffner, Francesco Emma, Lothar Seefried, Wolfgang Högler, Kassim M. Javaid, Detlef Bockenhauer, Justine Bacchetta, Deborah Eastwood, Martin Biosse Duplan, Dirk Schnabel, Philippe Wicart, Gema Ariceta, Elena Levtchenko, Pol Harvengt, Martha Kirchhoff, Oliver Gardiner, Federico Di Rocco, Catherine Chaussain, Maria Luisa Brandi, Lars Savendahl, Karine Briot, Peter Kamenický, Lars Rejnmark, Agnès Linglart

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Artificial intelligence approaches to enable early detection of CKD 人工智能方法使CKD能够早期发现

IF 28.6 1区医学

Nature Reviews Nephrology Pub Date : 2025-02-03 DOI: 10.1038/s41581-025-00933-6

Navdeep Tangri, Charumathi Sabanayagam

引用次数: 0