Kidney international最新文献

{"title":"Vascular endothelial growth factor B-mediated fatty acid flux in the adipose-kidney axis contributes to lipotoxicity in diabetic kidney disease.","authors":"Erika Folestad, Annika Mehlem, Frank Chenfei Ning, Timo Oosterveld, Isolde Palombo, Jaskaran Singh, Hannes Olauson, Anna Witasp, Anders Thorell, Peter Stenvinkel, Kerstin Ebefors, Jenny Nyström, Ulf Eriksson, Annelie Falkevall","doi":"10.1016/j.kint.2024.11.026","DOIUrl":"https://doi.org/10.1016/j.kint.2024.11.026","url":null,"abstract":"<p><p>A common observation in diabetic kidney disease is lipid accumulation, but the mechanism(s) underlying this pathology is unknown. Inhibition of Vascular endothelial growth factor B (VEGF-B) signaling was shown to prevent glomerular lipid accumulation and ameliorated diabetic kidney disease in experimental models. Here, we examined kidney biopsies from patients with Type 2 (84 %) and Type 1 diabetes (16 %), combined with data mining of RNA-seq dataset analyses in patients with diabetic kidney disease. In glomeruli, mesangial cell-derived VEGF-B expression was increased, and glomerular lipid accumulation positively correlated with impaired kidney function. Tubular lipid accumulation also associated with kidney dysfunction but was independent of tubular-derived VEGF-B expression. In vitro, the uptake of the fatty acid analogue, BODIPY-FA, was quantified. VEGF-B treatment increased BODIPY-FA uptake in endothelial cells, whilst pre-incubation with neutralizing antibodies against VEGF-B and its receptor VEGFR1 abolished this uptake. Transcriptome analyses of kidney and white adipose tissue from diabetic macaques showed that VEGF-B expression was higher in white adipose tissue than in kidney, and expression of VEGF-B was increased in white adipose tissue from patients with diabetic kidney disease. Analyzes in diabetic transgenic mice demonstrated that expression of VEGF-B in adipocytes determined the lipolytic activity, dyslipidemia, kidney lipid accumulation and the development of diabetic kidney disease. Overall, VEGF-B is a regulator of kidney lipotoxicity in diabetic kidney disease, by controlling white adipose tissue lipolysis as well as endothelial fatty acid transport in glomeruli. Our data propose that assessment of kidney lipid accumulation, and VEGF-B expression can serve as biomarkers for early diabetic kidney disease.</p>","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":" ","pages":""},"PeriodicalIF":14.8,"publicationDate":"2024-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142846960","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 final frontier: kidney function, omics and deterioration in space","authors":"Vera C. Wulfmeyer, Marlus M. Rinschen","doi":"10.1016/j.kint.2024.11.011","DOIUrl":"https://doi.org/10.1016/j.kint.2024.11.011","url":null,"abstract":"","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":"49 1","pages":""},"PeriodicalIF":19.6,"publicationDate":"2024-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142797871","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":"Allocation biopsies of deceased donor kidneys: a necessary tool to expand the donor pool","authors":"Syed Ali Husain ,&nbsp;Sumit Mohan","doi":"10.1016/j.kint.2024.09.014","DOIUrl":"10.1016/j.kint.2024.09.014","url":null,"abstract":"","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":"106 6","pages":"Pages 1029-1032"},"PeriodicalIF":14.8,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142693122","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":"Corrigendum to “Long-term impact of immediate versus deferred antiretroviral therapy on kidney health in people with HIV.” Kidney International 2024;106:136–144","authors":"Annegret Pelchen-Matthews ,&nbsp;Amanda Mocroft ,&nbsp;Lene Ryom ,&nbsp;Michael J. Ross ,&nbsp;Shweta Sharma ,&nbsp;Steven Coca ,&nbsp;Amit Achhra ,&nbsp;Elaine Cornell ,&nbsp;Russell Tracy ,&nbsp;Andrew Phillips ,&nbsp;Marta Montero Alonso ,&nbsp;Giota Toulomi ,&nbsp;Brian K. Agan ,&nbsp;Nicholas Medland ,&nbsp;Christina M. Wyatt ,&nbsp;INSIGHT START Study Group","doi":"10.1016/j.kint.2024.10.002","DOIUrl":"10.1016/j.kint.2024.10.002","url":null,"abstract":"","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":"106 6","pages":"Page 1196"},"PeriodicalIF":14.8,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142693166","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":"Misuse of the Cox proportional hazards model and alternative approaches in kidney outcome research","authors":"Lingyu Xu ,&nbsp;Yan Xu","doi":"10.1016/j.kint.2024.08.026","DOIUrl":"10.1016/j.kint.2024.08.026","url":null,"abstract":"","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":"106 6","pages":"Page 1186"},"PeriodicalIF":14.8,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142693175","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":"Purinergic receptor P2X7 regulates interleukin-1α mediated inflammation in chronic kidney disease in a reactive oxygen species-dependent manner.","authors":"Maryam Amini, Janina Frisch, Priska Jost, Tamim Sarakpi, Simina-Ramona Selejan, Ellen Becker, Alexander Sellier, Jutta Engel, Michael Böhm, Mathias Hohl, Heidi Noels, Christoph Maack, Stefan Schunk, Leticia Prates Roma, Barbara A Niemeyer, Thimoteus Speer, Dalia Alansary","doi":"10.1016/j.kint.2024.10.024","DOIUrl":"10.1016/j.kint.2024.10.024","url":null,"abstract":"<p><p>Onset, progression and cardiovascular outcome of chronic kidney disease (CKD) are influenced by the concomitant sterile inflammation. The pro-inflammatory cytokine family interleukin (IL)-1 is crucial in CKD with the key alarmin IL-1α playing an additional role as an adhesion molecule that facilitates immune cell tissue infiltration and consequently inflammation. Here, we investigate calcium ion and reactive oxygen species (ROS)-dependent regulation of different aspects of IL-1α-mediated inflammation. We show that human CKD monocytes exhibit altered purinergic calcium ion signatures. Monocyte IL-1α release was reduced when inhibiting P2X7, and to a lesser extent P2X4, two ATP-receptors that were found upregulated compared to monocytes from healthy people. In murine CKD models, deleting P2X7 (P2X7-/-) abolished IL-1α release but increased IL-1α surface presentation by bone marrow derived macrophages and impaired immune cell infiltration of the kidney without protecting kidney function. In contrast, immune cell infiltration into injured wild type and P2X7-/- hearts was comparable in a myocardial infarction model, independent of previous kidney injury. Both the chimeric mouse line harboring P2X7-/- immune cells in wild type recipient mice, and the inversely designed chimeric line showed less acute inflammation. However, only the chimera harboring P2X7-/- immune cells showed a striking resistance against injury-induced cardiac remodeling. Mechanistically, ROS measurements reveal P2X7-induced mitochondrial ROS as an essential factor for IL-1α release by monocytes. Our studies uncover a dual role of P2X7 in regulating IL-1α biogenesis with consequences for inflammation and inflammation-induced deleterious cardiac remodeling that may determine clinical outcomes in CKD therapies.</p>","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":" ","pages":""},"PeriodicalIF":14.8,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142687327","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":"Has APOL1 kidney disease treatment been hiding in plain sight?","authors":"Opeyemi A. Olabisi","doi":"10.1016/j.kint.2024.09.003","DOIUrl":"10.1016/j.kint.2024.09.003","url":null,"abstract":"<div><div>Two coding variants of <em>APOL1</em> account for much of the excess risk of focal segmental glomerulosclerosis in people of recent West African ancestry. There is an unmet need of treatment for apolipoprotein L1 kidney disease. In this issue, Sula Karreci <em>et al.</em> reported that lisinopril reduced proteinuria and glomerulosclerosis in a mouse model of apolipoprotein L1–induced focal segmental glomerulosclerosis, in a genotype-specific manner. By contrast, hydralazine and dapagliflozin had no effect. This study highlights the potential therapeutic utility of angiotensin-converting enzyme inhibitor in apolipoprotein L1 kidney disease.</div></div>","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":"106 6","pages":"Pages 1015-1017"},"PeriodicalIF":14.8,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142693169","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":"journal club","authors":"","doi":"10.1016/j.kint.2024.10.008","DOIUrl":"10.1016/j.kint.2024.10.008","url":null,"abstract":"","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":"106 6","pages":"Pages 1004-1007"},"PeriodicalIF":14.8,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142705913","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 | Acute kidney injury after endovascular aortic graft placement","authors":"Sadia Saboor ,&nbsp;Satoru Kudose ,&nbsp;Miroslav Sekulic","doi":"10.1016/j.kint.2024.10.001","DOIUrl":"10.1016/j.kint.2024.10.001","url":null,"abstract":"","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":"106 6","pages":"Pages 1191-1192"},"PeriodicalIF":14.8,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142693187","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":"New insights into mechanisms underlying cognitive impairment in chronic kidney disease","authors":"Mickaël Bobot ,&nbsp;Stéphane Burtey","doi":"10.1016/j.kint.2024.09.008","DOIUrl":"10.1016/j.kint.2024.09.008","url":null,"abstract":"<div><div>Chronic kidney disease (CKD) is associated with an increased risk of cognitive impairment. Patients with CKD display an increased permeability of the blood–brain barrier. Zimmermann <em>et al.</em> highlighted the implication of potassium efflux in the microglia and its activation, the activation of the interleukin-1b/interleukin-1R pathway, linked to blood–brain barrier permeability and cognitive impairment in CKD. Along with uremic toxicity, this study provides new solid insights about pathophysiological mechanisms of cognitive impairment in CKD, and potential therapeutic targets.</div></div>","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":"106 6","pages":"Pages 1020-1022"},"PeriodicalIF":14.8,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142693178","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}