Pub Date : 2026-04-01DOI: 10.1016/j.kint.2026.01.011
Liwen Zhang,John Cijiang He
Cheng et al. identify aldehyde dehydrogenase 1A1 as a novel risk factor for autosomal dominant polycystic kidney disease, by both activating proliferative pathways and acting as a transcription factor. Targeting aldehyde dehydrogenase 1A1 with disulfiram delays cyst growth in autosomal dominant polycystic kidney disease mice. Combining low-dose disulfiram with anti-programmed death ligand 1 antibody synergistically attenuates cyst progression and improves the immune microenvironment. Although aldehyde dehydrogenase 1A1 upregulation occurs in other kidney diseases and its transcriptional mechanism warrants further study, repurposing aldehyde dehydrogenase 1A1 inhibitors and programmed death ligand 1 blockades may represent a novel strategy for autosomal dominant polycystic kidney disease therapy.
{"title":"ALDH1A1 is a potential novel target for treatment of ADPKD.","authors":"Liwen Zhang,John Cijiang He","doi":"10.1016/j.kint.2026.01.011","DOIUrl":"https://doi.org/10.1016/j.kint.2026.01.011","url":null,"abstract":"Cheng et al. identify aldehyde dehydrogenase 1A1 as a novel risk factor for autosomal dominant polycystic kidney disease, by both activating proliferative pathways and acting as a transcription factor. Targeting aldehyde dehydrogenase 1A1 with disulfiram delays cyst growth in autosomal dominant polycystic kidney disease mice. Combining low-dose disulfiram with anti-programmed death ligand 1 antibody synergistically attenuates cyst progression and improves the immune microenvironment. Although aldehyde dehydrogenase 1A1 upregulation occurs in other kidney diseases and its transcriptional mechanism warrants further study, repurposing aldehyde dehydrogenase 1A1 inhibitors and programmed death ligand 1 blockades may represent a novel strategy for autosomal dominant polycystic kidney disease therapy.","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":"17 1","pages":"646-649"},"PeriodicalIF":19.6,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147493081","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}
Pub Date : 2026-04-01DOI: 10.1016/j.kint.2026.01.007
Dana V Rizk
The treatment of patients with IgA nephropathy at risk of disease progression often requires therapies addressing the underlying immunologic pathogenesis. To date, steroids remain a viable treatment option; however, their use should be balanced against known associated toxicity. Canney et al. developed a prediction tool that utilizes readily available clinical data to calculate the expected response to steroid therapy for an individual patient. This shift to data-informed, patient-specific decision is the essence of personalized care.
{"title":"Predicting steroid treatment benefit in IgA nephropathy: are we ready for precision care?","authors":"Dana V Rizk","doi":"10.1016/j.kint.2026.01.007","DOIUrl":"https://doi.org/10.1016/j.kint.2026.01.007","url":null,"abstract":"The treatment of patients with IgA nephropathy at risk of disease progression often requires therapies addressing the underlying immunologic pathogenesis. To date, steroids remain a viable treatment option; however, their use should be balanced against known associated toxicity. Canney et al. developed a prediction tool that utilizes readily available clinical data to calculate the expected response to steroid therapy for an individual patient. This shift to data-informed, patient-specific decision is the essence of personalized care.","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":"14 1","pages":"649-651"},"PeriodicalIF":19.6,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147493073","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}
Pub Date : 2026-04-01DOI: 10.1016/j.kint.2026.01.008
Marc G Vervloet
This editorial comment discusses novel insights into renal osteodystrophy from a parallel publication, highlighting that uremia per se independently impairs bone cell viability and induces skeletal parathyroid hormone resistance. Using multimodal bone analyses, Wagner et al. show that parathyroid hormone exerts compartment-specific effects: protective for trabecular osteocytes yet detrimental to cortical integrity via increased porosity and by bone fibrosis and increased resorption. These findings redefine optimal parathyroid hormone targets and emphasize addressing uremic toxicity to reduce fracture risk in chronic kidney disease.
{"title":"The Janus face of parathyroid hormone in renal osteodystrophy.","authors":"Marc G Vervloet","doi":"10.1016/j.kint.2026.01.008","DOIUrl":"https://doi.org/10.1016/j.kint.2026.01.008","url":null,"abstract":"This editorial comment discusses novel insights into renal osteodystrophy from a parallel publication, highlighting that uremia per se independently impairs bone cell viability and induces skeletal parathyroid hormone resistance. Using multimodal bone analyses, Wagner et al. show that parathyroid hormone exerts compartment-specific effects: protective for trabecular osteocytes yet detrimental to cortical integrity via increased porosity and by bone fibrosis and increased resorption. These findings redefine optimal parathyroid hormone targets and emphasize addressing uremic toxicity to reduce fracture risk in chronic kidney disease.","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":"2 1","pages":"644-646"},"PeriodicalIF":19.6,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147493080","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}
Pub Date : 2026-04-01DOI: 10.1016/j.kint.2026.01.005
Griffith B Perkins,Maarten Naesens
The 2025 Nobel Prize in Physiology or Medicine was awarded to Mary E. Brunkow, Fred Ramsdell, and Shimon Sakaguchi for their research into mechanisms by which the immune system avoids attacking the body's own tissues. At the heart of this research was the discovery of the regulatory T cell, a peculiar immune cell with the capacity to shut down autoimmunity. This Editorial: Special Report looks at the tenacious science and scientists behind the discovery of the regulatory T cell, and the clinical progress of regulatory T-cell therapies to treat autoimmune kidney diseases and transplant rejection.
{"title":"Nobel prize-winning Treg cells in autoimmune kidney diseases and transplantation.","authors":"Griffith B Perkins,Maarten Naesens","doi":"10.1016/j.kint.2026.01.005","DOIUrl":"https://doi.org/10.1016/j.kint.2026.01.005","url":null,"abstract":"The 2025 Nobel Prize in Physiology or Medicine was awarded to Mary E. Brunkow, Fred Ramsdell, and Shimon Sakaguchi for their research into mechanisms by which the immune system avoids attacking the body's own tissues. At the heart of this research was the discovery of the regulatory T cell, a peculiar immune cell with the capacity to shut down autoimmunity. This Editorial: Special Report looks at the tenacious science and scientists behind the discovery of the regulatory T cell, and the clinical progress of regulatory T-cell therapies to treat autoimmune kidney diseases and transplant rejection.","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":"21 1","pages":"624-629"},"PeriodicalIF":19.6,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147493082","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 Case | A young man with medullary nephrocalcinosis and chronic kidney disease.","authors":"Swathy Raju,Sai Spandana Gollapudi,Thasarathan Senthilkumar,Vellathussery Chakkalakkombil Sunitha,Priyamvada Ps","doi":"10.1016/j.kint.2025.09.007","DOIUrl":"https://doi.org/10.1016/j.kint.2025.09.007","url":null,"abstract":"","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":"50 1","pages":"803-804"},"PeriodicalIF":19.6,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147493075","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 Case | Severe metabolic acidosis with normal anion gap.","authors":"Eléonore Ponlot,Jean-François Cambier,Jean-Philippe Lengelé,Hélène Munyentwali","doi":"10.1016/j.kint.2025.08.021","DOIUrl":"https://doi.org/10.1016/j.kint.2025.08.021","url":null,"abstract":"","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":"3 1","pages":"805-806"},"PeriodicalIF":19.6,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147493071","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}
Pub Date : 2026-04-01DOI: 10.1016/j.kint.2025.08.043
Daniel Weis,Philippe Braconnier
{"title":"Displaced kidneys in a giant inguinoscrotal hernia: an unusual cause of hydronephrosis.","authors":"Daniel Weis,Philippe Braconnier","doi":"10.1016/j.kint.2025.08.043","DOIUrl":"https://doi.org/10.1016/j.kint.2025.08.043","url":null,"abstract":"","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":"17 1","pages":"800"},"PeriodicalIF":19.6,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147493072","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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