Nature Reviews Nephrology最新文献

{"title":"Infrastructure and policy reforms to facilitate collaboration in medical research","authors":"Anna K. Kuderna, Nick K. Schneider, Ralf Heyder, Georg Schmidt, Peter Boor","doi":"10.1038/s41581-026-01090-0","DOIUrl":"10.1038/s41581-026-01090-0","url":null,"abstract":"Medical research increasingly depends on data-driven, large-scale, multicentric cooperation; however, such cooperation remains obstructed by fragmented procedures, heterogeneity in ethics oversight, complex legal frameworks and regulatory divergence. These structural barriers slow progress, increase costs and ultimately limit benefits to patients. Harmonized, efficient processes and coherent legal frameworks that enable effective collaborative research are feasible and urgently needed.","PeriodicalId":19059,"journal":{"name":"Nature Reviews Nephrology","volume":"22 8","pages":"513-515"},"PeriodicalIF":46.7,"publicationDate":"2026-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148163904","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}

{"title":"A spatial atlas identifies tertiary lymphoid tissue-like structures in DKD","authors":"Ellen F. Carney","doi":"10.1038/s41581-026-01093-x","DOIUrl":"10.1038/s41581-026-01093-x","url":null,"abstract":"","PeriodicalId":19059,"journal":{"name":"Nature Reviews Nephrology","volume":"22 7","pages":"458-458"},"PeriodicalIF":46.7,"publicationDate":"2026-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148150598","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}

{"title":"HNF1B as a central gatekeeper of tubular homeostasis","authors":"Susan J. Allison","doi":"10.1038/s41581-026-01091-z","DOIUrl":"10.1038/s41581-026-01091-z","url":null,"abstract":"","PeriodicalId":19059,"journal":{"name":"Nature Reviews Nephrology","volume":"22 7","pages":"458-458"},"PeriodicalIF":46.7,"publicationDate":"2026-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148150605","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}

{"title":"The pathophysiology of pre-eclampsia","authors":"Annemarie Hennessy, Jolene Ng, Angela Makris","doi":"10.1038/s41581-026-01085-x","DOIUrl":"10.1038/s41581-026-01085-x","url":null,"abstract":"Pre-eclampsia is a serious complication of pregnancy that contributes to maternal and neonatal morbidity and mortality. Maternal endothelial dysfunction, particularly in the kidney, liver and cerebral vascular beds, causes the key clinical features of hypertension and proteinuria as well as the potentially fatal complications of eclampsia: stroke, acute kidney injury and liver dysfunction. The placenta has a key role in moderating these systemic maternal responses and potentially also changes in fetal growth. As pre-eclampsia progresses, the dysfunctional placenta produces toxins that contribute to maternal endothelial dysfunction and disease development. These toxins, including the anti-angiogenic factor soluble fms-like tyrosine kinase-1 (sFLT1), can be utilized as biomarkers. Other pathophysiological contributions to placental dysfunction, including ischaemia, inflammation and senescence, as well as risk factors such as older maternal age, obesity, diabetes mellitus, chronic hypertension or multifetal gestation, may help to explain differences in disease presentation. Chronic kidney disease is a risk factor for the development of pre-eclampsia during early pregnancy, and early pre-eclampsia may reflect undiagnosed underlying kidney disease in some patients. Furthermore, pre-eclampsia is a risk factor for kidney and cardiovascular disease in the mother and baby in later life. Understanding the pathways that contribute to pre-eclampsia facilitates the development of potential prevention strategies and treatments for early-presenting disease with severe features. Here, the authors discuss the pathophysiology of pre-eclampsia and potential targets for treatment to reduce maternal and perinatal mortality. They also discuss the utility of testing to predict pre-eclampsia and the pathogenesis of cardiovascular disease following pre-eclamptic pregnancy.","PeriodicalId":19059,"journal":{"name":"Nature Reviews Nephrology","volume":"22 9","pages":"622-634"},"PeriodicalIF":46.7,"publicationDate":"2026-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148005999","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}

{"title":"Gene–disease relationships for glomerular phenotypes: expert recommendations from ClinGen","authors":"Alicia B. Byrne, Anna S. Li \u0000 (, ), Edmund Y. M. Chung, Enyonam Edoh, Hannah Dziadzio, Pamela Ajuyah, Elisabet Ars, Yasar Caliskan, Ahmet Burak Dirim, Mark D. Elliott, Asheeta Gupta, Kushani Jayasinghe, Andrew J. Mallett, Julie C. Ratliff, Matthew G. Sampson, Judy Savige, Johannes S. Schlondorff, Zornitza Stark, Ryan F. Webb, Parker C. Wilson, Janewit Wongboonsin, The ClinGen Glomerulopathy Gene Curation Expert Panel, Martin R. Pollak, Hugh J. McCarthy, Catherine Quinlan, Rachel Lennon","doi":"10.1038/s41581-026-01087-9","DOIUrl":"10.1038/s41581-026-01087-9","url":null,"abstract":"Glomerular diseases are complex conditions, many of which have a genetic basis. However, although some genetic variants can affect glomerular and thereby kidney function, not all identified variants are pathogenic. The process of evaluating genetic and experimental evidence to determine the validity of gene–disease relationships is known as gene curation, and it is critical for the identification of genes that should be examined in diagnostic tests and used to guide clinical management. Gene curation is a key role of the Clinical Genome Resource (ClinGen) and aims to ensure that the evidence underlying asserted gene–disease relationships across a range of diseases is sufficiently robust through comprehensive review of evidence and standardized evaluation by genetic and disease area-specific experts. The ClinGen Glomerulopathy Gene Curation Expert Panel has evaluated 57 gene–disease relationships from 56 genes that have been putatively linked to glomerular phenotypes. This evaluation identified 34 genes that reached a definitive level of evidence for gene–disease clinical validity. Ten genes had moderate supporting evidence and 11 had limited supporting evidence. A further two genes had insufficient evidence for any clinically valid relationship to disease. This curation establishes a comprehensive framework for the ongoing assessment of gene–disease relationships and provides a valuable reference for diagnostic genetic testing panels that target glomerular disease. Many glomerular diseases have a genetic basis; however, not all identified variants are pathogenic. This Expert Recommendation from the Clinical Genome Resource (ClinGen) Glomerulopathy Gene Curation Expert Panel describes the outcomes of gene curation efforts to evaluate the evidence underlying asserted gene–disease relationships for 56 genes that have putatively been linked to glomerular diseases.","PeriodicalId":19059,"journal":{"name":"Nature Reviews Nephrology","volume":"22 8","pages":"575-588"},"PeriodicalIF":46.7,"publicationDate":"2026-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147988394","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}

{"title":"Anti-neutrophil cytoplasmic antibody-associated vasculitis: biological insights and biomarker-guided disease management","authors":"Marilina Antonelou, Kashif Jamil Anwari, Alan D. Salama","doi":"10.1038/s41581-026-01081-1","DOIUrl":"10.1038/s41581-026-01081-1","url":null,"abstract":"Earlier recognition of anti-neutrophil cytoplasmic antibody-associated vasculitis has led to more timely treatment initiation and improvements in patient survival, despite limited available therapeutic options. Current drugs can induce remission in most patients, but therapies are not individualized, with consequent over-treatment of some patients and under-treatment of others, leading to considerable morbidity from both disease and therapy. Diverse research strategies, from large clinical datasets to single-cell molecular analyses, have improved understanding of antibody-associated vasculitis biology substantially, with implications for patient management. Longitudinal data from registries and trial databases have highlighted variations in the patterns and progression of kidney disease. Efforts to improve current biological readouts of disease activity have tried to identify more dynamic and clinically applicable biomarkers to inform, in real time, the level of therapy required. Examples of such readouts include urinary levels of CD163 and CC-chemokine ligand 2, urinary T cell numbers and serum levels of various immune biomarkers, although further validation studies are required. Several important questions — how to prevent kidney disease progression, predict relapse and determine immunological quiescence to inform duration of therapy — remain incompletely answered. Here, we highlight some of the latest research advances that can help to inform clinicians about the biology of disease and might ultimately enable customization of treatment. Current gaps in the management of anti-neutrophil cytoplasmic antibody-associated vasculitis include treatment-associated morbidity and mortality risk. Here, the authors examine research findings on biological readouts of disease activity that might offer biomarkers for monitoring disease activity and inform therapeutic interventions.","PeriodicalId":19059,"journal":{"name":"Nature Reviews Nephrology","volume":"22 8","pages":"541-558"},"PeriodicalIF":46.7,"publicationDate":"2026-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147931797","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}

{"title":"Author Correction: The genetics of hypertension","authors":"Gabriel Stölting, Kieu Nhi Tran Vo, Janek Haus, Ute I. Scholl","doi":"10.1038/s41581-026-01088-8","DOIUrl":"10.1038/s41581-026-01088-8","url":null,"abstract":"","PeriodicalId":19059,"journal":{"name":"Nature Reviews Nephrology","volume":"22 7","pages":"512-512"},"PeriodicalIF":46.7,"publicationDate":"2026-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41581-026-01088-8.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147875099","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Selective autophagy in kidney health and disease","authors":"Ying Fu, Man J. Livingston, Guie Dong, Anqun Chen, Juan Cai, Zheng Dong","doi":"10.1038/s41581-026-01082-0","DOIUrl":"10.1038/s41581-026-01082-0","url":null,"abstract":"The kidney is a highly metabolically active organ that relies on tightly regulated organelle turnover to maintain cellular homeostasis and support its energetic demands. Autophagy, once viewed primarily as a non-selective degradation mechanism, is now recognized to encompass specialized pathways — including mitophagy, lipophagy and endoplasmic reticulum-phagy — that mediate cargo-specific quality control of subcellular organelles. These selective programmes form an integrated network that couples stress- and nutrient-sensing regulators with core autophagy machinery and lysosomal capacity, generating cell-type- and context-dependent outputs across distinct nephron segments. Selective autophagy is a central determinant of renal stress adaptation, repair and disease progression. In acute kidney injury, in transition from acute kidney disease to chronic kidney disease and in diabetic kidney disease, selective autophagy preserves organelle homeostasis; however, insufficient, excessive or mistimed autophagic flux drives tubular injury, immune remodelling and fibrosis. Lysophagy, Golgiphagy and nucleophagy are emerging pathways of selective autophagy that might also contribute to the renal stress-response network. Therapeutic strategies that target selective autophagy in the kidney will require carefully timed and precise cell-specific modulation, as well as biomarker-guided patient stratification, to improve efficacy and avoid adverse effects. Here, the authors describe organelle-specific autophagy pathways and explain how renal cells integrate metabolic and stress signals to shape cargo selection and organelle quality control. They also discuss translational challenges in targeting selective autophagy pathways in kidney disease.","PeriodicalId":19059,"journal":{"name":"Nature Reviews Nephrology","volume":"22 8","pages":"559-574"},"PeriodicalIF":46.7,"publicationDate":"2026-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147875068","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}

{"title":"Epidemiology of cardiovascular-kidney-metabolic syndrome.","authors":"Lucas A Mavromatis, Morgan E Grams","doi":"10.1038/s41581-026-01078-w","DOIUrl":"https://doi.org/10.1038/s41581-026-01078-w","url":null,"abstract":"<p><p>Cardiovascular-kidney-metabolic (CKM) syndrome, defined by the American Heart Association in 2023, describes the interconnected risks of metabolic dysfunction, chronic kidney disease and cardiovascular disease. By unifying these conditions, CKM highlights shared pathophysiology, overlapping risk factors and common therapeutic approaches. The staging framework, from ideal CKM health (stage 0) to clinical cardiovascular disease (stage 4), underscores the importance of prevention and captures the escalating risk of morbidity and mortality with advancing stage. Epidemiological data demonstrate increasing global prevalence and that most adults already meet criteria for stage ≥1 CKM syndrome, with stage 2 (defined by metabolic risk factors or the presence of kidney disease) being the most common. The burden of CKM syndrome is characterized by demographic, socio-economic and geographic disparities, with men and older adults most affected. Established determinants of CKM health include genetics, diet, smoking and physical inactivity, as well as social and structural factors; emerging environmental risk factors, such as climate-related stressors, are increasingly investigated but have a less established evidence base. Lifestyle interventions remain foundational and modern therapeutic classes - including glucagon-like peptide-1 receptor agonists, sodium-glucose co-transporter-2 inhibitors and non-steroidal mineralocorticoid receptor antagonists - offer multisystem benefits, although cost, access and variable uptake remain important barriers. Here, we examine current CKM epidemiological evidence and highlight priorities for prevention, equity and future research.</p>","PeriodicalId":19059,"journal":{"name":"Nature Reviews Nephrology","volume":" ","pages":""},"PeriodicalIF":39.8,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147840522","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}

{"title":"Author Correction: Salt and chronic kidney disease","authors":"Jacob Murray,&nbsp;Roos F. Marsman,&nbsp;Rik H. Olde Engberink,&nbsp;Liffert Vogt","doi":"10.1038/s41581-026-01086-w","DOIUrl":"10.1038/s41581-026-01086-w","url":null,"abstract":"","PeriodicalId":19059,"journal":{"name":"Nature Reviews Nephrology","volume":"22 8","pages":"589-589"},"PeriodicalIF":46.7,"publicationDate":"2026-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41581-026-01086-w.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147840532","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}